Pathology Exam 1

• lack of, or decreased blood flow to a cell, organ, or body tissue
• common in the heart as a result of CAD

• 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

Study of the cause of disease or injury

Diseases with no identifiable cause

disease or injury as a result of medical intervention

Any abnormal cconditions that follw and are the result of a disease rx or injury

• Top of crow's foot
• Normal male: 14–18 g/dl
• Normal female: 12–16 g/dl
• 1/3 of HCT

• Bottom of crow's foot
• Percent of RBCs in a given volume of blood
• Normal male: 47%
• Normal female: 41%

• 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

• 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

• 1-4% of WBC count
• Fight parasites
• Important in asthma and allergies
• Mediate inflammatory process

• Horse-shoe shaped
• Turn into macrophages at site of inflammationg
• Initiate inflammatory response

• 36% of WBC count
• Main ones are t- and b-cells
• middle to late in inflammatory process

• 5–10% of WBC count
• Attack viruses
• attack cells infected with a virus the body has not seen before

• Not cells
• Allow blood to clot

• too many RBCs
• ex: leukemia

• Too few RBCs
• ex: anemia

MCV (mean corpuscle value: size of RBC): reference range: 80–100 fl

• Immature RBC
• 0.5–1% of RBC volume
• decrease with bone marrow problems
• increase with increased RBC production

• Microcytic anemia
• Genetic disorder: found in Greeks, Italians, African American, American Indian, and Asian
• Microcytosis and mild anemia, may need blood transfusions if severe

• RBC's too big and too few
• Elevated MCV lab

• Elevated MCV
• Usually due to B12 and iron defficiency

• 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)

• 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)

• 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

• 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

• Myeloproliferative disorder: affects WBCs and RBCs
• Insidious
• Increased clotting
• Enlarged spleen and liver
• Ruddy complexion (pruritis)

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

• 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

High neutrophil count

• Causes:
• infection
• inflammation
• tissue necrosis
• acute hemorrhage/hemolysis
• drugs such as lithium

High lymphocyte count

• Causes:
• viral infection
• TB, pertussis, hepatitis

• Total WBC count < normal (4000): be cautious
• Total WBC count < 1000: immunocompromised, take infection control measures (gown, gloves, mask): protect patient from infection

• Right side of crow's foot
• Thrombocytopenia: too few platelet
• Thrombocytosis: too many platelets

• 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

• 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

• 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

• Indications: TIA, CVA, MI and angina prevention
• - PVD
• Complications: bleeding, GI bleeding, interaction with BP meds

• 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

• Diaphysis = mid shaft
• Metaphysis = flared portion of distal ends
• Physis = growth plate
• Epiphysis = adjacent to physis and most distal
• Articular cartilage forms over epiphysis

• 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)

Skin over and near fracture is intact

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

• Local: inflammation (red), warm, pain,
• Systemic: fever

• Kids
• Growth plates – potentional for limb length discrepency in future

• 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

Bone growing in relation to stress

• 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

• 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

• 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

• < 12 y/o: 4 servings a day
• 12–20: 3 servings a day
• 20–menopause: 2 servings a day
• > menopause: 3 servings a day

• 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

• 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

• 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

• 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

• 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

• 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

• 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)

• 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

helps body take calcium from blood and use it to build bone – Wolff's Law

• 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

• Screening often done after onset of symptoms/fracture
• Bone density measurements:
• DXA
• Ultrasound
• CT scan
• Lab tests: probably the best

• 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

• Rickets in children
• Insufficient mineralisation in bone matrix, results from calcium of phosphate deficiency
• Vitamin D deficiency is a causative factor

• Inadequate synthesis or dietary deficiency of vitamin D
• Decreased absorption of fat-soluble vitamin D
• Derangements in vitamin D metabolism
• Phosphate depletion

• 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

• 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

• 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

• Warmth, swelling, tenderness, delayed onset of pain
• Fever (endogenous > exogenous)
• Malaise – flu-like symptoms

• Evaluation: WBC count, culture/biopsy, imaging
• Treatment: acute: antibiotics. Chronic: surgical debridment, bone/skin grafts, hyperbaric oxygen

• Prevention: universal precautions
• Know weight-bearing status
• Use lab date and vital signs to guide exercise progression

• 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)

• Single joint
• not symmetrical
• Due to:
• Infection
• Trauma
• Crystal insduced gout
• Pseudo-gout

• 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

• 1% of US population
• Adult onset: 30–50 y/o
• Childhood onset: 6 mo – 2 yrs
• Female > male (3:1)

• 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

• 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

• 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

• 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

• 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

• 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

• Chronic fluctuating course
• More swollen and involved joints at onset, greater the activity and erosion
• Early, aggressive durg therapy may be the most effective

• Fatigue
• Malaise
• Weakness
• Fever
• Weight loss – very sudden, can be up to 10 lbs in less than two weeks

• 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

• Tendons slip out of place and joints swell --> ulnar deviation of wrist and MCPs, swan-neck, Boutonneire's deformity
• Symmetric but not necessarily equal

• 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

• 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

• 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

• 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

• 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

• 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

• 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

• A way to rule in or rule out different rheumatic conditions
• HLA-DR4 increased in patients with 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

• 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)

• 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

• 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

• ROM
• Muscle strength
• Endurance
• Proper joint alignment and function
• Bone density

• 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)

• 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

• 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

• 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

• 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

• 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

• 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

• 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

• 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

• 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

• 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

• 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 —

• 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

• 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

• 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

• NSAIDs in early stages: indomethecin — wathc for GI upset
• DMARD: sulfasalazine
• Immunosuppressants: inflixamib

• Anything that promotes rotation and extension
• PNF techniques
• aerobic, flexibility
• Postural education — stand in front of mirror at home
• Pain management and modalities

• 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

• Signs:
• warmth, tenderness, swelling
• "sausage-like" appearance
• acne and nail changes
• psoriatic plaques

• Symptoms:
• painful joints
• morning stiffness

• History/presence of psoriasis
• Rule out other disorders:
• negative serum RF
• negative elevated serum uric acid
• negative urate crystals with joint aspiration

• NSAIDs: reduce pain and inflammation
• For severe cases:
• antimalarials
• corticosteroids
• immunomodulators

• Pain managemtns
• Joint protection
• Maintain strength and flexibility in surrounding areas with active exercise with not in acute inflammation

• 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

• Conjunctivites/uveitis
• Urethritis
• Arthritis — knee, ankle

Short lived, can't see (uveitis), can't pee (urethritis), can't climb a tree (arthritis)

• NSAIDs — indomethecin
• DMARDs — MTX
• Biologics — TNFI
• Corticosteroids
• PT: focus on joint protection, maintanence of function

• 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

• 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

• Signs:
• warmth
• extreme tenderness
• hypersensitivty
• ? fever/chills

• Symptoms:
• bad pain, mostly at night
• Inability to weight bear

• Modify therapy during active attack
• Assistive devices
• Patient education on joint protections
• Not doing a lot, not seeing Gout patients as primary diagnosis

• 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