NUR202 Pathophysiology & Pharmacology II PDF

NUR202 PATHOPHYSIOLOGY & PHARMACOLOGY II DISORDER OF MUSCULOSKELETAL SYSTEM Rose Heung  OUTLINE Review of Musculoskeletal System Effects of Exercise, Hormones, and Nutrition Diagnostic Procedures for musculoskeletal system Arthritis:...

NUR202 PATHOPHYSIOLOGY & PHARMACOLOGY II DISORDER OF MUSCULOSKELETAL SYSTEM Rose Heung  OUTLINE Review of Musculoskeletal System Effects of Exercise, Hormones, and Nutrition Diagnostic Procedures for musculoskeletal system Arthritis: Osteoarthritis; Gouty Arthritis; Rheumatoid Arthritis Injury and Trauma of Musculoskeletal Structures: Strains; Sprains; Dislocation & Subluxation; Fracture Osteoporosis Prepared by Rose Heung  INTRODUCTION : SKELETAL SYSTEM The Skeletal System Bones of the skeleton Cartilages, ligaments, and connective tissues Prepared by Rose Heung  FUNCTIONS OF THE SKELETAL SYSTEM Primary Functions of the Skeletal System 1. Support 2. Storage of Minerals (calcium) and Lipids (yellow marrow) 3. Blood Cell Production (red marrow) 4. Protection 5. Leverage (force of motion) Prepared by Rose Heung  THE AXIAL SKELETON Forms the longitudinal axis of the body Has 80 bones The skull 8 cranial bones 14 facial bones Bones associated with the skull 6 auditory ossicles The hyoid bone Prepared by Rose Heung  REVIEW OF MUSCULOSKELETAL SYSTEM Prepared by Rose Heung  APPENDICULAR SKELETON 126 bones Allows us to move and manipulate objects Includes all bones besides axial skeleton The limbs The supportive girdles Prepared by Rose Heung  APPENDICULAR SKELETON Prepared by Rose Heung  APPENDICULAR SKELETON Prepared by Rose Heung  BONE (OSSEOUS) TISSUE Bone contains 4 types of cells: 1. Osteocytes 2. Osteoblasts 3. Osteoprogenitor cells 4. Osteoclasts Prepared by Rose Heung  BONE CELL - OSTEOCYTE Mature bone cells that function in the maintenance of bone matrix Play an active role in releasing calcium into the blood Prepared by Rose Heung  BONE CELL - OSTEOBLAST Basic bone-forming cells Synthesize and secrete the organic matrix of bone Participate in the calcification of the organic matrix Prepared by Rose Heung  BONE CELL - OSTEOPROGENITOR CELLS Undifferentiated cells that differentiate to osteoblasts Found in periosteum, endosteum, and epiphyseal growth plate of growing bones. Prepared by Rose Heung  BONE CELL - OSTEOCLAST Responsible for the resorption of bone matrix The release of calcium and phosphate from bone Prepared by Rose Heung  BONE (OSSEOUS) TISSUE Homeostasis Bone building (by osteoblasts) and bone recycling (by osteoclasts) must balance More breakdown than building, bones become weak Exercise, especially weight-bearing exercise, causes osteoblasts to build bone Prepared by Rose Heung  Process of BONE REMODELING The adult skeleton: Bone continually remodels, Maintains itself recycles, and replaces Replaces mineral Turnover rate varies: reserves If deposition is greater Recycles and renews than removal, bones get bone matrix stronger Involves osteocytes, If removal is faster than osteoblasts, and replacement, bones get osteoclasts weaker Prepared by Rose Heung  EXERCISE, HORMONES, AND NUTRITION Effects of Exercise on Bone Mineral recycling allows bones to adapt to stress Heavily stressed bones become thicker and stronger Bone Degeneration Bone degenerates quickly Up to one-third of bone mass can be lost in a few weeks of inactivity Prepared by Rose Heung  EXERCISE, HORMONES, AND NUTRITION Normal Bone Growth and Maintenance Depend on Nutritional and Hormonal Factors A dietary source of calcium and phosphate salts Plus small amounts of magnesium, fluoride, iron, and manganese The hormone calcitriol Made in the kidneys Helps absorb calcium and phosphorus from digestive tract Synthesis requires vitamin D3 (cholecalciferol) Prepared by Rose Heung  EXERCISE, HORMONES, AND NUTRITION Normal Bone Growth and Maintenance Depend on Nutritional and Hormonal Factors Vitamin C is required for collagen synthesis and stimulation of osteoblast differentiation Vitamin A stimulates osteoblast activity Vitamins K and B12 help synthesize bone proteins Growth hormone and thyroxine stimulate bone growth Estrogens and androgens stimulate osteoblasts Calcitonin and parathyroid hormone regulate calcium and phosphate levels Prepared by Rose Heung  HORMONES INVOLVED IN BONE GROWTH & MAINTENANCE Prepared by Rose Heung  JOINTS Body movement occurs at joints (articulations) where two bones connect Determines direction and distance of movement (range of motion or ROM) Joint strength decreases as mobility increases (Source: https://www.researchgate.net/publication/51093 273_Homeostasis_6_Nurses_as_external_control_a gents_in_rheumatoid_arthritis) Prepared by Rose Heung  JOINTS Two Methods of Classification 1. Functional classification is based on range of motion of the joint (a) Synarthrosis (immovable joint) (b) Amphiarthrosis (slightly movable joint) (c) Diarthrosis (freely movable joint) 2. Structural classification relies on the anatomical organization of the joint (a) Bony (b) Fibrous (c) Cartilaginous (d) Synovial Prepared by Rose Heung  MUSCLE TISSUE 3 types of muscle tissue: 1. Skeletal muscle tissue 2. Cardiac muscle tissue 3. Smooth muscle tissue Prepared by Rose Heung  MUSCLE TISSUE 1. “Voluntary” muscles: the actions can be directed by our thoughts via nervous system (skeletal muscles); 2. “Involuntary” muscles: the actions are not under conscious control. Their functions are directed by the autonomic nervous system (cardiac and smooth muscles); Prepared by Rose Heung  FUNCTIONS OF SKELETAL MUSCLE TISSUE Skeletal Muscles Are attached to the skeletal system Allow movement Requires neuronal stimulation for contraction, accounts for ½ of a human’s body weight Prepared by Rose Heung  DIAGNOSTIC PROCEDURES FOR MUSCULOSKELETAL SYSTEM: BLOOD TESTS Test Normal Value Significance of abnormal findings Calcium 8.5 – 10.5 mg/dL Hypercalcemia: e.g. Metastatic bone disease or extended immobilization. Hypocalcemia: e.g. poor dietary intake May lead to osteoporosis in older adults Phosphorus 2.6 – 4.5 mg/dL Usually elevated with calcium Hypophosphatemia: e.g. rare, as phosphate reabsorption in the intestine is efficient. Hyperphosphatemia: e.g. renal failure Alkaline M: 4.5 – 115 units/L ALP increases may indicate bone abnormality (e.g. Paget’s disease, metastatic bone Phosphatase (ALP) F: 30-100 units/L cancer) Myoglobin 50-120mcq/mL Increased myoglobin can indicate myocardial infarction or skeletal muscle destruction Creatine kinase (CK) M: 60-400 units/L Intramuscular injections can cause increase in CK F: 40-150 units/L Isoenzyme CK3 95% - 100% High levels e.g. myositis, trauma (MM) Uric acid M: 3.5-8mg/dL Elevated serum levels indicate gout F: 2.5 – 6.8 mg/dL Prepared by Rose Heung DIAGNOSTIC PROCEDURES FOR MUSCULOSKELETAL SYSTEM Procedure Definition Significance of Nursing Management abnormal findings X-Ray Visualization of skeletal Aids in treatment plan & Instruct patient to remove all metal objects (e.g. abnormality or provide additional necklaces, pins) so they do not block visualization deformity. information of care, e.g. of the body part. Visualize dense or broken ribs demand inflamed tissues and increased attention to joint. respiratory system Computed A noninvasive, yet accurate Obtain informed consent Tomography (CT) radiographic procedure Instruct the patient to lie still during the used to diagnose procedure. Assess the patient for allergies to pathologic conditions (e.g. contrast medium. Patient may need NPO before tumors) test Magnetic Electromagnets provide a Obtain informed consent Resonance three-dimensional Instruct the patient to remove all metal Imaging (MRI) visualization of the area. objects Inform the patient to remain still during the procedure. Ultrasonography High-frequency sound Obtain informed consent (USG) waves (ultrasonic waves) Inform the patient that the jelly-like are directed at internal conducting substance body structures. Prepared by Rose Heung  DIAGNOSTIC PROCEDURES FOR MUSCULOSKELETAL SYSTEM Procedure Definition Significance of Nursing Management abnormal findings Nerve conduction Electromyography (EMG) is Alternations usually indicate a Explain that there may be some discomfort during studies the electrical testing of problem with the nerves or nerve and muscle stimulation as well as when the nerves and muscles the muscles needles are inserted (if needed) Arthrography Contrast medium is Aids in the diagnosis of joint Inform patient that the test is uncomfortable during (Arthrogram) injected into the joint abnormalities e.g. arthritis injection. which is then x-rayed Joint swelling is common after the procedure. May need to apply ice and elevate limb. Discourage physical activity for 12-24 hours after procedure Nuclear Medicine A radioisotope is injected Finding a “hot spot” Inform patient about the procedure scans to help visualize bone and (increased uptake of the other soft tissue radionuclide) usually indicates abnormalities metastases or bone infection Gallium/thallium A radioactive element is Gallium concentrates in areas Inform patient about the procedure scans injected that migrates to of tumours, inflammation, and bone, and inflammatory infections. Thallium detects tissue osteosarcoma Prepared by Rose Heung DIAGNOSTIC PROCEDURES FOR MUSCULOSKELETAL SYSTEM Procedure Definition Significance of Nursing Management abnormal findings Arthroscopy An endoscopic procedure Identifies joint abnormalities Obtain informed consent that provides direct e.g. arthritis Assess color, warmth, circulation and movement visualization of a joint and often. its capsule using an Monitor patient for complications, e.g. swelling instrument inserted into Apply ice, and keep limb elevated if ordered. the space. Arthrocentesis Involves the withdrawal of Establish the diagnosis of joint Obtain informed consent (Joint Aspiration) synovial fluid from a joint abnormalities e.g. joint Monitor for signs of infection e.g. pain, fever, or space. infection, arthritis, neoplasms swelling. Used for analysis of involving the joint. After the procedure, apply ice to decrease pain and synovial fluid or reduction swelling. of excess fluid pressure. Myelography Radiographic visualization Identifies spinal problems e.g. Obtain informed consent (Myelogram) of the subarachnoid space spinal cord tumors, herniated After procedure: Keep bed rest; assess for headache of the spinal canal. intravertebral disk. and nausea (signs of meningeal irritation); head position may be elevated if contrast agent is used. Bone or Muscle Involves need aspiration or Obtain informed consent Biopsy surgical extraction of bone Monitor site of biopsy for bleeding. or muscle tissue Provide normal wound care for open biopsy. Prepared by Rose H eung Perform neurovascular assessment if needed.  COMMON DISORDERS OF MUSCULOSKELETAL SYSTEM Osteoarthritis Gouty Arthritis Rheumatoid Arthritis Prepared by Rose Heung  OSTEOARTHRITIS (OA) Osteoarthritis is a common, age-related disorder of synovial joints. Female > Male : After age 55 years It is characterized by local areas of loss and damage of articular cartilage, new bone formation of joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis and thickening of the joint capsule Primary defect in OA is loss of articular cartilage OA can arise in any synovial joint but is commonly found in the hands, knees, hips and spine Prepared by Rose Heung  RISK FACTOR OF OSTEOARTHRITIS Increasing age (primary risk factor) Obesity Genetic linkage Inactivity Repetitive joint use Prepared by Rose Heung  CAUSES OF OSTEOARTHRITIS Cause Effect on Joint Cartilage Trauma Dislocations or fractures may lead to avascular necrosis or uneven stress on cartilage Mechanical stress Repetitive physical activities (e.g. sports) cause cartilage deterioration Inflammation Release of enzymes in response to local inflammation can affect cartilage health Joint instability Damage to supporting structures causes instability, placing uneven stress on joint cartilage Neurologic Pain and loss of reflexes from neurologic disorders, such as disorders diabetic neuropathy, cause abnormal movements that contribute to cartilage deterioration. Skeletal deformities Congenital or acquired conditions, e.g. dislocated hip Haematologic/ Chronic haemarthrosis (e.g. from haemophilia) contributes to endocrine cartilage deterioration. disorders Prepared by Rose Heung  PATHOPHYSIOLOGY OF OSTEOARTHRITIS The cartilage that lines joints provides a smooth surface, so that the bones of joint glide over one another without friction Normally the cartilage contains water, collagen, and proteoglycans, with other noncollagenous proteins and glycoproteins present in lesser amounts Ratio of water: collagen in cartilage = 10:90; the colour of the fluid should be colourless/in straw colour In OA, proteoglycans and collagen are lost from the cartilage because of degradation ↑ Water content of the cartilage due to the ↓proteoglycan and collagen, the cartilage becomes yellow/brownish gray and loses its tensile strength Surface ulceration occur, fissures develop in deeper layers of the cartilage →large areas of articular cartilage are lost and underlying bone is exposed The bone thickens in exposed areas, ↓ its ability to absorb energy in joint loading Cysts can develop in the bone as synovial fluid leaks through damaged cartilage → inflammation and leading synovitis Prepared by Rose Heung  (Norris, T.L. 2020) Prepared by Rose Heung  CLINICAL MANIFESTATION OF OSTEOARTHRITIS Affecte Clinical Manifestations d Joint Spine Localized pain and stiffness Muscle spasm Limited range of motion Nerve root compression with radicular pain Osteophyte formation may cause vascular compression Hip Pain referred to inguinal area, buttock, thigh, or knee Reduced hip motion Limp or shuffling gait Difficulty getting in and out of chairs Knee Pain on motion Limitation of motion Crepitus Quadriceps atrophy (due to lack of use) (Source: Joint instability https://boroondaraosteopathy.c Genu varus or valgus om.au/knockknees/) se HeuJno g int effusion Prepared by Ro  CLINICAL MANIFESTATION OF OSTEOARTHRITIS Affected Joint Clinical Manifestations First Swelling, tenderness at base of carpometacarp thumb al joint Squared appearance of joint Interphalangeal Bony enlargements of distal joints interphalangeal (DIP) joints: Herberden nodes – occurs more frequently in females Bony enlargements of proximal interphalangeal (PIP) joints: Bouchard nodes Spur formation at joint margins Pain and discomfort after joint use Prepared by Rose Heung Prepared by Rose Heung  DIAGNOSIS OF OSTEOARTHRITIS Medical history Physical examination X-rays of affected joints: ✓ irregular and narrowing of joint space ✓ Spikes ✓ Osteophytes ESR: may be slightly elevated in older adults Synovial fluid: usually is normal Prepared by Rose Heung  TREATMENT OF OSTEOARTHRITIS Focus of treatment: ✓ Symptomatic and includes physical rehabilitative, pharmacologic, and surgical measures. Physical measures: Aimed at improving the supporting structures of the joint and strengthening opposing muscle groups involved in cushioning weight-bearing forces. This includes: a balance of rest and exercise, use of splints to protect and rest the joint, use of heat and cold to relieve pain and muscle spasm, and adjusting the activities of daily living. Weight reduction: when weight-bearing surfaces are involved Use of a cane or walker: if the hips and knees are involved Prepared by Rose Heung  TREATMENT OF Medication Aimed at reducing inflammation or provide analgesia. OSTEOARTHRITIS Oral Medication: NSAIDs e.g. ibuprofen (Brufen) Mild analgesics: Paracetamol Topical medication: NSAID e.g. Diclofenac diethylamine (Voltaren emulgel Mild opioid analgesic: Tramadol , metoclopramide (Maxalon) Intra-articular injection Systemic corticosteroids e.g. prednisolone Intra-articular hyaluronic acid injection: works as a cushioning and lubricating devices in the joints Intra-articular corticosteroid injection: may be used when other treatment measures have been unsuccessful in adequately relieving symptoms e.g. joint effusion OTC dietary supplement Glucosamine sulfate: promote cartilage repair in the joints Surgery Knee joint replacement (Source: For severe pain and loss of joint function https://medlineplus.gov/ency/ E.gPr.epjoariendtbryeRposleaHceeunmg ent article/002974.htm)  GOUTY ARTHRITIS Also known as gout Is a group of disorders characterized by increased serum uric acid (hyperuricaemia) and urate crystal deposits in the kidneys and joints. Male > Female Hyperuricaemia (definies as serum uric acid level ≥ 420 µmol/L for men and ≥ 390 µmol/L for women) may be classified as primary or secondary Primary hyperuricaemia: the disorder is unknown or hereditary error of purine metabolism Secondary hyperuricaemia: related to another acquired disorder Prepared by Rose Heung  CAUSES OF GOUTY ARTHRITIS Acidosis or ketosis Excessive alcohol use Atherosclerosis Chemotherapy drugs Diabetes Mellitus Drug-induced renal impairment Hyperlipidaemia Hypertension Malignant disease Obesity Renal insufficiency Use of certain common drugs e.g. aspirin, diuretics Prepared by Rose Heung  RISK FACTORS OF GOUTY ARTHRITIS Male gender Aging Hypertension Obesity Metabolic syndrome (hyperlipidaemia, hypertension) Type 2 diabetes mellitus Chronic kidney disease Medication: Aspirin, diuretics Consumption of a diet rich in meat and seafood, soft drinks with sugar/fructose Prepared by Rose Heung  PATHOPHYSIOLOGY OF GOUTY ARTHRITIS The pathogenesis of gout resides in an elevation of serum urid acid levels. Uric acid is the end product of purine metabolism and primarily excreted by the kidneys. Normal range of uric acid: Men: 3.5-8 mg/dl; Women 2.8-6.8 mg/dl If uric acid > 8.0mg/dl, the serum is saturated with urate →↑ risk for formation of monosodium rate crystals Hyperuricaemia results from either an underexcretion of uric acid by the kidneys or an overproduction of uric acid ↑ urate levels are present in other extracellular fluids, including synovial fluid and plasma Synovial fluid is poorer solvent for urate →↑ risk for urate crystal formation Monosodium urate may form in the synovial fluid or the synovial membrane, cartilage, or other joint connective tissues Crystal tend to form in peripheral tissues of the body, such as kidneys, these crystals stimulate and continue the inflammatory process, ↑ neutrophils responses by ingesting the crystals → tissue damage and destroy joint cartilage and underlying bone Prepared by Rose Heung  CLINICAL MANIFESTATIONS OF GOUTY ARTHRITIS Acute Gout Chronic Gout Acute pain in 1 or more joints Multiple joint involvement The typical acute attack of gout is Visible deposits of tophi (sodium monoarticular and usually affects the urate crystals) first metatarsophalangeal joint. Location: subchondral bone, Acute gout often begins at night and vertebrae, along tendons and in the may be precipitated by excessive exercise, certain medications (e.g. skin and cartilage Aspirin, Lasix) or food, alcohol, or Infrequent mild attacks or multiple dieting. severe episodes → slowly The tarsal joints, insteps, ankles, heels, progressive disability due to chronic knees, wrists, fingers, and elbows also inflammation and may lead to may be initial sites of involvement. secondary OA Red, hot, swollen and tender joint Fever, chills, malaise paW Pre↑ red B byC Rose Heung  DIAGNOSIS OF GOUTY ARTHRITIS Serum uric acid Blood for CBP, renal function 24 hour urine for uric acid Synovial fluid analysis: ✓A definitive diagnosis of gout can be made only when monosodium urate crystals are in the synovial fluid ✓To exclude other conditions e.g. septic arthritis, pseudogout, and RA X-ray of affected area Prepared by Rose Heung  TREATMENT OF GOUTY ARTHRITIS Objective ✓ termination and prevention of the acute attacks of gouty arthritis ✓ correction of hyperuricemia ✓ consequent inhibition of further precipitation of sodium urate ✓ absorption of urate crystal deposits already in the tissues. Drug Therapy ❑ Aimed at reducing joint inflammation ❑Hyperuricemia and related problems of tophi, joint destruction, and renal problems are treated after the acute inflammatory process has subsided. ✓ NSAIDs e.g. indomethacin, ibuprofen, naproxen (treat acute gout) ✓ Xanthine oxidase inhibitor e.g. Allopurinol (Zyloric) ✓ Colchicine : treat acute gout attack ✓ Corticosteroids: if NSAIDs & colchicine are ineffective e.g. prednisolone Prepared by Rose Heung  TREATMENT OF GOUTY ARTHRITIS Other Treatment ❑ Aim: Maintaining normal uric acid levels and is lifelong ✓ Education about the disease and its management are fundamental to the treatment and management of gout ✓ Lifestyle changes: ▪ Exercise ▪ Maintenance of ideal body weight ▪ Moderation in alcohol consumption ▪ Smoking cessation ▪ Purine restricted diet (low purine diet) ✓ Optimal management of comorbidities: e.g. coronary heart disease, diabetes mellites, hyperlipidaemia, hypertension Prepared by Rose Heung  RHEUMATOID ARTHRITIS (RA) RA is a chronic systemic inflammatory disease with bilateral involvement of synovial or diarthrodial joints. Female > Male : 3 times more frequently than are males Prevalence increases with age Exact cause is unknown It may result from a combination of genetics and environmental triggers The disease often commences insidiously with symmetric involvement (Source: https://www.pennmedicine.org/for-patients- and-visitors/patient-information/conditions-treated-a- of the small joints, such as the fingers, to-z/rheumatoid-arthritis) followed by inflammation and destruction of additional joints Prepared by Rose Heung  ETIOLOGY OF RA Cause of RA remains uncertain, but evidence points to a genetic predisposition and the development of joint inflammation that is immunologically mediated. It has been suggested that the disease is initiated in a genetically predisposed person by the activation of a T-cell-mediated response to an immunologic trigger, e.g. microbial agent. The importance of genetic factors in the pathogenesis of RA is supported by the increased frequency of the disease among first- degree relatives. An important genetic focus that predisposes to RA is present on the human leukocyte antigen (HLA) loci on the MHC class II molecules, with a specific focus on the DRB1 locus. Prepared by Rose Heung  PATHOPHYSIOLOGY OF RA First period of acute attack RA begins with the abnormal immune response, causing inflammation of the synovial membrane with vasodilation, ↑permeability and formation of exudate → typical red, swollen and painful joint Rheumatoid factor (RF), an antibody against immunoglobulin G (Ig-G) and other Ig factors is present in the blood and synovial fluid in most of the patients of RA After the first period of acute inflammation period, the joint may appear to recover completely Prepared by Rose Heung  PATHOPHYSIOLOGY OF RA Subsequent exacerbation, the process continues Synovitis: inflammation recurs, synovial cells proliferative Pannus formation: ▪ Pannus is the destructive vascular granulation tissue which extends from the synovium over the articular cartilage. ▪ The inflammatory cells found in the pannus have a destructive effect on the adjacent cartilage and bone → pannus develops between the joint margins and become fibrotic, leading to reduced joint motion and the possibility of eventual ankylosis. ▪ With progression of the disease, joint inflammation and the resulting structural changes lead to joint instability, muscle atrophy from disuse, stretching of the ligaments, and involvement of the tendons and muscles. Prepared by Rose Heung  CLINICAL MANIFESTATIONS OF RA RA often is associated with extra-articular as well as articular manifestations. It usually has an insidious onset marked by systemic manifestations e.g. fatigue, anorexia, weight loss, and generalized aching and stiffness. The disease is characterized by exacerbations and remissions May involve only a few joints for brief durations, or may become progressive and debilitating. Prepared by Rose Heung  CLINICAL MANIFESTATIONS OF RA ▪ Joint Manifestations ✓Inflammation may be apparent first in fingers, hands, wrists, knees, and feet ✓Affects joints in a symmetric fashion, usually more than 1 pair of joints is involved ✓ Joints appear red & swollen ✓Joint pain and stiffness that lasts for 30 minutes and frequently for several hours ✓Impaired joint movement (pain & fibrosis) Prepared by Rose Heung  CLINICAL MANIFESTATIONS OF RA ▪ Extra-Articular Manifestations ▪ RA is a systemic disease and can accompany with complaints of fatigue, weakness, anorexia, weight loss, and low-grade fever when the disease is active. ▪ Erythrocyte sedimentation rate (ESR) may be elevated during inflammatory processes ▪ Rheumatoid nodules: ✓granulomatous lesions that develop around small blood vessels ✓Typically found over pressure points e.g. extensor surfaces of the ulna Prepared by Rose Heung  DIAGNOSIS OF RA Diagnosis of RA is based on findings of the history, physical examination, and laboratory tests. At least 5 out of 10 possible points must be present to make a diagnosis of RA These criteria consisting of 4 categories: 1. Joint involvement 2. Serology 3. Acute phase reactants 4. Duration of symptoms Prepared by Rose Heung  DIAGNOSIS OF RA ❑ Joint involvement Early stages is difficult to diagnose: Changes in joint structure usually are not visible early in the disease Signs of inflammation e.g. swelling, tenderness, warmth Reduced motion Soft, spongy feeling : due to synovial thickening and inflammation ❑ Serology Rheumatoid Factor (RF): not diagnostic for RA but of value in differentiating RA from other forms of arthritis Antibody to citrullinated peptide (anti-CCP): +ve C-reative protein (CPR): ↑ Serum Erythrocyte Sedimentation Rate (ESR): ↑ HLA-DRB1antigen: +ve ❑ Synovial fluid analysis If inflammation, the synovial fluid has a cloudy appearance Prepared by Rose Heung  TREATMENT OF RA Treatment goals: prevent and/or reduce the pain, decrease stiffness and swelling, maximize mobility, and possibly halt the pathologic process. ▪ Drug Therapy Goal: reduce pain, decrease inflammation, maintain or restore joint function, and prevent bone and cartilage destruction Prepared by Rose Heung  INJURY AND TRAUMA OF MUSCULOSKELETAL STRUCTURES Dislocation Subluxation Sprain 脫位 不全脫位 扭傷 Prepared by Rose Heung  INJURY AND TRAUMA OF MUSCULOSKELETAL STRUCTURES Strains A strain is a stretching injury to a muscle or a musculotendinous unit caused by mechanical overloading. (a) Mild strain: minimal inflammation with swelling and tenderness (b) Moderate strain: partial tearing of muscle or tendon fibers; with pain and inability to move affected body part (c) Severe strain: a muscle or tendon is ruptured, with separation of muscle from muscle, tendon from muscle, or tendon from bone, with severe pain and disability. Causes: ✓ Result from an unusual muscle contraction or an excessive forcible stretch e.g. falls, excessive exercise, lifting heavy objects Most common sites: Lower back and the cervical region of the spine Elbow and the shoulder Foot strain: associated with the weight-bearing stresses of the feet Prepared by Rose Heung  INJURY AND TRAUMA OF MUSCULOSKELETAL STRUCTURES Sprains A sprain, which involves the ligamentous structures (strong bands of connective tissue) surrounding the joint, resembles a strain, but the pain and swelling subside more slowly. Usually caused by abnormal or excessive movement of the joint which may be incompletely torn or completely torn or ruptured. A complete separation of a tendon or ligament from its bony attachment site is known as “avulsion” Common sites: ✓ Ankle joint: most common ✓ Knee joint ✓ Elbow joint ✓ Wrist joint Prepared by Rose Heung  DIAGNOSIS – STRAINS & SPRAINS Clinical manifestations X-rays Musculoskeletal ultrasound Magnetic resonance imagiing (MRI) Arthroscopy Prepared by Rose Heung  TREATMENT – STRAINS & SPRAINS ❑ RICE (Acronym of treatment) ▪ Rest ✓ Immobilization for a muscle strain is continued until the pain and swelling have subsided. ✓ In a sprain, the affected joint is immobilized for several weeks. ✓ ↓ regular daily living activities & exercise as needed ✓ Limit weight bearing on the injured extremity for 48 hours ✓ Use a cane or crutch to avoid weight bearing ▪ Ice ✓ Local application of ice pack to the injured area for < 15 minutes at a time ▪ Compression ✓ Apply compression bandages/splints helps reduce swelling and provides support ▪ Elevation ✓ Keep the injured extremity elevated on a pillow above heart level Prepared by Rose Heung  DISLOCATION & SUBLUXATION ▪ Dislocation: Involves the displacement or separation of the bone ends of a joint with loss of articulation. Simple dislocation: not involve fracture Complex dislocation: with fracture ▪ Subluxation: a partial or incomplete displacement of the joint surface ▪ Causes of Dislocation: Congenital: hip and knee Traumatic: occur after falls, blows, or rotational injuries Pathologic: e.g. complication of infection, rheumatoid arthritis, neuromuscular disease ▪ Common sites: Upper extremity: thumb, elbow and shoulder Lower extremity: hip, kneecap Prepared by Rose Heung  PATHOPHYSIOLOGY OF DISLOCATION & SUBLUXATION Dislocations and subluxations are often accompanied by fracture because stress is placed on areas of bone not normally subjected to stress As the bone separates from the joint, it may bruise or tear adjacent nerves, blood vessels, ligaments, supporting structure and soft tissue Example: Dislocation of shoulder 1. Dislocation of shoulder → damage the shoulder capsule and axillary nerve 2. Damage to the axillary nerves → anaesthesia in the sensory distribution of the nerve and paralysis of the deltoid muscle 3. Torn periosteum, ligaments and muscle frequently accompany elbow dislocations 4. Bleeding from the damaged periosteum and muscles put pressure on adjacent arteries that stop circulation to and from the forearm and hand 5. If the pressure is not promptly relieved, ischemic paralysis develops Prepared by Rose Heung  DISLOCATION & SUBLUXATION Clinical Manifestation Diagnosis Sharp pain Clinical manifestation Soft tissue swelling X-rays Changes in tendon or ligament contour and Arthroscopy dislocation or subluxation of Arthrography bones Limited motion of the affected joint Prepared by Rose Heung  TREATMENT OF DISLOCATION & SUBLUXATION Depends on the site, mechanism of injury and associated injuries, such as fractures Pain management: ✓ NSAIDs ✓ Moist heat Manipulation Surgical repair, immobilization is necessary for several weeks after reduction of a dislocation to allow healing of joint structures Physiotherapy Prepared by Rose Heung  FRACTURES Fracture, or discontinuity of the bone, is the most common type of bone lesion. A fracture occurs when more stress is placed on the bone than it can absorb. 2 basic mechanisms produce fracture: 1. Direct force: e.g. fall or blow 2. Indirect force: e.g. head of the radius or clavicle can be fractured by the indirect forces that result from falling on an outstretched hand There are 3 major categories of fractures: 1. Fractures caused by sudden injury 2. Fatigue or stress fracture: results from repeated wear on a bone e.g. running 3. Pathologic fracture: e.g. spontaneous fracture at the site of the bones that are weakened by disease or tumours Prepared by Rose Heung  CLASSIFICATION OF FRACTURE Fractures are described and classified a/c (1) type, (2) communication or noncommunication with the external environment, and (3) location of the fracture. Initial definitions : Open fracture Closed fracture Fracture 骨折 開放性骨折 閉鎖性骨折 (Source : McRae, 2008) Prepared by Rose Heung  CLASSIFICATION OF FRACTURE ❑ Closed (Simple) fracture If the skin is intact, the fracture is considered a simple fracture ❑ Open (Compound) fracture If the skin integrity is interrupted, the fracture is known as open fracture Often complicated by infection, delayed union ▪ Complete fracture Involve the entire width of the bone ▪ Incomplete fracture Involve only a part of the width of the bone Commonly seen in children Prepared by Rose Heung  CLASSIFICATION OF FRACTURE Fractures can be classified according to the direction and broken pieces of the fracture line. 橫斷形骨折 斜斷形骨折 蝴蝶形骨折塊 旋轉形骨折 粉碎形骨折 分節狀骨折 Prepared by Rose Heung  CLINICAL MANIFESTATION OF FRACTURE Varies according to the type of fracture, site of the fracture and associated soft tissue injury. Manifestation Pathophysiology Pain & Muscle spasm as a result of involuntary reflex action of muscle, direct tissue tenderness trauma, increased pressure on sensory nerve, movement of fracture parts Swelling Oedema due to disruption of soft tissues or bleeding into surrounding tissues Numbness Nerve damage or nerve entrapment Bone deformity Abnormal position of bones secondary to fracture and muscles pulling on fractured bone Crepitus Grating or crunching together of bony fragments, producing palpable or audible crunching sensation Ecchymosis Discolouration of skin as a result of extravasation of blood in subcutaneous tissue Muscle spasms Muscle contraction near the fracture loss of function Decreased function & inability to bear wt. or use the affected part. The pt. Guards & protects the extremity against movement. Prepared by Rose Heung  STAGES OF FRACTURE HEALING Fracture healing occurs in a manner similar to soft-tissue healing. However, a more complex process and takes longer. There are 5 stages of the healing process : 1. Hematoma formation stage 血腫形成期 2. Cellular proliferation stage/granulation tissue 細胞增生期 3. Callus formation stage 骨痂形成期 4. Ossification stage骨化期 5. Consolidation and remodeling 重塑期 Prepared by Rose Heung  STAGES OF FRACTURE HEALING Stage Description Illustration 1. Haematoma formation When a fracture occurs, bleeding forms a haematoma that surrounds the ends of the bone fragment The haematoma is extravasated blood that changes from liquid to a semisolid clot This occurs in the first 72 hours after injury 2. Cellular proliferation During this stage, active phagocytosis /granulation tissue absorbs the product of local necrosis The haematoma converts to granulation tissue Granulation tissue (consisting of new blood vessels, fibroblasts and osteoblasts) forms the basis for new bone substance (osteoid) during days 3-14 after injury Prepared by Rose Heung  STAGES OF FRACTURE HEALING Stage Description Illustration 3. Callus formation As minerals and new bone matrix are deposited in the osteoid, an unorganized network of bone is formed and woven about the fractured parts Callus is primarily composed of cartilage, osteoblasts, calcium and phosphorus It usually appears by the end of the 2nd week after injury Evidence of callus formation can be verified by x-ray 4. Ossification It occurs from 3 weeks to 6 months after fracture and continues until the fracture has healed Callus ossification is sufficient to prevent movement at the fracture site when the bones are gently stressed In this stage, the patient may be allowed limited mobility or the cast may be removed Prepared by Rose Heung  STAGES OF FRACTURE HEALING Stage Description Illustration 5. Consolidation and Ossification continues and occurs when an x- remodeling ray shows complete bone union This phase can occur up to 1 year after injury Excess bone tissue is resorbed in the final stage of bone healing, and union is complete Bone remodels in response to physical loading stress Prepared by Rose Heung  COMPLICATIONS OF FRACTURE HEALING Direct complications: problems which caused by the fracture bone(s) Complication Description Infection A high incidence from open fracture & soft tissue injury Delayed Failure of fracture to heal within predicted time as union determined by x-ray Time frame cannot be set, but usually considered as ~8-9 months after a fracture Malunion Bony consolidation of fracture site, but in an anatomically incorrect position (Deformity) Nonunion Failure of bone to heal before the process of bone repair stops Has not shown radiographic progress for 3 months Prepared by Rose Heung  COMPLICATIONS OF FRACTURE HEALING Indirect complications: associated with blood vessel and nerve damage resulting in conditions of the following: Compartment syndrome 間室症候群 Deep Venous Thrombosis 深層靜脈栓塞 Fat Embolism syndrome 脂肪栓塞 Hypovolemic shock Prepared by Rose Heung  COMPARTMENT SYNDROME The muscles and nerves of an extremity are enclosed in tough, inelastic fascia often termed a muscle compartment. If the pressure in the compartment is sufficiently high, tissue circulation is compromised, causing death of nerve and muscle cells. Permanent loss of function may occur. Causes: Restrictive dressings, splints, casts, excessive traction or premature closure of fascia ↑ compartment volume: e.g. bleeding, inflammation, oedema, or intravenous fluids infiltration. Compartment syndrome is usually associated with trauma, fractures (especially of long bones), extensive soft tissue damage and crush injury. Prepared by Rose Heung Prepared by Rose Heung  CLINICAL MANIFESTATION OF COMPARTMENT SYNDROME 6 “P”s Pain (severe pain which cannot be relieved by opiod analgesics) Pallor Paralysis (weakness in movement) or loss of function (very late symptom) Paresthesia (numbness & tingling): due to nerve compression Pulselessness (diminished/absent peripheral pulses) Poikilothermia (the extremity is cool to touch) Prepared by Rose Heung  DIAGNOSIS OF COMPARTMENT SYNDROME Pain assessment Examination of sensory & motor function: Sensory function: light touch and two-point discrimination Motor function: movement and muscle strength Doppler: confirm the existence of a pulse Intra-compartmental measurement: Normal intra-compartmental pressure: ▪ between 0 mmHg to 8 mmHg. When the pressure increases to within 10 mmHg to 30 mmHg , this indicates inadequate perfusion and relative ischemia of the involved extremity Prepared by Rose Heung  TREATMENT & COMPLICATIONS OF COMPARTMENT SYNDROME Reduce compartmental pressure Remove restrictive dressing, casts/splints Fasciotomy Incision into the fascia that encloses the compartment to allow the tissue to expand and relieves the pressure The surgical wound remains open until the pressure decrease The close the wound Complications: Tissue necrosis, nerve damage, infection, contracture, cosmetic deficit, amputation, rhabdomyolysis (muscle break down releases myoglobin which is harmful to the kidneys) or renal failure & ultimately death Prepared by Rose Heung  FACTORS INFLUENCING BONE HEALING Positive Factors Negative Factors Local Immobilization Local Delay in correction of Timely correct of displacement displacement Open fracture Application of ice Presence of foreign body at Electrical stimulation fracture site Systemic Adequate amounts of Systemic Immunocompromised status growth hormone, vitamin D Decrease circulation (DM, and calcium PVD) Adequate blood supply Malnutrition Absence of infection or Osteoporosis diseases Advanced age Younger age Moderate activity level prior to injury Prepared by Rose Heung  DIAGNOSIS OF FRACTURE ▪ Diagnosis is the first step in the care of fractures and is based on: History Physical examination X-ray : confirm the diagnosis and direct the treatment Prepared by Rose Heung  TREATMENT OF FRACTURE The goals of treatment include: 1. Reduction 復位: anatomic realignment of bone fragments 2. Immobilization 固定: to maintain realignment 3. Rehabilitation復健 : Restoration of function of the injured part. Prepared by Rose Heung  FRACTURE REDUCTION 1. Closed reduction閉鎖(合)性復位 2. Traction牽引術 3. Open reduction開放性復位 Prepared by Rose Heung  FRACTURE REDUCTION ▪ Reduction: When bones are realigned to restore their original structure Closed reduction (closed manipulation by traction) Open reduction : correction of bone alignment through a surgical incision, including internal fixation with wires, screws, pins, plates or nails Prepared by Rose Heung  TRACTION is the application of a pulling force for medical purposes, to treat muscle or skeletal disorders Example: to reduce a fracture, maintain bone alignment, relieve pain, or prevent spinal injury. usually applied to the arms, legs, spine, or the pelvis treat fractures, dislocations, and long-duration muscle spasms, and to prevent or correct deformities. Prepared by Rose Heung  SKIN TRACTION Skin traction is applied by strapping the patient’s affected lower limb and attaching weights. Prepared by Rose Heung  BALANCED SUSPENSION SKELETAL TRACTION Uses : Femoral fracture Hip fracture Pelvic and acetabular fracture Prepared by Rose Heung  IMMOBILIZATION AND FIXATION ▪ Immobilization: prevents movement of the injured parts is the single most important element in obtaining union of the fracture fragments. External devices, e.g. splints, casts, traction External fixation devices: consists of a frame connected too pins that are inserted perpendicular to the long axis of the bone Internal fixation devices inserted during surgical reduction of the fracture. Prepared by Rose Heung Prepared by Rose Heung (Source : http://www.nlm.nih.gov/medlineplus/ency/imagepages/18021.htm)  (Source : http://www.nlm.nih.gov/medlineplus/ency/imagepages/1 8023.htm) Prepared by Rose Heung  DRUG TREATMENT OF FRACTURE Analgesic: to relieve pain e.g. Tramadol, Panadol NSAIDs : to decrease inflammation and supplement analgesia Prophylactic antibiotics : Prevent infection e.g. cephalosporin Prevent muscle spasms: Central and peripheral muscle relaxants Prevent deep vein thrombosis: Anticoagulants may be prescribed if surgery or prolonged immobilization Stool softeners: To prevent constipation due to the adverse effect of narcotics and immobility Antacids: reduce the adverse effect of NSAIDS (cause GI bleeding) Prepared by Rose Heung  OSTEOPOROSIS Osteoporosis, or porous bone (fragile bone disease) is a chronic, progressive metabolic bone disease characterized by low bone mass & structural deterioration of bone tissue, leading to increased bone fragility and fractures Female > Male (Normal bone) (Osteoporotic bone) Prepared by Rose Heung (WHO, 2004)  PATHOPHYSIOLOGY OF OSTEOPOROSIS Secondary osteoporosis is associated with many conditions: ▪ Endocrine disorders e.g. hyperthyroidism causes an acceleration fo bone turnover ▪ Malignancies secrete the osteoclast-activating factor, causing significant bone loss ▪ Alcoholism : Alcohol is a direct inhibitor of osteoblasts and may also inhibit calcium absorption ▪ Certain medications e.g. Corticosteroid use is the most common cause of drug-related osteoporosis, and long-term corticosteroid use in the treatment of disorders such as rheumatoid arthritis is associated with a high rate of fractures. Prepared by Rose Heung  PATHOPHYSIOLOGY OF OSTEOPOROSIS The exact pathophysiology is unclear Most data suggest an imbalance between bone resorption and formation such that bone resorption exceeds bone formation → thin, fragile bones that are subject to spontaneous fracture Hormonal factors play a significant role in the development of osteoporosis, which leads to an imbalance in osteoclast and osteoblast activity: ✓ In women, bone loss further increases after menopause (with loss of oestrogen), then slow but does not stop at about age 60 ✓ While testosterone levels in men decline with aging, this is a more gradual process and associated bone loss occurs more slowly Osteoporosis affects the bones consisting of higher proportions of cancellous bone and a predisposition to fractures of the vertebrae and femoral neck. Early stages are asymptomatic Prepared by Rose Heung  RISK FACTORS OF OSTEOPOROSIS Personal Characteristics Lifestyle Advanced age Sedentary Female Calcium deficiency White/Asian ethnicity Excessive alcohol intake Low body weight Excessive caffeine intake Postmenopausal Smoking Family History Drug and Disease Related Aluminum-containing antacids Gastrectomy Anticonvulsants Diabetes mellitus Heparin Chronic obstructive lung disease Corticosteroids or Cushing Malignancy disease Hyperthyroidism Hyperparathyroidism Prepared by Rose Heung Rheumatoid arthritis Prepared by Rose Heung  CLINICAL MANIFESTATION OF OSTEOPOROSIS Progressive curvature of the spine Fractures : hip, pelvis, humerus etc Loss of height: due to collapse of vertebrae Kyphosis: commonly referred to as dowager hump Low back pain Prepared by Rose Heung 脊柱後彎 kyphosis/dowager’s hump  DIAGNOSIS OF OSTEOPOROSIS Dual-energy x-ray absorptiometry (DEXA/DXA)雙能量 X 光 吸收測量儀 of the spine and hip ▪ most commonly taken to measure bone density and diagnose osteoporosis Values of T-score -1 or above : normal -1 to -2.5 : osteopenia (low bone density) ≦ -2.5 : osteoporosis Quantitative ultrasound (QUS) ▪ for screening purpose, not suitable for diagnosis Prepared by Rose Heung  REFERENCES Adams, M., Holland, N., & Urban, C. (2020). Pharmacology For Nurses: A Pathophysiologic Approach, (4thed.). Edinburgh Gate: Pearson. Greene, W.B. (2006). Netter’s Orthopaedics. Philadelphia: Saunders Elsevier. Huether, S.E., McCance, K.L., Brashers V.L., Tote, N.S. (2017). Understanding Pathophysiology. (6th ed.). St. Louis, MO: Mosby/Elsevier. (Book available in library). Norris, T., & Porth, Carol. (2020). Porth's essentials of pathophysiology (5th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. (Book available in library) Prepared by Rose Heung