Pathology Exam 1

  1. Ischemia
    • lack of, or decreased blood flow to a cell, organ, or body tissue
    • common in the heart as a result of CAD
  2. Systems Review
    • Cardiopulmonary: vitals signs etc
    • Musculoskeletal: strength and ROM to stand up and walk
    • Neurologic: balance control
    • Integumentary: skin intact
    • Cognition: are the alert and can they talk to you
  3. Etiology
    Study of the cause of disease or injury
  4. Idiopathic
    Diseases with no identifiable cause
  5. Iatrogenic
    disease or injury as a result of medical intervention
  6. Sequelae
    Any abnormal cconditions that follw and are the result of a disease rx or injury
  7. Hemoglobin
    • Top of crow's foot
    • Normal male: 14–18 g/dl
    • Normal female: 12–16 g/dl
    • 1/3 of HCT
  8. Hematocrit
    • Bottom of crow's foot
    • Percent of RBCs in a given volume of blood
    • Normal male: 47%
    • Normal female: 41%
  9. Leukocytes
    • Left side of crow's foot
    • Granulocytes: neutrophils, eosinophils
    • Agranulocytes (phagocytes): monocytes, lymphocytes, NK cells
    • Normal adult: 5,000–10,000
    • CBC with "left shift" with infection – due to increase of WBC count
  10. Neutrophils
    • Most numerous WBC – 55%
    • Big, 2–5 nuclei
    • Kill bacteria – increased neutrophils, ? bacterial infection
    • Phagocytes in early inflammation
    • Immature: bands or stabs – increased could mean early infection
  11. Eosinophils
    • 1-4% of WBC count
    • Fight parasites
    • Important in asthma and allergies
    • Mediate inflammatory process
  12. Monocytes
    • Horse-shoe shaped
    • Turn into macrophages at site of inflammationg
    • Initiate inflammatory response
  13. Lymphocytes
    • 36% of WBC count
    • Main ones are t- and b-cells
    • middle to late in inflammatory process
  14. NK Cells
    • 5–10% of WBC count
    • Attack viruses
    • attack cells infected with a virus the body has not seen before
  15. Platelets
    • Not cells
    • Allow blood to clot
  16. Cytosis
    • too many RBCs
    • ex: leukemia
  17. Cytopenia
    • Too few RBCs
    • ex: anemia
  18. RBC
    MCV (mean corpuscle value: size of RBC): reference range: 80–100 fl
  19. Reticulocyte
    • Immature RBC
    • 0.5–1% of RBC volume
    • decrease with bone marrow problems
    • increase with increased RBC production
  20. Thallasemia
    • Microcytic anemia
    • Genetic disorder: found in Greeks, Italians, African American, American Indian, and Asian
    • Microcytosis and mild anemia, may need blood transfusions if severe
  21. Macrocytic Anemia
    • RBC's too big and too few
    • Elevated MCV lab
  22. Megaloblastic Anemia
    • Elevated MCV
    • Usually due to B12 and iron defficiency
  23. Normocytic Anemia
    • Cell size and volume are fine
    • Due to acute or chronic blood loss
    • Seen in patients with failing kidneys
    • Hemolytic anemia
    • G6PD defficiency (genetic, rare)
  24. Hemolytic Anemia
    • Rupture of RBCs
    • Direct Coomb's Test measures metabolytes in blood plasma to see if there is too much intracellular contents in the plasma
    • Can be medication related; inherited; aquired via autoimmune diseases, injection, or mechanical (e.g. heart valves)
  25. PT Implications for Anemia
    • Patients who have hemoglobin <12 or hematocrit <26:
    • -spontaneous bruising or bleeding
    • -joint protection
    • -after bleeding episode: isometric exercises --> work up to resistive
    • -decreased oxygen carrying capacity --> fatigue
  26. Erythrocytosis
    • Too many RBCs
    • Men HCT > 52
    • Women HCT > 47
    • response to hypoxia (e.g. high altitude, smoking, CO exposure, cyanotic heart disease), kidney malfunction (increased epogin), over-productive stem cells
    • PT Implications: blood is thicker --> harder for heart to pump blood, more susceptible to clotting
    • Dehydration can look like erythrocytosis
  27. Polycythemia Vera
    • Myeloproliferative disorder: affects WBCs and RBCs
    • Insidious
    • Increased clotting
    • Enlarged spleen and liver
    • Ruddy complexion (pruritis)
  28. Leukopenia
    Low WBC count - typically neutrophils

    • Causes (not making enough):
    • drugs: chemotherapy, chloramphenacol – grey baby, sulfa drugs (diuretics and antibiotics), seizure meds, antipsychotics
    • infection: can actually destroy WBCs – often viruses (parvovirus: young children and elderly – affects WBC count and RBC count)
    • bone marrow failure, nutrition deficiency, connectice tissue disorders (SLE), radiation

    • Causes (destroying them):
    • overwhelming bacterial infection
    • hemodialysis
    • CP bypass
    • autoimmune diseases
    • drugs
  29. Neutropenia
    • Decreased neutrophil count
    • < 1000/uL = neutropenia
    • < 500/uL = cannot fight own gut bacteria
    • < 200/uL = no inflammatory response
    • seen after bone marrow transplants, other transplants, and HIV
  30. Neutrophilia
    High neutrophil count

    • Causes:
    • infection
    • inflammation
    • tissue necrosis
    • acute hemorrhage/hemolysis
    • drugs such as lithium
  31. Lymphocytosis
    High lymphocyte count

    • Causes:
    • viral infection
    • TB, pertussis, hepatitis
  32. PT Implcations for luekopenia
    • Total WBC count < normal (4000): be cautious
    • Total WBC count < 1000: immunocompromised, take infection control measures (gown, gloves, mask): protect patient from infection
  33. Platelets
    • Right side of crow's foot
    • Thrombocytopenia: too few platelet
    • Thrombocytosis: too many platelets
  34. Thrombocytopenia
    • Too few platelets
    • <150,000/uL is low: be especially carfeul of falls and trauma
    • <50,000/uL increases risk of bleeding with trauma: is intervention at risk of causing spontaneous bleeding
    • <10–20,000/uL risk of spontaneous bleeding: is it appropriate to treat at all

    • Causes:
    • -immune related response
    • -infection
    • -drugs and alcohol
    • -B12/folic acid deficiency

    non-blanching erythematous (press and redness doesn't go away), purpura on face
  35. Thrombocytosis
    • Too many platelets
    • <500,000/uL
    • Causes:
    • -chronic inflammation or infection
    • -solid tumors
    • -after splenectomy

    • Essential thrombocythemia: platelets cloning themselves at a quicker rate
    • Increased risk of clotting or thrombosis
  36. Clotting problems
    • Decreased:
    • Iatrogenic (caused by other medical intervention): too much anticoagulant: coumadin, heparin
    • Inability to produce fibrin and other clotting factors: hemophilia
    • Increased:
    • Pregnancy
    • Immobilization (valves, thoracic and musculoskeletal pumps decreased)
    • Post-op
    • oral contraceptives
  37. Antiplatelet therapy
    • Indications: TIA, CVA, MI and angina prevention
    • - PVD
    • Complications: bleeding, GI bleeding, interaction with BP meds
  38. PT Implications for platelets
    • Be cautious with patients who have:
    • -known DVT: Homan's test – dorsiflex and palpate
    • -platelet count <50,000/uL – spontaneous bleeding
    • -big spleen – painful
    • -are on anticoagulants – safety re falls/trauma
  39. Bone Anatomy
    • Diaphysis = mid shaft
    • Metaphysis = flared portion of distal ends
    • Physis = growth plate
    • Epiphysis = adjacent to physis and most distal
    • Articular cartilage forms over epiphysis
  40. Fracture
    • Defect in bone continuity
    • Bone doesn't look the way it did the day before – can be microscopic or macroscopic

    • Transverse: simplest to heal
    • Comminuted: often requries surgery
    • Avulsion: soft tissue structure broke part of bone off
    • Greenstick: (kids) didn't fully break (can be sign of child abuse)
    • Compression: bone collapses – usually some metabolic reason underlying
    • Pathologic: due to underlying disease process – often CA
    • Intra-articular: on a joint line – causes permanent problems
    • Stress fracture: usually from too much stress on the bone and it can't build back up (like pocket of osteoporosis)
  41. Closed Fracture
    Skin over and near fracture is intact
  42. Open Fracture
    Skin over and near fracture is lacerated or abraded by the injury (bleeding) – could be cause directly by the fracture, or due to surgical intervention
  43. Signs of Infection
    • Local: inflammation (red), warm, pain,
    • Systemic: fever
  44. Salter-Harris Fractures
    • Kids
    • Growth plates – potentional for limb length discrepency in future
  45. Describing Fractures
    • What bone is involved and location on bone (metaphysis, diaphysis, epiphysis), other anatomical description
    • Orientation/extent of fracture line (transvers, oblique ...)
    • Displacement and amount involved (angulated...nondisplaced)
    • Open vs closed

    Colles fracture: distal radius
  46. Exostosis
    Bone growing in relation to stress
  47. Physical Examination for Fracture
    • Localised tenderness, swelling, possible deformity: palpate gently, start with uninvolved side
    • Look at skin integrity: any break in the skin classifies as an open fracture
    • Eval surrounding/adjacent joints and function of nerves and vessels distal to site of injury
  48. Fracture Healing
    • Hematoma formation: a fibrin mesh forms as a bas for healing
    • Procallus formation: fibroblasts, capillary buds, and osteoblasts move into wound
    • Callus formation: osteoblasts form woven bone – looks fuzzy on xray
    • Callus replacement: osteoblasts replace callus with trabecular or lamellar bone
    • Remodeling: maturation of bone – can take up to a year
  49. Adverse Outcomes to Fracture Healing
    • Delayed Union
    • Nonunion
    • Malunion
    • Infection – must be treated before bone can grow
    • Osteomyelitis – inflammation of bone
    • Sever fx – can cause soft tissue, nerve, and vessle damage; wiggle fingers and toes, colour
    • Compartment syndrome – vascular and nerve compression due to swelling when have a cast (between radius and ulna or between tibia and fibula)
    • Heterotropic ossification (exostosis) – bones grew too much and got lumpy
    • Complex regional pain syndrome (reflex sympathetic dystrophy – RSD) – pain that's out of proportion to the injury due to overactive sympathetic nervous system. More aggressive rx early on will help prevent RSD
  50. Calcium Intake
    • < 12 y/o: 4 servings a day
    • 12–20: 3 servings a day
    • 20–menopause: 2 servings a day
    • > menopause: 3 servings a day
  51. Treatment of Fractures
    • Recognise it (xray)
    • Reduce (if needed)
    • Retention of reduction (cast, splint, sling, ORIF)
    • For every week in a cast, that's how many weeks it will take to get better once cast is removed
  52. Prognosis for Fracture Healing
    • Time until fracture is healed enough to take full loading:
    • Children: 4–6 weeks
    • Adolescents: 6–8 weeks
    • Adults: 10–18 weeks
    • Casting usually for 4–8 weeks
  53. Conditions that delay fracture healing
    • Renal of vascular insufficiency – on dialysis, not a good chemical environment for healing
    • Smoking – 1.5 times as long to heal; poor oxygenation
    • Alcoholism – often have poor nutrition
    • DM – pain changes glucose needs in body
  54. Stages of Fracture Healing and PT
    • Acute: being fixated (cast, sling etc.) bone healing happening. PT: move associated body parts: wiggle fingers, bend elbow etc. Whatever is not in the cast needs to be moved. Elevate to reduce swelling
    • Subacute: just took cast off. Still acute for soft tissue – swell. PT: swelling reduction, PRICE
    • Chronic: bone fully healed. PT: resume ADL's
  55. Osteoporosis
    • A multifactorial skeletal disorder that leads to decreased bone density and organisation, which ultimately reduces bone strength
    • MSK Pattern 4A: primary demineralisation: bone stock very weak
    • Measure of bone mineral density (BMD): >2.5 standard deviations away from norm
  56. Non Modifiable risks for Osteoporosis
    • Age: >50
    • Gender: famale > male
    • Genetic: family history
    • Race: caucasian, Northern European ancestry
    • Long periods of inactivity: SCI, CVA with paralysis, MS, ALS
    • Ectomorphic: small, thin, not a lot of muscle mass
  57. Other Risk Factors for Osteoporosis
    • Hormonal: early menopause (e.g. hysterectomy); amenorrhea
    • Dietary: low calcium intake, excess sodium and animal protein, high caffeine intake
    • Lifestyle: sedentary lifestyle, smoking, alcohol
    • Concurrent illness: medications (esp steroids)
    • RA, CVA, Parkinson's: meds and inactivity
    • Endocrine Disorders: hyperparathyroidism, hyperthyroidism, hypogonadism (males)
    • Medications > 6 months: corticosteroids (inhaler, COPD, RA, Crohn's: calm immune system suddenly and effectively); immunosuppressants (RA, psoriatic arthritis etc.); heparin and coumadin (difficult ot heal if blood can't clot); antacids containing aluminum (calcium not usable to the body)
  58. Hormones that increase risk of osteoporosis
    • Parathyroid hormone (PTH): if increases (bad), bone is broken down; calcium levels in blood are high because the calcium is not in the bones
    • Calcitonin (thyroid): if increases (good), more calcium is higher in the blood and available for bone building
  59. Physical Activity for Osteoporosis
    helps body take calcium from blood and use it to build bone – Wolff's Law
  60. Clinial Manifestations of Osteoporosis
    • Often silent
    • Usually detected after a fracture occurs
    • Bone collapse with of without fracture can cause back pain and possibly radicular symptoms
    • Kyphosis and decreased height can occur
  61. Diagnosis of Osteoporosis
    • Screening often done after onset of symptoms/fracture
    • Bone density measurements:
    • DXA
    • Ultrasound
    • CT scan
    • Lab tests: probably the best
  62. Management for Osteoporsosis
    • Reduce risk factors: get patients up and moving – walking preferable to biking
    • Eliminate negatives: talk to patients about proper diet and nutrition
    • PT: educate, exercise (weight bearing is best), prevention in children and teens, posture – start early, periscapular muscles (esp lats, rhomboids, mid trap)
    • Medications: bisphosphonates (injections – injection site problems); hormone replacement therapy, calcitonin
  63. Osteomalacia
    • Rickets in children
    • Insufficient mineralisation in bone matrix, results from calcium of phosphate deficiency
    • Vitamin D deficiency is a causative factor
  64. Risk factors for Osteomalacia
    • Inadequate synthesis or dietary deficiency of vitamin D
    • Decreased absorption of fat-soluble vitamin D
    • Derangements in vitamin D metabolism
    • Phosphate depletion
  65. Clinical Manifestations of Osteomalacia
    • Bone pain and tenderness – like growing pains
    • Softening of cranial vault in children
    • Swelling of costochondral joints – enormous rib cages in children
    • Femoral neck fractures in adults
    • Proximal myopathy – waddling gait, trendelenburg gait
  66. Management of Osteomalacia
    • Address causative factors: nutrition especially, vitamin D and calcium
    • PT: gradual loading (Wolff's Law), joint protection (don't carry heavy things), positioning – need to sit up straight so their bones don't form in the wrong shape
  67. Osteomyelitis
    • Usually bacterial infection of bone (staph aureus) but can be viral, fungal, or parasitic
    • Poor healing, longer healing time, poor outcomes
    • Exogenous: bacteria came from outside the body (often from open fractures) – usually more easily and affectively treatable
    • Endogenous: bacteria came from inside body and just deposited in the bone
    • Acute: lasts < 1 month. Very painful
    • Chronic: last > 1 month. Much more difficult to treat
    • Pathophysiology: infection --> inflammation --> bone necrosis if not treated in time/properly. May have to surgically remove dead bone and/or pus pockets
  68. Clinical Manifestations for Osteomyelitis
    • Warmth, swelling, tenderness, delayed onset of pain
    • Fever (endogenous > exogenous)
    • Malaise – flu-like symptoms
  69. Management of Osteomyelitis
    • Evaluation: WBC count, culture/biopsy, imaging
    • Treatment: acute: antibiotics. Chronic: surgical debridment, bone/skin grafts, hyperbaric oxygen
  70. PT Implications for Metabolic Bone Disorders
    • Prevention: universal precautions
    • Know weight-bearing status
    • Use lab date and vital signs to guide exercise progression
  71. Osteonecrosis (Avascular necrosis)
    • Beath of bony tissue as a result of los of blood supply in the absence of infection
    • 20–50 y/o
    • Male > female
    • Most common in bilateral femoral heads
    • Treatment: make things bleed
    • Idiopathic, sometimes related to trauma, associated with corticosteroid and alcohol use
    • Clinical manifestations: pain, loss of motion, antalgic gait, degenerative changes
    • Intervention: activity modification (sometimes getting weight off of joint helps blood flow), surgical (drill holes to make it bleed and then controlled motion it; joint replacement)
  72. Monoarticular Arthritis
    • Single joint
    • not symmetrical
    • Due to:
    • Infection
    • Trauma
    • Crystal insduced gout
    • Pseudo-gout
  73. Polyarticular Arthritis
    • Multiple joints involved
    • Degenerative: Primary, Secondary, Trauma, Mechanical
    • Metabolic: Gout, Amyloid, Hyperlipidemia, CPPD
    • Rheumatoid-like (inflammatory nature, affects joints, but also other organ tissue: RA, SLE, Systemica Sclerosis, Polymayalgia Rheumatica
    • Spondyloarthropathy (predominantly affects axial skelton, hips, and shoulders): Ankylosing Spondylitis, Reactive Arthritis, Psoriatic Arthritis
  74. Epidemiology of RA
    • 1% of US population
    • Adult onset: 30–50 y/o
    • Childhood onset: 6 mo – 2 yrs
    • Female > male (3:1)
  75. Causative Factors of RA
    • Infection: can trigger
    • Heart disease: very prevalent --> high mortailty rate. RA as signifcant a risk factor for CVD as DM
    • Respiratory failure
    • Renal failure
    • GI disease
  76. Pathogenesis of RA
    • Autoimmune disease: affecting immune system
    • Genetic: some identified alleles that correlate to increased risk
    • Problem with the intrasynovial lining --> vascular component
    • Damage from pro-inflammatory activity
  77. Development of RA
    • Stage 1: Genetic: asymptomatic, but have family history
    • Exposure (e.g. smoking) that causes RA to flare up
    • Stage 2: Inflammation: pro-inflammatory activity, but still asymptomatic
    • Stage 3: Early symptoms: morning stiffness > 1 hour, joint pain, swelling and warmth of joints
    • Stage 4: Inflammatory Arthritis. Can lead to joint death
  78. Characteristics of RA
    • Systemic: people present as if they have the flu
    • Chronic fluctuating course: exacerbates and remits unpredictably
    • Symmetric
    • Disease of the synovium – can eventually kill cartilage and erode bone
    • Extra-articular manifestions
    • Risk of premature death
  79. Calssification for RA
    • Must have 4/7
    • Morning stiffness > 1 hour
    • Swelling or fluid ≥ 3 joints
    • Arthritis in hands
    • Symmetric involvement
    • Subcutaneous nodules – under the skin at areas of pressure
    • Abnormal serum RF – can have a negative RF but still have RA
    • Radiographic changes – new patients will have a baseline xray
  80. Functional Status Classification of RA
    • Class I: Completely able to perform ADL's
    • Class II: Performs self-care and vocational activities, but lmited avocational activities
    • Class III: Able to perform self-care but limited voactional and avocational activities
    • Class IV: Limited in all areas
  81. Disease Course
    • Chronic fluctuating course
    • More swollen and involved joints at onset, greater the activity and erosion
    • Early, aggressive durg therapy may be the most effective
  82. Systemic Symptoms of RA
    • Fatigue
    • Malaise
    • Weakness
    • Fever
    • Weight loss – very sudden, can be up to 10 lbs in less than two weeks
  83. RA Joint
    • Inflammation of synovium – synovitis (warm to touch, not hot)
    • Thinning of cartilage – body eats away at cartilage, if it reaches bone, can have OA arthritis changes too
    • Inflammation of tendon sheaths – tenosynovitis, and pain at tendon insertions
  84. Hands and Wrists in RA
    • Tendons slip out of place and joints swell --> ulnar deviation of wrist and MCPs, swan-neck, Boutonneire's deformity
    • Symmetric but not necessarily equal
  85. C-spine Involvement in RA
    • 50% of patients:
    • AO subluxation
    • Subaxial subluxation
    • Basilar invagination of foramen magnum
    • Signs and symptoms:
    • Occipital headache, neck pain
    • Paresthesias in UE
    • Basilar – tinitus, vertigo, visual disturbances, dysphagia
    • Involvement of alar ligament: swelling of ligament --> neck becomes highly unstable --> must do alar ligament test
  86. Changes in Feet in RA
    • Cock-up toes: flexed toes stuck in that position --> difficult to get into/find shoes that fit
    • Fat pads on plantar surface of foot start disappearing: heads of MTs have no padding --> need more padded shoes
    • Busitis in talocalcaneal region
    • Pronation
    • Hallux valgus and bunions
    • Depression of MT heads
    • Hammer or claw toes
    • Subplantar spur formation
  87. Extra-articular Rheumatoid Nodules
    • 15–40% of patients
    • Seen in areas of repeated friction (e.g. elbow) and in viscera of heart and lungs
    • Associated with low dose methotrexate
    • Painful, but can often be removed from joints, but not lunges and heart
    • When present in lungs, can make aerobic activity very difficult and painful
  88. Extra-articular RA – Pleaura and Lungs
    • Pleura and lung disease evident in 75% of patients
    • Pleural effusion only 5%
    • 1/3 of patients with pleaural effusion have interstitial disease
    • Interstitial fibrosis:
    • Men > women
    • with rheumatic nodules
    • +RF
    • How they look:
    • SOB: don't know if it's interstitial fibrosis or just inactivity: 6 minute walk test
    • Incorporate aerobic activity into POC to maximise lung capacity
  89. Extra-articular RA – Cardiac
    • Risk of CVD same as DM
    • Usually asymptomatic — changes seen on autopsy:
    • mitral valve prolapse or thickening
    • posterior pericardial effusion
    • aortic root dilation and thickening
  90. Laboratory Tests for RA
    • Non-specific markers on inflammation: don't tell what is wrong, just show that there is inflammation in the body. Used more for prognosis than diagnosis — are they more likely to have more severe disease down the line
    • Frequent findings:
    • Reduced RBC count --> fatigue
    • elevated erythrocyte sedimentation rate (ESR) --> inflammatory
    • may or may not have +RF -->if + more likely to be sicker down the line. Marker of disease progression
    • Occasional findings:
    • increased or decreased WBC count
    • increased or decreased platelet count
    • +ANA (Antibodies to Nuclear Antigens)
    • +pANCA (Antineutrophil Cytroplasmic Antibodies)
    • ANA and pANCA are markers of disease activity more than diagnostic

    often do assessment of synovial fluid
  91. Non-specific markers on Inflammation in RA
    • Elevated ESR: infication of inflammation, does not give a lot of info
    • -age and gender specific
    • -could be a result if anemia

    • C-Reactive protein (CRP): better than ESR because it's not affected by anemia
    • -rises and falls with inflammation
    • -more stable measure of inflammation
    • -independent marker of coronary heart disease --> increased CRP, more likely to have heart involvement
  92. HLA Typing for RA
    • A way to rule in or rule out different rheumatic conditions
    • HLA-DR4 increased in patients with RA
  93. Outcome Measures in RA
    • Disease specific outcome measures:
    • DAS-CRP 3 — mix of CRP plus joint score (Disease Activity Score). Joint score graded on effusion in joint, derangement of joint, and pain in the joint
    • - >3.7: highly active disease: when touch joints, warm, boggy, painful
    • - < 2.4: mild

    Health Assessment Questionaire (HAQ): asks questions about functional ability: 0 = no limitations. 3 = very limited in everything
  94. RA Drugs/Treatment Options
    • NSAIDs: reduce pain but don't change the course of the disease at all
    • DMARDs: (disease modifying agents): MTX (methotrexate — gold standard), TNFI, anti-malarials, corticosteroids, immunomodulators (Imuran). Leflumonide (works well, but many side effects, tetrogrenic agent so not good for women trying to get pregnant)

    Involvement of other organs (liver, kidneys etc) can preclude patient from taking certain drugs

    • Biologic Therapy: for patients who are non-responsive to other DMARDs
    • B-lymphocyte therapy: "reboots" immune system (B cells produce RF)
  95. Rehabilitation Goals and Considerations for RA
    • Maximise:
    • muscular strength — weakness can result from deconditioning, or from the inflammatory response
    • flexibility — so joints stay in good alginment
    • endurance
    • mobility
    • patient independence and self-management skills — can have sudden flare, need to know what to do and when

    • Always screen BP and HR before, during, and after exercise
    • Be cognizant of fatigue — often have decreased aerobic capacity

    • Some drugs take months to start working, some hours, so be aware of that and also how long the drug is effective for when planning treatments
    • Be aware of drug side-effects
  96. Rehabilitation Interventions for RA
    • Joint protection — splinting reduces biomechanical strain. Resting (at night) and functional
    • Energy Conservation and Rest — need to pace themselves, get 8–10 hours of sleep, rests during the day
    • Self-Management Skills
    • Work Modification
    • Education
    • Exercise
  97. Exercise for RA
    • ROM
    • Muscle strength
    • Endurance
    • Proper joint alignment and function
    • Bone density
  98. RA Intervention Algorithm
    • Acute Inflammatory (flu like symptoms, swollen joints, warm to touch): Rest, splints, modalities isometrics, ROM, keep active. Joint checks: stiff joint do ROM exercises
    • Subacute (some joint still have inflammation, but not boggy or warm anymore): dynamic and ROM exercises, ergonomic interventions; physical activity. Progressive strengthening program if joints are not deranged
    • Chronic/Inactive (no inflammation): aerobic exercises, work accomodations. Get the patiens as strong and fit as possible. Make physical activity an integral part of their lives (stairs, walking, etc)
  99. Systemic Lupus Erythematosus (SLE)
    • Most prevalent in childbearing aged women
    • Female > male (9:1)
    • 2–3 times more common in people of African, Hispanic, or Asian decent
    • More severe than RA: can have neurocognitive components, high incidence of nephritis, higher mortality
  100. Etiology of SLE
    • Autoimmune disease
    • Environmental — people who live near benzene or petrochemical plants have higher incidence, EBV can trigger, UV light, dietary
    • Genetic — runs in families and racial groups; autoimmune complex disorder (lupus, hemolytic anemia, thyroid disease, DM, MS)
    • Hromonal
  101. Symptoms of SLE
    • Red "butterfly" rash (like sunburn)
    • Nephritis --> unstable BP
    • Pleural effusions
    • Cardiac conditions
    • Raynaud's syndrome — don't have good blood supply to hands and feet
    • Joints not really involved, if they are, usually due to lack of blood supply to joint
  102. ACR and Diagnostic Criteria for SLE
    • Malar rash
    • Discoid rash
    • Photosensitivity — sunburn, headaches, cannot tolerate sun
    • Oral ulcers
    • Arthritis
    • Serositis — Inflammation around heart and lungs
    • Renal disorder — High blood pressure
    • Neurocognitive lupus — get confused, can't do count backward by 3's test
    • Alopecia — hair loss
  103. Diagnostic Laboratory Criteria for SLE
    • Many of the same tests as RA
    • ESR
    • CRP
    • Antiphospholipid antibodies (APL) — high risk for developing clots. Women may have multiple miscarriages, because develops antibodies that produce clots
    • Lupus anticoagulant
    • Anti-DNA antibodies
    • ANA

    Show inflammation, but not where it is coming from

    • Anemia
    • Leukopenia — common in active disease. Patients more susceptible to infection, must be very careful to sterilise equipment
    • Thrombocytopenia
    • Serologies: anti-rho (associated with photosensitivity) and anti-la; complement proteins to monitor kidney disease; +ANA most often found in lupus
    • Kidney and Cardiovascular diease
  104. Changes in Outcome of SLE
    • Historically patients died of kidney disease
    • Now, patients die of heart disease:
    • CHD 9–11 times great in people with SLE than general population
    • Premature "accelerated" athersclerosis
  105. Treatment of SLE
    • Prednisone, NSAIDs — to decrease pain and inflammation
    • Hydroxychloroquine and methotrexate — DMARDs
    • Cyclophosphamide — anti-inflammatory, very effective with kidneys
    • Vitamin D and calcium — bone and muscle strength
    • Coumadin — if the patient is at risk for a clot
    • Avoid steroids
  106. PT Interventions for SLE
    • Education about photosensitivity
    • Education about aerobic condition for BP and heart issues
    • Rest and support
    • Diet, nutrition, vitamins
    • Exercise
    • Contraceptions and pregnancy advice and planning — usually addressed by physician
    • Immunization with killed vaccines
    • Always monitor BP and HR
  107. SLE WHO Calssification of Renal Pathology
    • I: Normal
    • II: Mesangial hypertrophy
    • III: Focal glomerulonephritis
    • IV: Diffuse glomerulonephritis
    • V: Membranous glomerulonephritis
    • VI: Advanced sclerosing glomerulonephritis

    • Types I, II, and III: nothing or low dose steroids, follow closely
    • Type IV: pulse steroids, pulse cyclophosphamide, azathiprine, Mycophenylate Mofetil
    • Type V: steroids, cyclosporine
  108. Ankylosing Spondylitis
    • Host factors: men > women 14–40 y/o, HLA-B27+, rare in African Americans
    • Disease Process: Inflammatory, arthropathy, enthesopathy
    • Joint Involvement: Spine, SI, shoulders and hips most common peripheral joints
    • Systemic features: acute iritis, Cardiac valvel involvement insuffiency, apical pulmonary fibrosus
    • Etiology: unknown
    • Laboratory: elevated CPK, ? increased ESR
  109. Clinical Presentation of Ankylosing Spondylitis
    • Back pain and morning stiffness > 1 hour
    • Enthesopathy — inflammation of tendons. Complain of pain/discomfort at insertions of tendons
    • SI joint pain — can't sit cross legged
    • SOB especially with leaning over — due to cardiac involvement, usually valves
    • UVitis —
  110. Signs and Symptoms of AS
    • Early:
    • Fever
    • Weight loss
    • Fatigue
    • Synovitis
    • Pain/stiffness with inactivity (AM stiffness prminent) — don't like to be straight/ extended, prefer flexed spine position
    • Tenderness of SI joint
    • Enthesitis – achilles and
    • Late:
    • Osteophytes
    • Fibrosis
    • Loss of ROM in spine and hips
    • OA hip joints
    • Glaucoma, iritis
    • Bamboo Spine — joints of spine fused together in flexed position
  111. Signs and Symptoms of AS Cont.
    • Signs:
    • decreased spinal motion in all planes
    • increased thoracic kyphosis, decreased lumbar lordosis
    • gait deviations
    • C1–C2 subluxation
    • spinal stenosis with neurogenic claudication

    • Symptoms:
    • back stiffness
    • low back, hip, buttocks, or neck pain (achy or intermittently sharp)
    • improve with activity, worsen with rest
    • significant AM stiffness >1 hour
    • enthesitis — PF, achilles, tib tub, CS, ischial tub
  112. Diagnostic Tests for AS
    • X-rays: blurring of joint margins, erosion and joint space narrowing
    • MRI: not done often
    • +HLA-B27: helps rule out other diagnoses, but not definitive for AS
  113. Medical Management of AS
    • NSAIDs in early stages: indomethecin — wathc for GI upset
    • DMARD: sulfasalazine
    • Immunosuppressants: inflixamib
  114. PT Interventions for AS
    • Anything that promotes rotation and extension
    • PNF techniques
    • aerobic, flexibility
    • Postural education — stand in front of mirror at home
    • Pain management and modalities
  115. Psoriatic Arthritis
    • Similar to RA, but with psoriatic rash
    • Age 25–50
    • Usually get psoriasis first
    • HLA-B27
    • Family association
    • Slower progression and less erratic than RA
    • Damage to cartilage and bones can lead to joint replacement
    • Involvement mostly in hands and feet, but can affect knees and ankles
    • dactylitis — sausage fingers
    • Unilateral SI joint involvement
    • Asymmetrical, oligo-articular disease
  116. Signs and Symptoms of PA
    • Signs:
    • warmth, tenderness, swelling
    • "sausage-like" appearance
    • acne and nail changes
    • psoriatic plaques

    • Symptoms:
    • painful joints
    • morning stiffness
  117. Diagnostic Tests for PA
    • History/presence of psoriasis
    • Rule out other disorders:
    • negative serum RF
    • negative elevated serum uric acid
    • negative urate crystals with joint aspiration
  118. Medical Management of PA
    • NSAIDs: reduce pain and inflammation
    • For severe cases:
    • antimalarials
    • corticosteroids
    • immunomodulators
  119. PT Interventions for PA
    • Pain managemtns
    • Joint protection
    • Maintain strength and flexibility in surrounding areas with active exercise with not in acute inflammation
  120. Reactive Arthritis — Reiter's Syndrome
    • Seronegative spondyloarthropathy (affecting the spine)
    • Usually caused by an infectious agent (often after an STD)
    • Reiter's is most common reactive arthritis
    • symptoms start 2–4 weeks after infection
    • men > women
    • more common in HIV infected
    • feet, knees, ankles, and spine involved
    • can be treated and it goes away (usually <1 year), but damage to the joints increases risk for OA later in life
  121. Triad of Symptoms Associated with Reiter's Syndrome
    • Conjunctivites/uveitis
    • Urethritis
    • Arthritis — knee, ankle

    Short lived, can't see (uveitis), can't pee (urethritis), can't climb a tree (arthritis)
  122. Medical Management for Spondyloarthropathies
    • NSAIDs — indomethecin
    • DMARDs — MTX
    • Biologics — TNFI
    • Corticosteroids
    • PT: focus on joint protection, maintanence of function
  123. Gout
    • Metabolics disorder
    • Hyperuricemia — deposition of urate crystals in joints, soft tissues (tophi), and kidneys
    • Crystal aggregate triggers inflammatory response
    • Mono-articular, inflammatory — often 1st MTP
    • Dietary component: made worse by alcohol and fatty foods
    • Joints are warm and red
    • Male > female
    • 40–50 y/o
    • Obesity increase UA production
    • Diurectic use decreases UA excretion (not as much fluid in body)
    • HTN and kidney disease
  124. Gout — Course of Disease
    • Acute gouty arthritis: 1st attack
    • Very painful
    • Short lived: hour to days, sometimes weeks
    • Intercitical Gout: longer, after multiple acute flares
    • More exacerbations --> spread to other joints
    • Chronic Tophaceous Gout:
    • destructive disease
    • can be crippling
    • alters joints considerably
  125. Signs and Symptoms of Gout
    • Signs:
    • warmth
    • extreme tenderness
    • hypersensitivty
    • ? fever/chills

    • Symptoms:
    • bad pain, mostly at night
    • Inability to weight bear
  126. PT Interventions for Gout
    • Modify therapy during active attack
    • Assistive devices
    • Patient education on joint protections
    • Not doing a lot, not seeing Gout patients as primary diagnosis
  127. Medical Treatment of Gout
    • Acute Gouty Attack:
    • NSAIDs —indomethecin, NEVER ASPIRIN —> can thin blood too much, irritates gut
    • Costicosteroids is NSAIDs don't work
    • Colchine
    • 2–3 attacks per year: start preventative rx
    • most common is allupurinol
Card Set
Pathology Exam 1
Pathology Exam 1