Rheumatology PDF

Rheumatology Autoimmune disorders - one of two things happen (sometimes both): 1. T cells attack body’s own tissues, and/or 2. auto-immune complexes form in the blood and deposit in the tissues (type III hypersensitivity) B and T cells (lymphoid cells) have memory...

Rheumatology Autoimmune disorders - one of two things happen (sometimes both): 1. T cells attack body’s own tissues, and/or 2. auto-immune complexes form in the blood and deposit in the tissues (type III hypersensitivity) B and T cells (lymphoid cells) have memory cells that prompt them into action episodic – triggered: meaning you can have “FLARE-UPS” of the disease where it gets worse. What organs are typically attacked? Eyes, Lungs, Heart, Blood Vessels, Skin, Joints. 1. The eyes Inflammation and scarring. Some people with RA develop inflammation of the whites of the eyes (scleritis) that can lead to scarring. Symptoms include pain, redness, blurred vision and light sensitivity. Usually treatable with prescription medication Dryness. The inflammatory process can damage the tear-producing glands, a condition known as Sjögren’s syndrome. Sjorgren’s syndrome no tears (& no saliva) inflammation of the secretory glands Can result from: RA, SLE, AS, MS, sarcoidosis, psoriatic arthritis Depending on the particular disease, there can be inflammation of every structure of the eye; can lead to cataracts, glaucoma, blindness Drug effects. Corticosteroids may cause glaucoma and cataracts. 2. Mouth Dryness. Inflammation can damage the moisture-producing glands of the mouth resulting in a dry mouth. Good dental hygiene is a must, as bacteria tend to flourish in a dry mouth, leading to tooth decay and gum disease. Drug effects. Methotrexate can cause mouth sores or oral ulcers. 3. Lungs Inflammation and scarring. Up to 80 percent of people with RA have some degree of lung involvement, If severe, prolonged inflammation of the lung tissue can lead to a form of lung disease called pulmonary fibrosis. Nodules. Rheumatoid nodules might form in the lungs Drug effects. Methotrexate can cause methotrexate pneumonia 4. Heart Pericarditis. Inflammation of the heart lining, the pericardium, Causes pain interferes with pumping of blood to and through the heart. Atherosclerosis. Chronic inflammation can damage endothelial cells that line the blood vessels Damaged vessels will absorb more cholesterol and form plaques. Heart attack and stroke. Plaques from damaged blood vessels can break off and block a vessel, leading to heart attack or stroke. risk of heart attack for people with RA was 60 percent higher just one year after being diagnosed Drug effects. Some RA medications may reduce cardiovascular risk 5. Blood vessels Vasculitis can cause restricted blood flow to extremities. Especially through the small distal vessels. Decreased blood flow to the nerves may cause –neuropathies – 6. Skin - Nodules. ½ of people with RA develop rheumatoid nodules – sometimes disappear on their own or with treatment with disease-modifying antirheumatic drugs (DMARDs). Rashes. Vasculitis of the skin, a rash of small red dots is the result. Can cause skin ulcers on the legs or under the nails. Drug effects - Corticosteroids to reduce inflammation, can cause thinning of the skin and susceptibility to bruising 7. Joints Immune system attacks the synovium — the lining of the membranes that surround your joints. inflammation thickens the synovium, - which can eventually destroy the cartilage and bone within the joint. Immune complexes are deposited in the joints - causing even more damage to the joint surfaces. Bones – osteoporosis - Chronic inflammation from RA leads to loss of bone density, Drug effects. - Corticosteroids can also cause bone thinning. Rheumatoid arthritis (RA) a chronic systemic inflammatory disease of unknown cause. An external trigger causes an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation potential for extra-articular manifestations. 1% prevalence, most commonly shows up in the 30s and 40s Predominantly affects woman - 3:1 ratio. genetic propensity environment – immune system response may be initiated by a virus? Bacteria? hormone component –especially sex hormones - improves in pregnancy and worsens or “flares” post-pregnancy Rheumatoid factor – an antibody produced by the immune system, is present in many diagnosed with RA but doesn’t have to be present Early in the disease = PIPs and MCPS in both hands OA is opposite where the DIPs and PIPs are more involved in the joints of highest use (wear and tear). As the disease progresses more joints may become involved. Length of time the morning stiffens lasts is often used as a measure of disease severity and/or a flare. The longer the stiffness the worse the sign. Classic sign is joint destruction over time and deformity Inflammatory Progression: Active inflammation is first seen in the synovial membranes of the joints, which become red and swollen. Later, a layer of roughened granulation tissue, or pannus, protrudes over the surface of the cartilage. Under the pannus the cartilage is eroded and destroyed. Joints can become fixed in place (ankylosed) by thick and hardened pannus Breakdown of adjacent ligaments and cause subluxation of the joints Pressure on surrounding structures may lead to tendon rupture Specific Deformities As the disease progresses, deformities may form from the ongoing joint destruction of the inflammatory process. Due to overstretching and rupture of tendons Boutonniere’s - Hyper-extension of MCP, Flexion of PIP, Hyper-extension of DIP Swan Neck - Flexion of MCP, Hyper-extension of PIP, Flexion of DIP Ulnar Drift - Ulnar deviation at the MCP joints and radial deviation at the wrist (radiocarpal joint) Z Deformity - at the thumb - consists of hyperextension of the interphalangeal (IP) joint, and fixed flexion and subluxation of the metacarpophalangeal (MCP) joints Flat foot - tenosynovitis of tib. post tendon resulting in loss of longitudinal arch. Hallux valgus (bunion) – valgus deformity at MTP joint Cock up toes – subluxation of MTP joints – dorsiflex -of MTPs, with plantarflex -of PIPs & DIPs Claw toe – MTP hyper-ext, PIP and DIP flexed Mallet toe – MTP neutral, PIP neutral, DIP flexed Hammer toe – MTP hyper-ext, PIP flexed. DIP hyper-ext Nodules Usually indicates more severe disease. (sero +ve) firm, noticeable lumps underneath the skin Typically appear in the following locations: Fingers and knuckles, Elbows, Forearms, Knees, Backs of heels Meds – critical importance for managing pain, decrease inflammation and slow the progression of the disease to prevent deformity and loss of function Acetaminophen – Tylenol – may cause liver damage from long term use. NSAIDS non-steroidal anti-inflammatories– burn out the stomach can lead to kidney damage from long term use Steroids – can cause multiple side effects (eg. Glaucoma) Disease-modifying anti-rheumatic drugs (DMARDs). Can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate  Biologics (Humira & Remicade) – immunosuppressants – suppress the immune system increasing risk of other infection Rehab in RA Joint Protection Exercise Pain management Juvenile rheumatoid arthritis - AKA juvenile idiopathic arthritis most common type of arthritis in children under the age of 16. 1-2/1000 children (< age 16) persistent joint pain, swelling and stiffness. Some have symptoms for only a few months, while others have symptoms for the rest of their lives. Sx begin between ages 3-7 Cause –autoimmune same as adult RA precipitated by infection Classic differences between adult RA and JRA- Kids often don’t take the disease into adulthood (but can last months to years) Affects larger joints in kids (hips and knees) Usually more acute than the adult type of RA Pauciarticular - 4 joints or fewer Polyarticular – 5 or more joints Systemic onset - Still’s disease More rapid onset, more tissues involved that just joints Systemic pathology: skin rashes, pericarditis (pericardial sac inflammation), enlargement of spleen & liver Still’s Dz Secondary effects – loss of aerobic capacity (w/c users) complications from meds – steroids (osteoporosis, moon face, deposition of fat on the trunk) Rx – orthotics, rest during acute episodes, ex. when not acute, assistive devices 75% go into remission in adolescence Ankylosing spondylitis or AS, affects primarily the spine causes inflammation of the spinal joints (vertebrae) that can lead to severe, chronic pain and stiffness. Genetic predisposition (HLA-B27) Onset 15-40 years, men 3:1 Inflammation of the SI joints., lumbar spine, thoracic spine, costovertebral joints, manubriosternal joints Classic sign of AS is “bamboo” spine on x-ray. A flattening or loss of normal spinal lordosis, narrowing of intervertebral space and a fusion of the joints. Other complications might include: Eye inflammation (uveitis). eye pain, sensitivity to light and blurred vision. Compression fractures. increasing the severity of stooped posture. Heart problems. can cause problems with the aorta Treatment Meds – biologics (expensive: $10,000-30,000/yr) Exercises for spinal extension, respiratory expansion of chest, yoga Psoriatic Arthritis Chronic rheumatic inflammatory condition with Inflammation of joints and skin (psoriasis) and occasionally systemic symptoms. (Sero-negative) S & S – synovitis mainly in distal joints of hands & feet, but can also be sacroiliac jts., spine There are 5 types Rehab – rest strategies, heat & ex. for hands & other affected joints Arthritis Mutilans – the most severe form Reiter’s Syndrome Men 25:1, ages 30-40 (35) Etiology unknown- usually occurs 1-4 weeks after a venereal or intestinal infection S & S - Synovitis knees, ankles, feet; connective tissue of Achilles tendon & plantar fascia, LBP, swollen fingers & toes, rash on feet, hands, genitalia, mouth ulcers, urethritis, uveitis, conjunctivitis, & sacroiliitis Rehab - Address pain, joint problems & muscle weakness Connective Tissue Diseases Scleroderma hardening and tightening of the skin and connective tissues Some beyond the skin — such as blood vessels, internal organs and the digestive tract. Signs and symptoms vary, depending on which structures are affected. women > men most commonly ages of 30 and 50. no cure treatments can ease symptoms and improve quality of life. Mild form – tightening of skin of face & hands, Raynaud's Syndrome –bilateral/symmetrical vasospasm triggered by cold or stress) Severe form – scarring in heart, lungs, (often causing death), kidneys (many deaths), & esophagus, 70% have lung involvement Systemic lupus erythematosus (SLE), also known simply as lupus, Systemic, chronic autoimmune inflammatory disease. Primarily involving collagen. Common symptoms include: painful and swollen joints, Fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes Fatigue, red rash which is most commonly on the face, Flare-ups and periods of remission when there are few symptoms Discoid lupus – skin rash only with no organ involvement Intense inflammation develops in the skin, particularly in sun-exposed areas. More severe symptoms of SLE include: Bilateral jt. Pain, stiffness & swelling, Malar rash Skin lesions that appear or worsen with sun exposure (photo sensitive) Vasculitis – (Raynaud’s phenomenon/disease) SOB due to pleurisy, pleural effusions Pericarditis – chest pain Kidney damage/failure Dry eyes, alopecia Headaches, confusion, memory loss, coma Fibromyalgia (FM) Chronic pain heightened pain response to pressure. Fatigue affecting normal sleep problems restless legs syndrome sensitivity to noise, lights or temperature. Fibromyalgia is frequently associated with depression, anxiety, and posttraumatic stress disorder. Other types of chronic pain are also frequently present. Have 11 out of 18 points on the body of hypersensitivity to palpation (not trigger points as no referral of pain) Exercise is the most successful treatment to date. Temporal arteritis Chronic inflammation of major (large) arteries: carotid, aorta, femoral, subclavian, temporal sudden onset symptoms: blindness, severe temporal and/or occipital head-aches, TIA, stroke, MI PMR chronic and systemic condition associated with giant cell arteritis. Women 2:1 over the age of 60 Similar symptoms to arthritis (aching, stiffens with pain) in neck, low back, shoulders, & legs (mostly inflammation in shoulder and pelvic girdles) Rx – meds to reduce pain and stiffness, exercise to maintain mobility Myofascial Pain syndrome Not the same as fibromyalgia or polymyalgia rheumatica. Key feature is Trigger points – hyperirritable bands of taut muscle with specific and predictable referral patterns Polyarteritis Nodosa Systemic vasculitis affects the collagen and connective tissue of the skin systemically. Inflammation of small and medium arteries resulting in nodule formation in walls of arteries joint, muscles, kidneys, GI tract, reproductive organs, & skin  Prognosis is poor if left untreated. May develop into generalized vasculitis and cause death Complex Regional Pain Syndrome; Reflex Sympathetic Dystrophy Unknown cause - Trauma precipitates onset of disturbance in vasomotor control of limb (upper > lower) Why some people with the same conditions develop RSD other don’t is unknown severity of the injury is not related to the severity of RSD. S&S: - Severe pain- out of proportion for injury, Edema Trophic changes; Skin changes – thins, shines, sweats, acutely sensitive, excessive hair growth Sarcoidosis Systemic Granulomas (lumps of tissue) develop in lymph nodes, lungs, liver, eyes, skin, joints, muscles, & nervous system S&S – fatigue, chest pain, shortness of breath, skin lesions, & jt. Pain Prognosis – often self-limiting 24-36 months; but widely variable from complete recovery, to permanent damage, to death Sjorgren’s syndrome Mucous membrane dysfunction due to autoimmune response Immune system destroys salivary and lacrimal (tear) glands (minimal diagnostic criteria) women 9:1 50% - primary with no other disease process or, 50% secondary to another autoimmune disease (eg RA) S & S - Dry eyes & mouth Myasthenia Gravis autoimmune disorder where antibodies block, alter or destroy the receptors for ACH (acetylcholine) at the synapse in the neuromuscular junction resulting in muscle weakness. Etiology Sometimes related to thymus tumor – B and T cells Example of type II hypersensitivity reaction (immune mediated) 3 Forms 1. Ocular form – weakness of the eye lid causing ptosis and diplopia 2. Generalized form – eye and facial muscle weakness 3. Severe Form - Ptosis – one or both eyes, Blurred or double vision (diplopia), Unstable or waddling gait, Facial paralysis, Dysphagia, dysarthria, Weakness of respiratory muscles Inflammatory Myopathies Several types of inflammatory myopathies exist including polymyositis and dermatomyositis S & S - Gradual or sudden weakness in shoulder, shoulder girdle, and neck muscles due to T cells attacking muscle fibers May be triggered by virus or other autoimmune disorder (RA, SLE, scleroderma, Sjorgen’s) “myositis” = muscle weakness Polymyositis – includes CHF, pericarditis, wt. loss Dermatomyositis – includes facial rash along with other symptoms that may progress to upper body, mainly on extensor aspects of limbs. Rx – meds, rehab – energy conservation, careful exercises, for shoulder girdle strengthening  Neurology Forms of dementia: Alzheimer’s Lewy Body Disease (AD, Parkinson’s, hallucinations) Vascular dementia secondary to other neurological disorders (Huntington’s, MS, TBI, Down Syndrome, meds) growing body of evidence that Alzheimer’s is related to insulin resistance Alzheimer’s Very Mild Forgetfulness Problems coming up with the right word or name Losing common objects (keys) Mild Trouble remembering names when introduced to new people Trouble with planning or reading comprehension Challenges performing some ADLs or challenges at work Losing or misplacing a valuable object Moderate Forgetfulness of recent events or about one's own personal history Trouble with planning and organization of daily tasks Feeling moody or withdrawn Mod. Severe Confusion about time, place, day, or what season it is Personality and behavioral changes Trouble controlling bladder and bowels in some individuals Changes in sleep patterns Severe May need round-the-clock assistance with daily activities and personal care Lose awareness of recent experiences as well as of their surroundings Worsening changes in sleep-wake Changes in physical abilities Have increasing difficulty communicating Very Severe Most of time in bed, help with feeding Incontinent Limited recognition of loved ones, if at all Coma ALS 1500 – 2000 Canadians currently have ALS Usually aged 55 – 65; as young as 20 5-10% genetic; rest is of unknown cause Recent studies indicate a protein responsible for nerve repair becomes ineffective Hyperreflexia – CNS damage leads to return of primitive reflexes like Babinski, or loss of protective reflexes like gag CVA Ischemic strokes (loss of blood flow) Hemorrhagic strokes (bleeding in the brain) Types of ischemic stroke 1. Thrombotic stroke Diseased or damaged cerebral arteries blocked by the formation of a blood clot within the brain. 2. Embolic stroke is a clot within an artery forms somewhere other than in the brain itself, often from the heart. Emboli travel in the bloodstream until they become lodged in the brain. Hemorrhagic- A diseased blood vessel within the brain bursts Blood leaks inside the brain. Usually occurs in selected parts of the brain: basal ganglia, cerebellum, brain stem, or cortex. Common cause is hypertension (high blood pressure) Signs of a stroke: Sudden numbness or weakness of the face, arm or leg, especially on one side of the body. (facial droop) Sudden confusion, trouble speaking or understanding. (slurred speech) Sudden trouble seeing or blurred vision in one or both eyes. Sudden headache. Sudden trouble walking, dizziness, loss of balance or coordination Circle of Willis At the base of the brain, the carotid and vertebrobasilar arteries form a circle of communicating arteries known as the Circle of Willis. From this circle, other arteries arise and travel to all parts of the brain. anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA) If one of the main arteries in the circle is occluded, distal smaller arteries can receive blood from other arteries (collateral circulation). The middle cerebral artery is the artery most often occluded in stroke. Epilepsy - Types: Absence- brief loss of conscious Atonic – loss of motor tone Myoclonic – jerking, twitching Tonic-clonic – LOC, stiffness, shaking, loss of B&B Partial Sz – affect smaller parts of the brain (simple or complex) Guillain-Barre the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. symmetrical weakness and abnormal sensations spread to the arms and upper body. Can lead to near-total paralysis. life-threatening - potentially interfering with breathing ventilator to assist with breathing if required Can have good recovery even from severe cases of GBS, but it can be very slow approx. 20% still are unable to walk without assistance at 6 months Huntington disease (HD) an inherited brain disorder. causes cells in parts of the brain to die: specifically, the caudate, putamen, and, as the disease progresses, the cerebral cortex becomes less able to control movements, recall events, make decisions and control emotions. Multiple Sclerosis 1. Primary Progressive: constant progression of symptoms 2. Relapsing Remitting: flares with return to near baseline, very slow progression. Diagnosed by MRI – plaque build ups in the brain show up as white >2 on MRI = MS Characteristics o CNS demyelination  sensory changes and muscle weakness o Visual disturbance o Ataxia o Cognitive and emotional changes o Bowel and bladder control o Fatigue o Body temperature homeostasis Neuropathy Interference with nerve conduction that affects the periphery of the body Motor, sensory, or autonomic Variety of causes Weakness, sensory disturbance, other Parkinson’s Disease Destruction of cells in the substantia nigra that produce dopamine Tremor, atrophy, cogwheel rigidity, bradykinesia, mask-face, shuffling gait, imbalance, etc. Post-polio syndrome Secondary to Poliomyelitis infection earlier in life Theory: motor neurons not affected earlier during poliomyelitis infection become fatigued and over-worked leading to post-polio syndrome Avoid fatiguing patients with a history of polio SCI C1-6 = quadriplegia (above C3 low survival rate) C6-8 = complete hand, trunk, legs paralysis (will have some shoulder/elbow movement) T1-12 = paraplegia L1-5 = paraplegia Functional impact depends on the level of injury and complete vs incomplete SCI Know the important levels associated risks TBI Mild, moderate, or severe Contra-coupe injury Loss of consciousness, headache, dizziness, changes in behaviour/personality, altered cognition Possible motor and sensory deficits  Genetic & Hereditary Chromosome Diseases and Pediatric Neurological Conditions Teratology – Study of embryonic/fetal developmental malformations Chromosomes 23 pairs of chromosomes (contain genes coded within our DNA) 22 pairs of autosomal chromosomes and 1 pair of sex chromosomes - Male XY; female XX. Females receive an X chromosome, and males receive a Y chromosome from the father A genetic disorder is a genetic problem caused by one or more abnormalities in the genome, especially a condition that is present from birth (congenital). Autosomal Dominant one mutated copy of the gene will be necessary for a person to be affected Each affected person usually has one affected parent. The chance a child will inherit the mutated gene is 50% if one parent has the gene Autosomal Recessive Two copies of the gene must be mutated for a person to be affected Both parents must be carriers or have the disease Two unaffected people who each carry one copy of the mutated gene have a 25% risk with each pregnancy of having a child affected by the disorder. X-linked dominant Caused by mutations in genes on the sex chromosome - X Only a few disorders have this inheritance pattern, 50% chance of inheriting if one parent is affected X-linked recessive Also caused by mutations in genes on the X chromosome. Males are more frequently affected than females Sons of a man with an X-linked recessive disorder will not be affected (they receive his Y chromosome) ○ Daughters will carry one copy of the mutated gene. (Carrier only) A woman who is a carrier has a 50% chance of having sons who are affected ○ 50% chance of having daughters who are carriers. Teratogens: non-genetic factors that interfere with normal embryonic and fetal development and morphogenesis. In general, the fetus is more sensitive to major deformity earlier in gestation. 1-2 weeks- often results in death of the fetus (spontaneous miscarriage) 3-8 weeks- risk of major morphological abnormalities (heart, upper limbs, neurological system) 8-36 weeks- functional deficits and minor morphological deficits Children exposed to teratogens in utero will not pass their defect on to their children. Not a genetic condition. Sometimes they can mimic genetic disorders but are not The four important factors in teratogenicity are 1. Time. 3. The genotype of the fetus. 2. Dosage. 4. The genotype of the mother. Common teratogens are: Alcohol, smoking, drugs, viruses, uncontrolled diabetes Chromosome Abnormalities Some types of chromosomal abnormalities are inherited, but most are not Many are due to a random structural abnormality in a chromosome Deletion: A portion of the chromosome is missing or deleted. Translocations: A portion of one chromosome is transferred to another chromosome. Inversions: a portion is broken off and flipped over and reattached Duplications: A portion of the chromosome is duplicated, resulting in extra genetic material. Down Syndrome Extra chromosome – trisomy of chromosome #21 Exact cause unknown, but more common in babies born to mothers over 40. (older mothers) S&S At risk for Mild to moderate cognitive impairment underdeveloped intestines & intestinal Characteristic facial features - Eyes that problems have an upward slant, oblique fissures increased risk of congenital heart Flat nasal bridge defects Protruding tongue Developmental dysplasia of the hips Small stature and short neck Hearing deficits Single, deep creases across the center C1/C2 laxity of the palm (called Simean) hypotonic/low tone & often have Large space between first and second slower motor development (seen in toe rehab) A single flexion furrow of the fifth finger early cognitive decline – dementia Fragile X sex (x) linked dominant disorder detected with DNA testing named due to fragile section on X chromosome (Also known as Martin-Bell syndrome) Etiology – can become worse from generation to generation as the fragile section becomes more fragile. S&S low intelligence and learning difficulties. Speech and language challenges Behavioral challenges - ADD, ADHD (said to have a sluggish nervous system that needs stimulation). Identifying physical features – narrow long face, big ears, flat feet Girls affected by the condition are often less severely affected Klinefelter Chromosomal abnormality affecting males - additional X chromosome (XXY) S&S - Abnormalities of the sexual organs: Low testosterone, breast development, small testicles ADHD, learning disability may have comorbidities: osteoporosis, auto-immune disorders, depression, lung disease Patau Rare chromosomal disease. Usually from trisomy of chromosome #13 S&S severe neurological impairments, microcephaly, heart defects, cleft palate, Prognosis - high mortality – usually die by 3 days of age due to the number of congenital defects (especially neuro impairments/lack of brain development). Few survive to teenagers – delayed motor development Turner Syndrome cause unknown only affects females -lack an X chromosome S&S tend to not develop secondary sex characteristics (breasts, pubic hair) short stature, growth inhibition, non-functioning ovaries, infertility Tend to have short webbed necks and wide chest with nipples far apart. Higher incidence of – type 2 diabetes, aorta defects, high blood pressure, among others Developmental Diseases, Birth Injuries and Multifactorial Disorders Conditions Cerebral Palsy a group of neurological disorders that appear in infancy or early childhood and permanently affect body movement and muscle coordination caused by damage to or abnormalities inside the developing brain that disrupt the brain’s ability to control movement and maintain posture and balance. The term cerebral refers to the brain; palsy refers to the loss or impairment of motor function. The majority of children have congenital cerebral palsy (born with it) A small number of children have acquired cerebral palsy, (begins after birth) The following types of brain damage may cause its characteristic symptoms: Damage to the white matter of the brain (periventricular leukomalacia). Abnormal development of the brain (cerebral dysgenesis). Bleeding in the brain (intracranial hemorrhage). Severe lack of oxygen in the brain (anoxia). Doctors classify CP according to the type of movement disorder involved -- ○ spastic (stiff muscles) ○ athetoid (writhing movements) ○ ataxic (poor balance and coordination) ○ plus any additional symptoms, such as weakness (paresis) or paralysis (plegia). Spastic cerebral palsy - the most common type of the disorder Characteristics of stiff muscles and awkward movements. Types: Spastic hemiplegia/hemiparesis typically affects the arm and hand on one side of the body, but it can also include the leg. Spastic diplegia/diparesis involves predominantly the legs and less severely affects the arms Spastic quadriplegia/quadriparesis is the most severe form of cerebral palsy often associated with moderate-to-severe intellectual disability. Dyskinetic cerebral palsy (also includes athetoid, choreoathetoid, and dystonic cerebral palsies) characterized by slow and uncontrolled writhing/jerky movements of hands, feet, arms, or legs. Hyperactivity of the muscles in the face and tongue  grimacing or drooling. Some have problems hearing, controlling their breathing, and/or coordinating the muscle movements required for speaking. Intelligence is rarely affected in these forms of cerebral palsy. Ataxic cerebral palsy affects balance and depth perception. Children will often have poor coordination and walk unsteadily with a wide-based gait. Hypotonic cerebral palsy- low muscle tone - noticeably weaker muscle tone than normal. generally caused by damage to the cerebellum Mixed types of cerebral palsy refer to symptoms that don’t correspond to any single type of CP but are a mix of types. Classification of Severity – Gross Motor Functional Classification System A 5-level system looking at movements such as sitting, walking and use of mobility devices. CP Co-morbidities: Seizures Incontinence Intellectual impairments Depression Vision/Speech/Hearing deficits Osteopenia / osteoporosis Sensory deficits Orthopedic conditions Birth Injuries Erb’s palsy paralysis of the arm caused by injury to the upper group of the arm’s nerves Damage or severing of the upper trunk C5-C6 nerves, part of the brachial plexus Sensation loss “Waiter’s tip” deformity Klumke’s paralysis involves the muscles of the forearm and hand brachial plexus injury affecting the 8th cervical (C8) and 1st thoracic (T1) nerve roots. Affects the intrinsic muscles of the hand and the flexors of the wrist and hand. “Claw hand” deformity where the forearm tends to lie flat and the wrist and fingers are flexed. Neural tube defects during development. Caused by failure of the neural tube closure before 28 days of gestation. Most common spina bifida, anencephaly, encephalocele One of the most common congenital anomalies / birth defects world-wide (WHO). Spina Bifida spina bifida occulta – small defect in vertebral ring occurs in 15% of people and many don’t know they have it. No deficits meningocele – meninges protrude posteriorly – usually surgically repaired right after birth myelomeningocele – spinal cord and meninges protrude through vertebral deficit and the skin – likely to have neurological damage Higher rates prior to 1998. Since, all flour must be fortified with folic acid, which reduces neural tube deficits by ½ Comorbidities of Spina Bifida Hydrocephalus – ”water on the brain” due to a blockage of CSF in the brain ventricular system. Chiari II malformation – due to downward pull of spinal cord on the brainstem & cerebellum Zika Virus Infection during pregnancy can cause severe birth defects including microcephaly and blindness primarily spreads through infected mosquitoes or sex with someone infected. Autism, or autism spectrum disorder, a range of conditions characterized by challenges with communication skills and behaviour 1 in 50 children are currently diagnosed with autism spectrum disorder. The prevalence of ASD has increased by over 100% in the last 10 years. Now the fastest-growing and most commonly diagnosed neurological disorder in Canada. ASD is caused by a combination of genetic and environmental influences. Fetal Alcohol Spectrum Disorder FASD describes the impacts to the brain and body that can occur when an unborn baby is exposed to alcohol. (teratogen) A lifelong disorder with effects that include physical, mental, behavioural and learning disabilities. can vary from mild to severe. Chiari Malformations (p. 304-305) Chiari malformation Type I (most common form of CM) Only the lower part of the cerebellum extends into the foramen magnum. Chiari malformation Type II Symptoms usually appear during childhood. Can cause life-threatening complications during infancy or early childhood, treatment is surgery. Both the cerebellum and brain stem tissue protrude into the foramen magnum. Nerve tissue that connects the two halves of the cerebellum may be missing or only partially formed. Usually accompanied by a myelomeningocele — form of spina bifida Chiari malformation Type III very rare and the most serious form. some of the cerebellum and the brain stem stick out, or herniate, through an abnormal opening in the back of the skull. This can also include the membranes surrounding the brain or spinal cord. cause debilitating and life-threatening complications. Similar symptoms to Type II but can also have additional severe neurological defects such as mental and physical delays, and seizures. Chiari malformation Type IV incomplete or underdeveloped cerebellum (a condition known as cerebellar hypoplasia). rare form of CM, the cerebellum is in its normal position but parts of it are missing, and portions of the skull and spinal cord may be visible. Premature Birth defined as a baby born before 37 weeks or weighing less than 2500 grams (5 ½ lb.) Age of viability –most doctors define the age of viability as being about 24 wks of gestation. In many hospitals, 24 weeks is the cut-off point when doctors will use intensive medical intervention to attempt to save the life of a baby born prematurely. high risk for hyaline membrane disease (HMD), AKA neonatal respiratory distress syndrome Rhesus Disease/Hemolytic Disease of the Newborn Rh factor incompatibility between mother and baby If first baby (+) and mom is (–), mom develops antibodies against the +Rh factor at time of birth when their blood mixes Then on subsequent pregnancy, mom’s blood attacks the second baby’s (+) blood causes anemia in baby, if severe, baby dies in utero or suffers neurological damage Example of immune type 2 hypersensitivity response Scoliosis Congenital (autosomal dominant) or idiopathic 2% of pop., girls twice as often than boys Often first observed around the age of 10. Can be a “C” or “S” curve Measure the curve on x-ray to monitor for progression. Treated first with bracing (TLSO) may require surgical fixation for severe curves and if progress even with bracing. (orthopedically fixated) Genetically-Linked Diseases Hemophilia Inheritance by X chromosome-linked recessive gene (affects males only) Variable deficiency in clotting agents There are two main types of haemophilia: haemophilia A and haemophilia B. Low clotting factors VIII or IX Muscular Dystrophy X-linked recessive disorder. Usually affects boys. Girls (only a single copy of the defective gene) have mild symptoms Dystrophin strengthens muscle fibres and protects them from injury as they contract & relax Muscular dystrophy ○ group of diseases that cause progressive weakness and loss of muscle mass. ○ abnormal genes (mutations) interfere with the production of proteins needed to form healthy muscle. Duchenne’s usually begins around age 4 and worsens quickly. weakness starts in the pelvis and lower extremities, then progresses to trunk & UE’s starts proximally and moves distally in the extremities usually lose the ability to walk by age 12. typically die in their late teens or early adulthood due to respiratory insufficiency Becker’s similar to Duchenne’s but symptoms begin later and progress much slower. starts proximally & moves distally in UE’s & LE’s Sickle Cell  Autosomal recessive (both parents need to be carriers) 25% chance 80% of African-Canadians are carriers of some traits related to sickle cell anemia related to resistance to malaria RBCs (erythrocytes) contain abnormal hemoglobin that forms inflexible rods rather than the donut-shaped RBCs. Sickle-shaped cells rupture easily and reduce O2 delivery and clog arteries. cells live only 10-20 days compared to 90-120 days, so it causes anemia. Spinal Muscular Atrophy Autosomal recessive “Floppy infant syndrome” or Werdnig Hoffman disease Progressive destruction of the Anterior Horn Cells of the lower motor neurons (similar to polio) with death occurring ages 3-7 Death is by respiratory insufficiency Congenital heart defect (CHD) also known as a congenital heart anomaly or congenital heart disease, a problem in the structure of the heart that is present at birth. Signs and symptoms depend on the specific type of problem. Tetralogy of Fallot (TOF) is a congenital heart defect that is present at birth. The cause is typically not known. Risk factors include: a mother who uses alcohol, has diabetes, >age of 40, or rubella during pregnancy. also associated with Down syndrome. Classically there are four defects: 1. a ventricular septal defect, a hole between the two ventricles 2. pulmonary stenosis, narrowing of the exit from the right ventricle 3. right ventricular hypertrophy, enlargement of the right ventricle 4. an overriding aorta, which allows blood from both ventricles to enter the aorta Cancer a disease of uncontrolled and abnormal growth of cells in the body. Malignancy or tumor resulting from the division of abnormal cells. Biological Principles of Cancer Oncogenesis –the formation of a cancer. Normal cells are transformed into cancer cells; Requires development of self-sufficiency in growth signal May begin when one of the cells gets damaged or altered and breaks free of normal controls. Loss of sensitivity to normal anti-growth signals. (tumor suppressors) Cell divides without a signal to do so and continues to divide b/c it doesn’t responds to normal signals to stop dividing. Develops into a tumor. Apoptosis – loss of sensitivity of normal cell death (apoptosis). Immortality – cancer cells can divide and live forever. Nutrition – altered metabolic properties (can attract more nutrients than other cells) Speed of reproduction – higher mutation rates (reproduce quickly) genetic mutation. Angiogenesis - ability to attract blood vessels (angiogenesis) develops its own blood supply. Allows the tumor to receive increased nutrients and continue the increased growth rate Metastasis – the capacity to invade other tissues to travel from the site of the original tumor to distant locations in the body. (accountable for about 90% of deaths from cancer) Colonization - failure of the colonized organ. Cancer takes over the organ and it loses its original function Death Neoplasm An abnormal mass of tissue doesn’t contribute to homeostasis referred to as a tumor The study of neoplasia = oncology Benign Means “harmless” A “Non-cancerous” tumor or a “non-malignant” tumor Does not invade nearby tissue or spread to other parts of the body the way cancer can but takes up space Retains cellular differentiation. ie. The cells has the same appearance as the original cells. Usually a slower growth rate, do not metastasize, have smooth borders, little vascularity and rarely reoccur. Can progress to cancerous (tumor progression) Premalignant Cells at risk for becoming malignant Cells proliferate but don’t spread Categorize them Mild to severe. There are different ways of describing precancerous changes based on how mild or severe the changes are: Hyperplasia - abnormal cells are dividing and increasing in number faster than normal. Atypia - cells are slightly abnormal (atypical). Metaplasia - there has been a change to the types of cells that are normally found in this area of the body. Dysplasia – cells are abnormal, there are more cells than normal, the cells are growing faster than normal and they aren’t arranged like normal cells. Dysplasia is a precancerous condition. Carcinoma in situ - is the most severe type of precancerous change. The cells are very abnormal but have not grown into nearby tissue. Carcinoma in situ is usually treated because it has a high risk of developing into cancer. Malignancy not self-limited in its growth, and is capable of invading adjacent tissues, and may be capable of spreading to distant tissues. Spread via blood, lymph, or seeding (travel across hollow organs and start to grow). Cells do not look like the host tissue cells, they are “undifferentiated” Appear irregular and not encapsulated. They are invasive and out of control. They are highly vascularized and recur readily. Usually ends in “sarcoma” or “carcinoma” depending on the embryonic layer from which the cells originated Metastasis Spread of cancer cells to other organs Organ of origin is the name of the cancer (e.g. melanoma can metastasize in the liver but it’s still melanoma, osteosarcoma in the lung is still an osteosarcoma) There are common metastatic patterns Certain types of cancer cells require specific tissue conditions to proliferate. Seed and soil theory: specific “seeds” (cancer cells circulating in the body) will grow better in certain “soils” (different organ tissues). Travel through the circulatory or lymph systems Angiogenesis Growth of new blood vessels as cancer cells develop their own blood supply. Feed rapid growth rate and high metabolic needs of the cancer cells. Cancerous cells mutate to produce angiogenic activators – attract capillary growth Sentinel Lymph Node First lymph node cancer cells are most likely to spread to Commonly checked via biopsy Carcinogen substance capable of causing cancer in a living tissue. Many factors interact to disrupt normal cell growth and division. Internal factors such as heredity, immunology, and hormones External factors such as chemicals, viruses, diet, and radiation. only 5% of cancers can be linked to chemical exposure. The chief causes of cancer are lifestyle factors: diet, cigarette smoke, alcohol, and sun exposure. Dietary factors - associated with 35% of all human cancers Cigarette smoke - another 30%. Agents that cause cancer (carcinogens) can be classified as genotoxic or nongenotoxic Genotoxins cause irreversible genetic damage or mutations by binding to DNA. Include chemical agents or non-chemical agents such as ultraviolet light and ionizing radiation. Nongenotoxic means they can cause cancer without direct damage to the DNA After the carcinogen enters the body, the body makes an attempt to eliminate it Certain viruses can also act as carcinogens by interacting with DNA. Stages of Carcinogenesis Cancer develops through four definable stages: initiation, promotion, progression and malignant conversion. These stages may progress over many years. Initiation, A change in the genetic makeup of a cell. May occur randomly or when a carcinogen interacts with DNA causing damage. Initial damage rarely results in cancer because the cell has in place many mechanisms to repair damaged DNA. If repair does not occur and the damage to DNA is in a location on the gene that regulates cell growth and proliferation, DNA repair, or a function of the immune system, then the cell is more prone to becoming cancerous. Promotion The mutated cell is stimulated to grow and divide faster and becomes a population of cells. Eventually a benign tumor becomes evident. Hormones, cigarette smoke, or bile acids are substances that are involved in promotion. This stage is usually reversible as evidenced by the fact that lung damage can often be reversed after smoking stops. Progression, there is further growth and expansion of the tumor cells over normal cells. Genetic material of the tumor is more fragile and prone to additional mutations. Mutations occur in genes that regulate growth and cell function such as oncogenes, tumor suppressor genes, and DNA mismatch-repair genes. This contributes to tumor growth until conversion occurs, Conversion, when the growing tumor becomes malignant and possibly metastatic. Many of these genetic changes have been identified in the development of colon cancer and thus it has become a model for studying multi-stage carcinogenesis. Staging systems for cancer The TNM staging system = Tumour, Node, Metastasis. The system also uses numbers to describe the cancer. T = size of the cancer and how far it has spread into nearby tissue – it can be 1, 2, 3 or 4, N = if the cancer has spread to the lymph nodes – 0 = no lymph nodes containing cancer cells Up to 3 = lots of lymph nodes containing cancer cells M = has it spread to another part of the body – 0 = cancer hasn't spread or 1 = cancer has spread Number Staging Stage 0 = cancer in situ still located in the place it started and has not invaded nearby tissues. Asymptomatic, almost undetectable often highly curable, by removing the entire tumour with surgery. Stage I = small cancer or tumour that has not grown deeply into nearby tissues has not spread to the lymph nodes or other parts of the body. size increased, but still fairly small. May start to produce symptoms Stage II and III = cancers or tumours that are larger in size Has grown more deeply into nearby tissue. Starting to spread and invade/displace tissues Spread to lymph nodes, but not to other parts of the body. Stage IV = cancer has spread to other organs or parts of the body. Cancer has its own blood supply and may be quite large in size. Has metastasized to other tissues. Difficult to treat. Grading A lower grade indicates a slower-growing cancer and a higher grade indicates a faster-growing one. Grade I – cancer cells that resemble normal cells and aren't growing rapidly Grade II – cancer cells that don't look like normal cells and are growing faster than normal cells Grade III – cancer cells that look abnormal and may grow or spread more aggressively Another grading system is… Tumors are graded as 1, 2, 3, or 4, depending on the amount of abnormality. Grade 1 = the tumor cells and the organization of the tumor tissue appear close to normal. These tumors tend to grow and spread slowly. Grade 2 = Moderately abnormal Grade 3 and Grade 4 = tumors that do not look like normal cells and tissue. Grade 3 and Grade 4 - tend to grow rapidly and spread faster than tumors with a lower grade. Medical Treatments Surgery – Who Has Surgery? Surgery works best for solid tumors that are contained in one area. It is a Local treatment, not used for leukemia (a type of blood cancer) or for cancers that have spread. Sometime sole treatment, but most often combined with another Tx. Remove the entire tumor - If it is contained in one area. Debulk a tumor - Removes some, but not all, of a tumor. Used when removing an entire tumor might damage an organ or the body. Removing part of a tumor can help other treatments work better. Ease cancer symptoms - Surgery is used to remove tumors that are causing pain or pressure. Palliative Chemotherapy – Often used with other forms of treatment & often used when cancer has metastasized. Works by stopping or slowing the growth of cancer cells Can be given oral, IV, Injection, intrathecal (Spinal), intraperitoneal, intra-arterial, topical How Chemotherapy Is Used with Other Cancer Treatments: Make a tumor smaller before surgery or radiation therapy. (called neoadjuvant chemotherapy) Destroy cancer cells that may remain after surgery or radiation therapy. (called adjuvant chemotherapy) Can Help other treatments work better. Kill cancer cells that have returned or spread to other parts of your body. Side Effects Kills or slows the growth of healthy cells too Ex. cells that line your mouth and intestines and those that cause your hair to grow. Leads to mouth sores, nausea, and hair loss. The most common side effect is fatigue or exhaustion Radiation – Used to treat cancer and ease cancer symptoms (curative or palliative) At high doses, RT kills cancer cells or slows their growth by damaging their DNA. Cancer cells with DNA damaged beyond repair stop dividing or die and can be removed from the body. Takes days or weeks of treatment before DNA is damaged enough for cancer cells to die. External Beam Radiation Therapy Aims radiation at the cancer. The machine does not touch you but can move around you and send radiation into a part of your body from many directions.  Local treatment - meaning it treats a specific part of your body. Ex. Lung Ca = RT to chest NOT whole body Internal Radiation Therapy Source of radiation is put inside your body. (Can be solid or liquid) Targeted Therapy – targets the changes in cancer cells that help them grow, divide, and spread. How they work- Most targeted therapies help treat cancer by interfering with specific proteins that help tumors grow and spread throughout the body. 1. Help the immune system destroy cancer cells. Mark cancer cells so it is easier for the immune system to find and destroy them. 2. Stop cancer cells from growing. Interfere with the proteins on cancer cells' surface, preventing them from telling the cells to divide. 3. Deliver cell-killing substances to cancer cells. Monoclonal antibodies are combined with toxins, chemotherapy drugs, and radiation. Once these monoclonal antibodies attach to targets on the surface of cancer cells, the cells take up the cell-killing substances, causing them to die. 4. Cause cancer cell death. Some targeted therapies can cause cancer cells to go through this process of cell death. Angiogenesis inhibitors Stop signals that help form blood vessels. Without a blood supply, tumors stay small or shrink. Immunotherapy Helps your immune system fight cancer Hormone Therapy cancer treatment that slows or stops the growth of cancer that uses hormones to grow. Stem Cell Transplant – restore blood-forming stem cells in people who have had theirs destroyed by the very high doses of chemotherapy or radiation therapy that are used to treat certain cancers. Blood-forming stem cells are important because they grow into different types of blood cells. WBC for immune, RBC for O2 transport, Platelets for clotting Skin Conditions The skin is the body’s largest organ. It serves many important functions, including: 1) Protecting the body against trauma 2) Protecting the internal environment from the external environment 3) Regulating body temperature 4) Maintaining water and electrolyte balance 5) Sensing painful and pleasant stimuli 6) Participating in vitamin D synthesis Skin is an organ of the body and is made up of 3 main layers: 1. Outer layer – Epidermis (5 sub-layers) 2. Middle layer – Dermis (2 sub-layers) 3. Inner layer subcutis / subcutaneous layer Epidermis - no blood vessels - relies on the dermis layer for nutrients Relatively thin, tough, outer layer of the skin. Most of the cells in the epidermis are keratinocytes. Keratinocytes originate in the deepest basal layer. New keratinocytes slowly migrate up toward the surface of the epidermis layer. As keratinocytes reach the skin surface, they are gradually shed and are replaced by newer cells pushed up from below. The surface is called the Stratum corneum It is relatively waterproof and prevents most bacteria, viruses, and other foreign substances from entering the body. Thicker where greater protection is needed. Melanocytes in the basal layer produce the pigment melanin, the main contributor to skin color. Melanin’s primary function is to filter out ultraviolet radiation from sunlight, which damages cellular DNA. Dermis The dermis, the skin's next layer, is a thick layer of fibrous and elastic tissue mostly collagen, with a small, important component of elastin that gives the skin its flexibility and strength. The dermis contains: nerve endings, sweat glands, oil (sebaceous) glands, hair follicles, and blood vessels. Nerve endings sense pain, touch, pressure, and temperature. The fingertips and toes contain many more nerves than other body parts and are extremely sensitive to touch. Sweat glands produce sweat in response to heat and stress. As sweat evaporates off the skin, it helps cool the body. Sebaceous glands secrete an oil into hair follicles that keeps the skin moist and soft. Hair follicles also coming from the dermis have a number of important physical roles including: regulating body temperature, providing protection from injury, and enhancing sensation. A portion of the follicle also contains stem cells capable of re-growing damaged epidermis. Blood vessels of the dermis provide nutrients to the skin and help regulate body temperature. Heat makes the blood vessels enlarge (dilate), allowing large amounts of blood to circulate near the skin surface, where the heat can be released. Cold makes the blood vessels narrow (constrict), retaining the body's heat. Fat layer Below the dermis lies a layer of fat Helps insulate the body from heat and cold, provides protective padding, and serves as an energy storage area. The fat is contained in living cells, called fat cells, held together by fibrous tissue. The fat layer varies in thickness, from a fraction of an inch on the eyelids to several inches on the abdomen and buttocks. Sensory Nerve Endings Free nerve endings – (dermis & epidermis) pain & itching, discrimination in fingers and toes Ruffini corpuscles – (hair follicles in dermis) pressure sensation – slow-acting Ruffini end organs – warmth sensation Pacinian corpuscles (deep dermis) – vibration sensation Krause end bulb (superficial dermis) – cold sensation Merkel’s endings/disc – (in hairy skin) touch sensation Meissner’s corpuscles – (in hairless skin) touch sensation Burns Current system: Superficial (epidermis) Superficial partial thickness (epidermis & into the papillary dermis) Deep partial thickness (epidermis, papillary dermis and into the reticular layer) Full thickness (epidermis & dermis and into the superficial fat) Fourth degree – bone, muscle Superficial burn – Layer of skin – Epidermis Appearance – red = erythema Inflammation duration – 5-10 days Scarring? No Painful? Yes Superficial partial thickness – Layers of skin – epidermis and papillary/superficial dermis Danger of infection? yes Healing time – ~10 days – epithelium lines the hair follicles and migrates over to missing areas (2-3 weeks for full healing). Painful? yes, free nerve endings are intact Deep Partial Thickness - Layers of skin – epidermis and dermis - has destroyed collagen (strength, elasticity, & extensibility.) What structures are destroyed? sweat glands, free nerve endings (pain & itching), Krause end bulbs (cold), Merkel’s discs (touch), Pacinian corpuscles (vibration), Ruffini end organs (heat)/corpuscles (pressure) Painful? not at the center of the wound, but yes at the margins Scarring? yes Does it require surgery? often excision & grafting. Healed skin is dry and flaky due to loss of sebaceous & sweat glands. Healing time – 3-8 weeks Full Thickness - Layers of skin – Epidermis, dermis & underlying fat. Does it require surgery? Yes, excision of eschar and grafting Painful? Not where all layers of tissue are lost, but pain at the graft sites, and edges Healing time – Months to heal completely (if at all) Electrical burns What does the current follow? Follows the route of least resistance (blood vessels, heart, & kidneys, nerves) Entry & exit burns often full thickness. Full extent of injuries are often not known right away. Current can interfere with cardiac function. Burn Classifications Areas of burn wound may have areas of different classifications within the same wound Typically classified into Burn zones (3) 1) coagulation – irreversible cell damage, skin dies, eschar forms, high risk of infection 2) stasis – cells may die if no intervention within 48 hours after injury 3) hyperemia – minimal cell damage and recovery within a few days. A major complication after a burn injury is often infection in the wound. Also, smoke inhalation lung injuries and resultant pneumonias increase morbidity risk. Wound treatment Wounds may be debrided – cleaning the wound by removing the dead and non-viable tissue to allow healthy tissue to grow. Larger wounds that are deeper may need to be covered with a skin graft. Most grafts are fenestrated or cut like mesh This allows the donor tissue to cover a larger area and to allow the tissue to stretch with movement. Success of the graft depends largely on an adequate blood supply Capillaries penetrate grafts 48-72 hours Grafts: Full thickness- both epidermis and dermis taken from the graft site Split thickness- epidermis and some dermis grafted Autograft (from self) grafted from an area of viable skin somewhere on the pt. Permanent Allograft – (from another human) typically a cadaver. Will slough off once the patient’s epidermis heals below the graft. Xenograft - (non-human) typically a pig, as it’s histologically closest to human Pressure Garments - Used to minimize the risk of Keloid scarring and hypertrophic scarring. Keloid scar – an excessive amount of healed tissue that extends beyond the parameters of the wound. Hypertrophic scar – is a raised scar but it stays within the parameters of the wound Frostbite damages the skin and sometimes the underlying tissue as a result of exposure to extreme cold. Higher risk in extremities. Frostnip- epidermis layer - fingers, nose, ears, erythema, no loss of sensation Superficial – losing sensation, moving into the dermis layer. May appear white, hard Deep – freezing of fat, subcutaneous layer. Tissue will die and become black due to necrosis. Dead tissue cannot recover. May need to be cut away to allow tissue below to heal. Joints are vulnerable (poorly vascularized) Wind up with stiffness & muscle atrophy If prolonged exposure to cold temperatures. The body moves to preserve vital organs and shunts blood from the periphery to the core. Hypothermia = core temp 35 C (95 F) or colder, Normal = 37 C (36.5-37.5) S & S – limb numbness, sleepiness, confusion, shivering, slurred speech, bradypnea (slowed breathing) Conditions Affecting Hair Alopecia areata, also known as spot baldness, is a condition in which hair is lost from some or all areas of the body. Alopecia totalis is the loss of all skull and facial hair. Autoimmune Hirsutism is excessive body hair in men and women on parts of the body where hair is normally absent or minimal Infection of Skin Cellulitis Infection and inflammation of dermal and subcutaneous layers of skin. Common on the lower legs. Incidence is higher in people that are obese, with diabetes, or malnutrition Methicillin-resistant staph aureus (MRSA) is a common antibiotic-resistant cause Vancomycin resistant enterococci. Vancomycin is an antibiotic medication. Used to treat MRSA infections, but there are bacteria that are now resistant to it. Can infect many different areas of the body Impetigo Assoc. with malnutrition and poor living conditions Bacteria colonize cuts, bites, open areas  Contagious – people scratch and spread it to other parts of the body Rx – antimicrobial meds Fungal Spread by contact – swimming pool deck areas, infected person, pet S & S – nails, groin, scalp, face Rx – antifungal meds Candidiasis (yeast) Prevalent in Immunosuppressed – normal flora from intestinal tract colonizes in mouth area, genitals, nails At risk – babies (diaper rash, thrush), diabetic, debilitated (cancer, malnutrition, chronic disease, recent broad-spectrum antibiotics), psoriasis S & S – skin rash, itching, redness, can be systemic and cause myalgia, arthralgia, migraines, food allergies, hay fever, asthma, cystitis Rx – antifungal meds Tinea cruris most commonly known as jock itch. A fungal infection of the skin. Herpes Virus Type 1 – cold sore (latent infection) always present in the body, wait until immunosuppressed. E.g. under stress Type 2 – sexually transmitted affects genitals. Controlled by medication Herpes Zoster (shingles) Viral infection (varicella zoster virus), virus goes latent and remains in the posterior root ganglion. Lesions along distribution of nerves (dermatome). Typically around the trunk. Common in >55yo. Now treated with vaccine. Very painful because it affects sensory nerves. Burning, itching pain from blister-like rash. Warts common skin lesions. Often found on hands, feet and genitals. Genital warts (caused by HPV), Plantar’s warts (also caused by HPV) Scabies Bites from spider mites – mite burrows under the skin, lays eggs in epidermis, 4-6 week gestation; larvae rise to surface of skin and then may burrow back in – may leave tracks (dark lines) S & S – inflammation, itching and rash from burrowing and fecal deposits Usually in warm, moist body areas, elbow creases, web spaces, under breasts, groin, waistline Rx – topical lotions Lice - 3 types body lice, head lice (most common), pubic lice (STD) Eggs – nits – hatch and suck blood from the head Lice can spread other diseases – typhus, trench fever Rx – shampoos, lotions, oral meds, fine tooth comb to remove nits Eczema refers to any chronic, non-infectious skin lesion often – hereditary disposition Inflammatory papules and vesicles Lichenification – skin looks leathery; called “the itch that rashes” Psoriasis autoimmune disorder, new skin cells grow very rapidly (days instead of weeks) and pile up to form thick patches (plaques); Rx – meds, UV light Dermatitis any inflammation of the skin Urticaria hives (allergy) Skin Cancer - see notes from slides Basal Cell Carcinoma Squamous Cell Carcinoma Malignant Melanoma Kaposi’s Sarcoma Immunopathology and Infective Agents Microbiome - The human microbiome is the sum of the bacteria living in and on us. The human body has ~100 trillion micro-organisms, a thriving megapolis of living and hardworking microbes. Most of the healthy flora (bacteria) live in our intestines and aid in the breakdown and digestion of food. If the bacteria of our gut is well balanced it allows our immune system to operate effectively Innate immunity (natural immunity system) that resists infections. (1st line of defense) Includes: 1. Skin and the fluid layer outside the skin (sweat and oil) 2. Mucous membranes – trap pathogens and allow them to be removed by cough or swallow. Remember the cilia in the airways and their role? 3. Bactericidal substances in tears, nose, intestinal tract and friendly bacteria 4. And WBC’s Acquired immunity (2nd line of defense) The immune system attacks pathogens that have eluded the 1st line of defense, as part of the immune response. Antibodies form in response to antigens Antigens are stimuli that elicit an immune response (chemical or irritant) The body recognizes the antigen as foreign, and the immune system responds by producing antibodies to destroy the invader. An added defense our body has is a vaccinations exposure to limited-strength antigens allows the body to build up antibodies to increase the immune response provides active acquired immunity to a particular disease. typically contains an agent that resembles a disease-causing microorganism often made from weakened or killed forms of the microbe, its toxins, or a surface protein. It stimulates the body's immune system to recognize the agent as a threat, destroy it, and recognize and destroy any of these microorganisms that it later encounters. Hematopoietic stem cells (HSCs) the stem cells that give rise to all the other blood cells through the process of hematopoiesis. give rise to both the myeloid and lymphoid lineages of blood cells. Myeloid stem cells give rise to granulocytes which include… Basophils – secrete histamine cardinal signs of inflammation/infection (heat, swelling, redness, pain, loss of function) & heparin (blood thinner to prevent clotting) Neutrophils – first responder phagocyte Eosinophils – phagocytic (ingest bacteria & parasites) Monocytes also develop from the myeloid stem cells – become macrophages or dendritic cells Lymphoid stem cells give rise to Lymphocytes: B Cells – produce antibodies to neutralize bacteria & virus’ (memory cells) T Cells – direct the immune response and induce death of infected cells Natural Killer cells – release cytotoxic granules that kill tumor cells and virus infected cells White Blood Cells White blood cells vary in size but in general are the largest blood cells in the body. Live in the lymph system and circulate in the blood and they are also found in the tissues. Make up less than 1% of blood’s volume. 5 major types of White Blood Cells (leukocytes) 1. 2. 3. 4. 5. Immune Response Four main components: 1. Pathogen recognition by cells of the innate immune system, with cytokine release, complement activation and phagocytosis of antigens 2. An acute inflammatory response is triggered by the innate immune system 1. If the innate immune response is unable to control the invader, the acquired immune response is initiated. 3. Antigen presentation takes place with activation of specific T helper cells 4. Helper T cells then co-ordinate a targeted antigen-specific immune response involving two adaptive cell systems: 1. humoral immunity from B cells and antibodies, 2. cell-mediated immunity from cytotoxic T cells Cells involved Macrophages – 1st arrival, engulf invaders. They signal to neutrophils if more help is needed. Neutrophils – so active that they kill everything in sight. Even healthy tissue. Dendritic cells – break apart invaders and present the antigen to other WBCs. Signal to other cells the type of invasion (bacteria, virus, etc). Signal Helper T cells by travelling to lymph nodes. T cells (directors of the show) – some become cytotoxic T cells and kill the invaders some become Memory T cells to improve response to same invader on subsequent exposures (immunity) some become Helper T cells to travel to the center of the lymph nodes to activate & stimulate B cells to produce antibodies. Helper T cells regulate the immune response by releasing cytokines – some inhibit action and some enhance the action of other cells and other cytokines Memory T cells and the memory B cells remain after the invader has been controlled, while the rest of the cells die off. Creating immunity if exposed to the same antigen again. Chemical Messengers The chemical messengers of the immune system are “Lymphokines” (a type of cytokine which are substances secreted by the immune system, a protein). are produced by lymphocytes to signal other WBCs Released by sensitive lymphocytes on contact with specific antigens that help affect cellular immunity by stimulating activity of monocytes and macrophages They regulate the immune response (length and intensity) Complement aspect of the adaptive immune system whereby proteins produced in the liver can respond by amplifying the immune response. improve the ability of antibodies and phagocytic cells to clear pathogens from the body. Antibodies – aka Immunoglobulins – produced by B Cells in response to foreign antigens. They are proteins specific to an antigen that help fight the current and future intrusions by that particular antigen Immunoglobulins- Y shaped proteins produced mainly by plasma cells. Five antibody classes or” types” 1. IgM – It is expressed on B cell surfaces and produced early in the immune response while IgG is being generated. 2. IgG – provides the majority of antibody-based immunity. It is more active with each subsequent exposure to the same antigen. It is found mainly in circulating blood and tissues, also crosses the placenta to provide passive immunity to the fetus. 3. IgA – It is found in mucosal areas such as the GI, respiratory and urinary tracts. It is also secreted in saliva, tears and breast milk. 4. IgE – It binds to allergens and mediates allergic reactions, as well as providing immunity against multicellular organisms such as parasitic worms. 5. IgD – It is found in very low levels in the serum and appears to interact with basophils and mast cells. Antibodies fight extracellular infections in a number of ways: neutralize toxins by directly binding to them bind to antigens on pathogen surfaces. This agglutinates them to impair their mobility and also opsonizes them to enhance phagocytosis. binding of antibodies to antigens to form complexes activates the classical complement pathway directly activate effector cells such as dendritic cells, NK cells and cytotoxic T cells What Are Infectious Agents? An infectious agent is something that infiltrates another living thing. Classes of Infectious Agents 1. Bacteria single-celled organisms without a nucleus. Have a single chromosome and no mitochondria (cannot produce energy). An Antibiotic is harmful to bacteria. Doctors prescribe antibiotics to help the immune system out when there is a bacterial infection. Bacteria Ex. strep throat, tuberculosis, E. coli, anthrax, salmonella, syphilis, and bubonic plague. Often named according to their shape and how they group – (eg. Chains, groups or clusters) Millions of types Bacteria are long-living and can live even without a host 2. Virus Smaller than bacteria. Not “technically” alive because they cannot function unless it has a host.  little packages of a DNA or RNA genome inside a protein shell called a capsid. If they get inside a host, their goal is to hijack the host cell's machinery, replicate and mutate. After new viruses have been made, they go out into the world and the cycle starts over. Like a bacterial infection, a viral infection can have different symptoms depending on which virus is doing the infecting. Ex. of viral infections: common cold, influenza, rabies, ebola, herpes, HIV, HPV, coronavirus. 3. Fungi multi-cellular or single-celled organisms with a nucleus and organelles, unique from plants or animals. feed by absorbing nutrients from their surroundings. Ex. Yeasts, molds and mushrooms Most types are not dangerous, but some can infect humans and be harmful. Often, fungal infections affect the skin and cause a minor rash (like athlete’s foot), but other fungi can also cause more serious problems, like a lung infection or a blood infection. 4. Parasites. Live on or in a host organism and get its food from or at the expense of its host. Range from simple to complex. Small multicellular creatures with a lifecycle. Multiply in humans leading to serious infections to develop from just a single organism. Transmission of protozoa that live in a human's intestine to another human typically occurs through a fecal-oral route (Ex. contaminated food or water or person-to-person contact). Protozoa that live in the blood or tissue of humans are transmitted to other humans by an arthropod vector (for example, through the bite of a mosquito or sandfly). Ex. Worms, lice, mosquitoes, and protozoa Forms of Infection Local –has not spread but remains contained near the entry site. Has only local symptoms (pain, swelling, redness). Systemic -the pathogen is distributed throughout the body rather than concentrated in one area. Sx - body ache, fever, chills, nausea vomiting. The neutrophils, basophils or eosinophils have alerted the hypothalamus to raise our body temperature ie. fever – helps fight the infection b/c chemical reactions happen more quickly Acute illness – characterized by rapid onset of disease, a relatively brief period of symptoms, and resolution within days. It is usually addressed quickly by the immune system. Brief but not a descriptor of severity Chronic –infection of long duration, characterized by a lesser degree of inflammation and reduced immune response can’t get rid of it Primary – A primary infection is the first time you are exposed to and infected by a pathogen. During a primary infection, your body has no acquired defenses against the organism, such as antibodies. Secondary – A secondary infection is an infection that occurs during or after treatment for another infection. It may be caused by the first treatment or by changes in the immune system. Latent – infection (usually virus) remains dormant and inactive in cells. Stages of Infection Incubation - period from the initial entrance of the organisms until 1st signs and symptoms appear. It is the time it takes for the pathogen to multiply enough to produce symptoms. Could be 2-3 days (flu) or weeks-months (Hep B) or even years (HIV) Prodromal - from the end of incubation period to the point at which classic signs of the illness appear. A person usually displays early vague/non-specific signs and symptoms malaise- not feeling well, headache, fever, upset stomach Acute / Illness - phase of rapid multiplication of the pathogen with exponential growth The peak of pathogen population. Symptoms are very pronounced, both specific to the organ affected as well as in general due to the strong response of the immune system. maximum symptoms most contagious Signs of Infection in the Elderly Seniors are less likely to have classic symptoms such as fever, chills, and vomiting. Instead, they might have atypical symptoms such as subnormal temperature, confusion, fatigue, and decreased appetite. Seniors are more susceptible to infection because multiple chronic illnesses that occur with age put extra stress on the body, and the medications for these conditions can block the immune system. In addition, the immune system naturally weakens as we grow older. Signs and Symptoms changes in eating habits/ decreased appetite lack of body control (incontinence, balance) fever (low grade) confusion, quietness changes in ability to complete day to day activities fatigue with increase in aches and pains Treatment To successfully treat an infection, first the infecting agent must be identified. Blood tests, urine analysis, or tissue samples are sent to the laboratory. Once the infecting agent is identified, the appropriate treatment must be prescribed. Antibiotics for bacteria, antivirals for viruses, antifungals for fungus, etc. It also important the correct antibiotic is used to treat the specific bacteria. Antibiotic-resistant bacteria is becoming more common. Super bugs the general term for antibiotic-resistant bacteria. Bacteria has become resistant to the antibiotics that previously could kill them. Three super infections that pose a threat in our acute care settings are: 1. Methicillin-resistant Staphylococcus aureus (MRSA) 2. Vancomycin-resistant enterocolitis (VRE) 3. Clostridium difficile (C diff), Hypersensitivity When something foreign enters our body, our immune system reacts in one of two ways: 1. Protection 2. Damaging Hypersensitivity is used to describe the latter. When the immune response is damaging to our bodies. 1. Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by re- exposure to a specific type of antigen. Exposure may be by ingestion, inhalation, injection, or direct contact. In type 1 hypersensitivity, B-cells are stimulated to produce IgE antibodies (instead of IgA, IgG, or IgM) specific to an antigen. The 1st time you are exposed to the antigen, B cells produce antibodies to the antigen. They become “sensitized” to it and the next time you are exposed the reaction is intense and immediate. The immune system responds to a common antigen (eg. pollen, dust, peanuts) as though the body was under attack. 2. In type II hypersensitivity (aka tissue-specific, or cytotoxic hypersensitivity) the antibodies produced by the immune response bind to antigens on the cell surfaces (ie. Thinks the cells are marked as non-self). The antigens recognized in this way may either be intrinsic or extrinsic Intrinsic = "self" antigen, innately part of the patient's cells Extrinsic = absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen These cells are recognized by macrophages or dendritic cells, which act as antigen- presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen. 3. Type III hypersensitivity occurs when there is accumulation of immune complexes (antigen- antibody complexes) that have not been adequately cleared by innate immune cells, This gives rise to an inflammatory response and attraction of leukocytes. Reactions can progress to the point of disease and produce immune complex diseases. 4. Type IV hypersensitivity is often called delayed type hypersensitivity as the reaction takes time to develop. Unlike the other types, it is not antibody-mediated but rather is a type of cell- mediated response. Inflammation and Healing Cytology  The study of cells – structure, function & chemistry Homeostasis – balance/equilibrium, the body’s maintenance of a relatively stable internal environment When homeostasis is challenged or disrupted, the cell responds. If the change is small the cell can recover, but if the trauma / damage / injury is severe the cell will die (necrose) Needed to maintain the health of a cell: o Enough water & nutrients o Normal temperature o Appropriate pressure o waste removal o intact nucleus Cell Injury and Death – Reversible cell injury = repair Irreversible cell injury  Normal cell death = Apoptosis  Programmed cell death  Damaged beyond repair  Necrosis Whether or not a cell can recover from an injury depends on the severity of the injury and what type of cell it is. 3 main types/categories of cells labile (renewing) cells – continue to divide throughout life and any damage is completely repaired (e.g. Skin, mucous membranes) stable cells – do not divide after growth ceases but can regenerate in response to injury (e.g. Liver, pancreas) Permanent cells – cannot replicate and are often replaced by fibrous tissue (e.g. Neurons, cardiac tissues) Principle causes of injury 1. Infections (e.g. viral, bacterial, fungal, parasitic) 2. Physical agents (e.g. heat, cold, trauma, ionizing radiation) 3. Chemicals (e.g. corrosives, acids, alkalis, bacterial toxins) 4. Hypoxia, anoxia, ischemia (lack of oxygen or blood flow) Types of cell death (necrosis) Liquefactive Cells die & liquefy due to the action of leukocytes (WBC’s) – becomes pus Common in stroke & brain injury. Coagulative The cells die due to ischemia (lack of blood flow and the O2 it brings) Gangrene - cells die due to loss of blood supply Wet – pockets of pus, blistery Dry – blackened mass of necrotic tissue. Caseous cheese-like Occurs in TB (lymph nodes) Fat Necrosis due to lack of blood supply to the remaining subcutaneous tissue after a procedure which leads to necrosis or when specific enzymes released from damaged cells attack only fat cells Dystrophic Calcification “dys” – abnormal, “tropic” – response to a stimulus, “calcification” – hardening, the necrotic or dead tissue calcifies Heterotopic Calcification “hetero” – other, “topic” – place – means occurring in an abnormal anatomical location Development of bone in muscles and fascia of the hip, knee, sh., & elb. Cellular Responses to Damage or Stimuli Atrophy Decreased size of cells; “a” – without; “trophic” – a stimulus Due to immobilization, aging brain, osteoporosis, lack of nutrition – cancer, malnutrition Hypertrophy “hyper” – extreme; “trophy” – stimulus. Not always a positive response to cell stimuli Increased size of cells, can include cell splitting Hyperplasia – increased number of cells, which is different than hypertrophy where the cells get larger “hyper” – extreme; “plasia” – development Hypoplasia “hypo” – below normal; “plasia” – development. Decreased no. of cells. Metaplasia “meta” – change “plasia” – development Cells change from one type to another type. Anaplasia “ana” – without”; “plasia” – development. Cell lose their function. Loss of structural and functional differentiation in cells, as occurs in cancer Cells reproduce so rapidly, they don’t develop a function. Dysplasia Abnormal growth or development of cells Inflammation and healing Inflammatory response - a defense to localize and eliminate the injurious agent Consists of changes in blood flow, changes in the permeability of blood vessels, and the migration of fluid, proteins, and white blood cells (leukocytes) to the site of tissue damage. The function of inflammation is to: eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process to initiate tissue repair Inflammation is a generic response = mechanism of innate immunity. Cardinal Signs of Inflammation 1. Redness- due to increased blood flow to the site, dilation of small blood vessels in area of injury 2. Heat- due to increased blood flow to the site, dilation of small blood vessels in area of injury 3. Swelling- (edema) caused by accumulation of fluid leaking out of damaged cells 4. Pain- due to initial injured tissue, compression of tissues from swelling, and the release of chemicals such as bradykinin and histamine that stimulate nerve endings. 5. Loss of function- what we address as rehab professionals. It has multiple causes, including pain and swelling Causes 1) microorganisms, 2) physical agents, 3) chemicals, 4) inappropriate immunological responses, 5) tissue death. Infectious agents such as viruses and bacteria are some of the most common stimuli of inflammation. Bacteria release substances called endotoxins that can initiate inflammation. Viruses give rise to inflammation by entering and destroying cells of the body; Physical trauma, burns, radiation, and frostbite can damage tissues and also bring about inflammation Corrosive chemicals such as acids, alkalis, and oxidizing agents. Acute Inflammation Acute inflammation may last for a few hours to a few days. Vascular changes When tissue is first injured, the small blood vessels in the damaged area constrict momentarily (vasoconstriction) then the blood vessels dilate (vasodilation), increasing blood flow into the area. Vasodilation may last from 15 minutes to several hours. Inflammatory response With tissue damage Mast cells in the tissues release histamine Histamine is also released by platelets and basophils (WBC) Histamine causes transudation (edema) and increased blood vessel permeability A “histamine-mediated response” in the initial phase of inflammation results in swelling, redness and warmth in the damaged area. Histamine lasts about 30 minutes before histaminase (produced by the tissue) prevents further tissue damage. The most important feature of inflammation is the accumulation of white blood cells at the site of injury. Most of these cells are phagocytes, certain “cell-eating” leukocytes that ingest bacteria and other foreign particles and also clean up cellular debris caused by the injury. Transudation – passage of fluid or solute through a membrane due to a pressure gradient This causes edema (swelling) After the initial phase Congestion of the dilated blood vessels occurs due to slowing of the blood flow. RBCs begin to pile up in the vessels. WBCs attach to the walls of the vessels. Prostaglandins (lipid compounds) are associated with the pain and fever of inflammation. They increase the effects of other substances that promote vascular permeability. affect the aggregation of platelets, part of the clotting process. Anti-inflammatory drugs are effective in part because they inhibit prostaglandin synthesis Blood Plasma contains four interrelated systems of proteins — that generate various mediators of inflammation. Complement proteins- increase vascular permeability and stimulate the release of histamine from mast cells. Also, adhere to the surface of bacteria, easier targets for phagocytes. Kinin system- increases vascular permeability as well. Bradykinin - prolongs the inflammatory response  pain and itching experienced with inflammation. Coagulation system- converts the plasma protein fibrinogen into fibrin, which is a major component of the fluid exudate. Fibrinolytic system- breaks down fibrin into products that affect vascular permeability. Cells of inflammatory response Neutrophils - phagocytic – migrate to the area to engulf debris - release cytokines that stimulate a systemic response of fever via the hypothalamus Eosinophils - phagocytic - Give off chemicals that kill bacteria and parasites Monocytes – develop into macrophages Macrophages – large phagocytic cells Basophils – precursors of mast cells, contain histamine Platelets (thrombocytes) – release histamine, help with clotting Chemical factors released by the different cells bring about vascular and cellular changes. The chemicals come primarily from blood plasma, white blood cells, platelets, endothelial cells lining the blood vessels, and damaged tissue cells. Classification of Inflammation Acute Sub-Acute Chronic Acute on Chronic Outcomes of Inflammation Healing and repair suppuration (pus) chronic inflammation The outcome depends on the type of tissue involved and the amount of tissue destruction that has occurred. Suppuration - The process of pus formation, occurs when the agent that provoked the inflammation is difficult to eliminate. Pus - a viscous liquid - mostly of dead or dying neutrophils and bacteria, cellular debris, and fluid leaked from blood vessels.  The most common cause of suppuration is an infection with pus-producing bacteria, such as Staphylococcus and Streptococcus. Regeneration - development of cells of the same type as those damaged Replacement - the development of a new type of tissue- often causing scarring Different cells vary in their ability to regenerate Repair/replacement occurs when tissue damage is substantial, or the normal tissue architecture cannot be regenerated successfully resulting in a fibrous scar new blood vessels and fibroblasts grow to form a loose framework of connective tissue called granulation tissue. Stages of Healing 1. Hemostasis – Vascular response to stop the bleeding – cascade reaction leading to fibrin clot formation 2. Inflammation – up to first 3 weeks 3. Proliferation – usually 3- 6 weeks 4. Remodeling – weeks to months (up to 2 years) Steps of the healing process (skin) 1. Contraction of the wound during the proliferation phase. Myofibroblasts gather around the wound and cause shrinking of the edges. Phagocytes (especially macrophages) remove necrotic tissue. A scab forms to protect the granulation tissue 2. Granulation tissue forms under the scab. Blood vessels start to grow at the base of the wound. It is fragile and needs protection The granulation tissue provides the nutrition for the collagen network. 3. Scar tissue is mainly type-3 collagen produced from fibroblasts. 4. Remodeling or maturation phase. The wound loses the red color, and the tissue becomes more like the original tissue. Wound healing can be classified into two categories: Primary - Characterized by the edges of the wound having clean and clear margins that are close together. o Like in a surgical incision e.g. surgical suturing o Scar can take up to 18 months to remodel o Follows the same steps as healing by secondary intention but initial wound closure is much faster (7-10 days) and usually less scar tissue formation Secondary - Takes longer and leaves a bigger scar o Some extensive wounds may never heal fully What can delay healing? Excessive movement Infection Foreign bodies Size Age Medical comorbidities Circulatory condition Interference (physical contact) Meds (anticoagulants, corticosteroids) Pressure ulcers, bone, muscle, tendons, ligaments  Pain Video – PAIN = Combination of complex interactions. Pain is a consequence of many diseases, injuries, & conditions. Subjective and is considered a “symptom” vs. a “sign”. Pain behavior is affected by cultural factors, gender, & family teachings. Pain can lead to disability, limiting participation in home, work, & recreational activities. Acute Pain Usually well localized and well-defined. An important warning that tissue damage is occurring. (injury, infection, disease process) Serves an important protective function following an injury: limits activity, promotes recovery. Duration 0-3 months – usually resolves within this time. Chronic Pain Begins as acute pain. Lasts from 3 months to years. Pain that lasts longer than normal healing time. Often accompanied by social, psychological, & physical dysfunction. Treated using a multidisciplinary model. Referred Pain Pain felt at a location distant from its source. Thought to occur because the areas may share the same dermatome, myotome, or sclerotome. Visceral Pain Pain from the viscera involves stretch receptors. Poorly localized. Often described as deep, aching, squeezing, cramping Gate Control Theory Theory – A gate mechanism exists in the spinal cord. When the gate is “closed” pain information is blocked and is not transmitted to the brain. When the gate is “open” pain information flows freely to the brain. Providing conflicting stimuli (heat, cold, massage, etc.), closes the gate thereby blocking the transmission of painful stimuli to the brain. Large fibers are stimulated primarily by mechanical distortion (mechano receptors) Interneurons in the dorsal or anterior horns of the spinal cord are responsible for Gate Theory Interneurons connect with many different pathways. The mechano-receptor input on the large fibers will synapse with the interneuron, and the interneuron’s signal will block or lessen pain. Endorphins The body produces its own pain-mediating substances (endorphins) that are chemically similar in structure to opiates (morphine, codeine). Production of these substances occurs during prolonged exercise and when the body is under stress This is also how acupuncture works, stimulating an increased release of endorphins by the body. Endorphins will close the gate in the gate control theory Until the 1900s Infectious diseases were the greatest killer because methods to treat them were not very effective. Examples of infectious diseases Pneumococcal pneumonia - a lung infection that killed numerous people Staphylococcus aureus, tuberculosis, syphilis, and bubonic plague were all killers In the 1930s, with the discovery of penicillin, antibiotic treatments became more effective. Now we are seeing the organisms adapt and become resistant to the drugs (Super Bugs) or new viruses that our bodies have not seen before (Coronavirus) Ancient world Greeks – used diet & ex. for warrior health; they developed early hospitals Romans – physicians travelled with the armies; ancient pandemics started when smallpox or measles were brought back by soldiers Egyptians – first sophisticated pharmacies (using plants) 5th-15th Centuries Disease was due to sin Holy wars– unleashed pandemics – nunneries and monasteries became the places where the sick were