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Clinical Medicine 1 > Lecture 2- Rheum > Flashcards

Lecture 2- Rheum Flashcards

1
Q

Elderly patient bones:
* What decreases in bone?
* What is the most common fractures?

A
  • Mineral content decreases
  • Less water content in cartilage
  • Connective tissues lose elasticity
  • The most common fractures in the elderly osteoporotic patients in the chart
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2
Q

What is an important assessment in the aging patient

A

Monitoring for Height Changes via the spinal column

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3
Q

Elderly patient muscles:
* What happens and what accelerates it?
* What decreases (3)?
* What declines in efficiency?
* What slows down?
* What increases?

A
  • Shrink and lose mass – as sedentary life accelerates
  • # and size of muscle fibers decrease
  • Water content of tendons decreases
  • Handgrip strength decreases
  • Heart muscle declines in efficiency
  • Metabolism slows
  • Lipids increase
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4
Q

How do you counteract the process of muscle wasting in elderly patients?

A
  • Many of these changes result from disuse
  • The most sedentary group in US is >50
  • Exercise (weight-resistant specifically) and stretching is key
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5
Q

Sacropenia:
* What is sacropenia?
* What does it correspond with?
* What tightens?
* What is replaced with adipose tissue?

A
  • Age related decrease in muscles
  • Corresponding loss in balance and coordination
  • Joint capsules tighten and lose flexibility
  • Lean muscle mass replaced by adipose tissue

Cannot do ADLs so neeed to ensure muscle is okay

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6
Q

What is going on with these images?

A
  • Increase adipose and decrease muscle
  • Major health concern affecting 25% of people younger than 70 years and 40% of those 80 years and older
  • Healthcare related costs – 18. 5 Billion in 2000 (NIH, 2011)
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7
Q
  • What is the treatment for increase adipose and decrease muscle?
  • What did Tufts university study revealed?
  • What did a New Zealand study reveal?
A
  • Resistance strength training even in the very aged and frail
  • A Tufts University study revealed a 43% decrease in arthritic knee pain along with increased strength, decreased disability and general physical performance after a 16 week program of strength training
  • A New Zealand study revealed a 40% reduction in falls (Women > 80)
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8
Q
  • The effects of aging on the musculoskeletal system may be counteracted, to a degree, with what?
  • All seniors, regardless of disability should have what?
  • What should you not assume about geriatric pain?
A
  • The effects of aging on the musculoskeletal system may be counteracted, to a degree, with exercise – specifically weight/resistance training.
  • All seniors, regardless of disability should have some sort of exercise built into treatment plan
  • Don’t assume all geriatric pain is osteoarthritis! (if they are losing height then check the spine)
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9
Q

Osteoporosis:
* What is it?
* What decreases?
* What is there a greater chance of?

A
  • Abnormal bone remodeling disease.
  • Decreased in total bone volume. Bone is less dense as you get older.
  • Greater chance of fractures
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10
Q

What is the difference between osteopenia and osteoporosis?

A
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11
Q

Osteoporosis:
* What varys with age?
* How much do men and women need?

A

Calcium need vary with age and gender BUT need to be careful giving out supplements (ex. CHD and kidney disease)
* Women 51-70 need 1200mg/day
* Men 51-70 need 1000mg/day (a little less because not as estrogen dependent)
* Men and Women >70 need 1,200/day

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12
Q

Epidemiology of osteoporosis:
* When is low bone mass more common? What might it be related to?
* What may lead to an increase risk fracture?

A
  • Low bone mass is more common in postmenopausal women and, when present, may be related to either inadequate peak bone mass acquisition, or previous or continuing bone loss.
  • The clinical significance of isolated low bone density (without fracture) in young women is unknown. Some premenopausal women with low bone mineral density (BMD), particularly those with a known secondary cause of osteoporosis, may have abnormal bone strength that may lead to an increased risk of fracture.

Patho fracture, menopause, osteopenia= you need to look at bone den scan

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13
Q

What are the two types of primary osteoporosis?

A

Primary Osteoporosis (more common form) most
* Type 1 – Postmenopausal – due to decrease in estrogen or testosterone
* Type 2 – Senile – Inability to produce adequate Vit. D3 resulting in decreased
bone formation

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14
Q

What is secondary osteoporosis?

A

Secondary Osteoporosis (when other disease conditions predispose
to bone loss)
* Medications
* HyperPTH (more calcium in blood than bone)
* Excess ETOH use
* Smoking

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15
Q

Osteoporosis:
What are the typical symptoms and signs?

A

Typical symptoms:
* Back pain, loss of height, spinal deformities and protruding abdomen (dt lordosis and kyphosis)

Typical Signs:
* T score <-2.5 or FRAX >3% for hip fractures or >20% for major osteoporotic fx

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16
Q

What might be detected in x-ray with osteoporosis?

A

Bone Density Deficiency May Be Detected on X-ray (osteopenia), but Not diagnosed because you need a dexa scan

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17
Q

What is the dexa t-scores for diagnosis of osteoporosis?

A
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18
Q

What is the fracture risk assessment tool (FRAX)?

A
  • The FRAX® tool has been developed to evaluate fracture risk of patients. It is based on individual patient models that integrate the risks associated with clinical risk factors as well as bone mineral density (BMD) at the femoral neck.
  • The FRAX® algorithms give the 10-year probability of fracture. The output is a 10-year probability of hip fracture and the 10-year probability of a major osteoporotic fracture (clinical spine, forearm, hip or shoulder fracture)

ex. get a 2.2 for t scale so do a frax test to help educate

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19
Q

What is the treatment of osteoporosis?

A
  • Weight-bearing exercises with resistance training
  • Calcium, Vitamin D, and Phosphorus
  • No Smoking
  • Limited ETOH
  • Bisphosphonates-Alendronate (Fosamax)
    * Osteonecrosis of jaw (SE)
  • HRT
  • SERMS
  • PTH analog meds (teriparatide)-> for hyperparathyriod
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20
Q

What is osteoarthritis?

A

Degenerative disease
* overuse problem
* genetic or no genetic
* 70-80 year olds

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21
Q

OA Epidemiology:
* How many people are affected by OA?
* Women vs men?
* Who has a higher prevalence and severity of OA?

A
  • Globally, approximately 300 million people are affected by hip and knee OA, including over 32 million in the United States, which has increased from 21 million in 1990 and 27 million in 2010.
  • Worldwide estimates are that 10 percent of men and 18 percent of women aged over 60 years have symptomatic OA
  • Female gender is associated with a higher prevalence and severity of OA.
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22
Q
  • What is the strongest predictor of OA?
  • What are the possible causes?
A
  • Age is one of the strongest predictors of OA, with incidence of hand, hip, and knee OA increasing with age, especially after the age of 50 years.
  • Possible causes are sarcopenia, loss of proprioception, and joint laxity that may affect joint function and predispose the joint to injury. Changes affecting joint tissues include loss of normal bone structure, increased stiffness of ligaments and tendons, and meniscal degeneration.
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23
Q

What is primary and secondary classification of OA?

A

Primary (idiopathic)
* No underlying cause apparent

Secondary
* Predisposing factor present - trauma, repetitive stress (occupation, sports),
congenital abnormality, metabolic disorder, or bone/joint disease

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24
Q
  • What are the primary symptoms of osteoarthritis (OA)?
  • Where do you they usally present?
  • What bones are most likely affected?
A
  • The primary symptoms of osteoarthritis (OA) are joint pain, stiffness lasting < 1 hour, crepitus, no systemic symptoms and locomotor restriction. ( not a systemic issue like fever, inflammation)
  • They usually present in just one or a few joints in a middle-aged or older person.
  • Hand DIP/PIP are most likely affected
    * MCP joints except thumb (1st CMC) are spared

RA is most likey to be bilateral

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25
Q

OA:
* What type of patients?

A
  • Older patients
  • F>M
  • Asymmetric
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26
Q

OA:
* What are the nodes of DIP and PIP called?
* What are the diagnostic levels?
* What are other issues?

A
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27
Q
  • What are non-pharm txt of OA?
  • Pharmacological txt?
  • What is the last resort?
A
  • Weight reduction, moderate physical activity, NSAIDs, intra-articular steroids, bracing, canes, and muscle-strengthening exercises
  • Acetaminophen vs NSAIDs (depends on risk factors, but NSAIDs are preferred)
  • Intraarticular glucocorticoid injections provide symptomatic relief but do infrequently as cartilage breakdown may be accelerated if performed too often
    * Systemic glucocorticoids have no place in Rx of OA (RA might get this)
  • Surgery last resort

NSAIDs: kideney clearance so be careful with diabetes, HTN, and kidney disease

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28
Q

Fill in

A
  • OA – assymetrical, weight bearing, NO redness or heat, Pain gets worse as day goes on and is alleviated by rest.
  • RA – symmetrical (PIP/MCP), worse in AM and gets better as day goes on.
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29
Q

Epidemiology of RA:
* What is the prevalence worldwide?
* What is the prevalence and northern european countries?
* How many people are affected?

A
  • The worldwide prevalence of RA has been estimated as 0.24 percent based upon the Global Burden of Disease 2010 Study.
  • Estimates of RA prevalence in the United States and northern European countries are typically higher, usually between 0.5 to 1
    percent dt auntoimmune, diet
  • The annual incidence of RA in the United States and northern European countries is estimated to be approximately 40 per 100,000 persons (also undiagnosised)
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30
Q

What is RA? What are the causes?

A
  • Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by an inflammatory polyarthritis that preferentially affects the small joints.
  • RA is a “multicausal” disease that most likely results from a combination of genetic predisposition and various environmental and lifestyle factors. Articular and systemic manifestations in RA can lead to poor long-term outcomes such as disability and death
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31
Q

What are RA clinical presentation?

A
  • MCP joints are involved, others are spared.
  • Joint pain and deformity
  • Muscle weakness, myositis, osteopenia, and osteoporosis
  • Extra-articular manifestations include changes in skin, lungs, kidneys, eyes, liver, blood system, and heart-> pul hem, chronic kidney disease, rash, eye issue
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32
Q

What are the clinical symptoms of RA (articular manifestations)

A

Symmetric polyarthritis involving small joints, may start as simple inflammation or synovitis, will progress to bone/cartilage erosions

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33
Q

What are the extra articular manifestations of RA?

A
  • General: Fatigue, fever, weight loss
  • Derm: Nodules
  • Heme: Anemia (Felty’s Syndrome)
  • Pulmonary: pleuritis/pneumonitis
  • Cardiac: Peri or myocarditis and higher chance of having DVT (has autoimmune then need high awareness)
  • Renal: Interstitial nephritis
  • Ophthalmic: Episcleritis
  • GI: Xerostomia
  • MS: myositis
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34
Q

What is the cervical spine involvement of RA?

A
  • Common at C1-C2, but remainder of spine is usually spared
  • Instability of C spine is a life threatening complication of RA.
  • Instability results from a cervical ligament synovitis in region of C1-C2. * Occurs in 30-40% of pts who develop RA
  • 5% of these eventually develop a myelopathy or cord injury

Issue since breathing is C4 so anything above-> DEAD

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35
Q

RA Diagnosis/Imaging:
* What needs to be quantified?
* What are the diagnosisic levels?
* What may be seen on x-ray?
* What may be evident?

A
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36
Q

What is the diagnostic criteria for RA?

A

A score ≥ 6 is needed for classification of a patient as having definite RA

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37
Q

What is the treatment of RA?

A

Consult with rheumatology
* PT/OT
* Pharm tx early and aggressive to reduce pain, preserve function, and prevent deformity
* NSAIDs with DMARDs (usually started together)
* DMARDs-initially methotrexate

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38
Q

What are the other DMARDs and newer biologic DMARDs for RA?

A
  • Others DMARDs are steroids, sulfasalazine, antimalarials (hydroxychloroquine), and leflunomide.
  • Newer biologic DMARDs are etanercept, abatacept, rituximab, infliximab, and adalimumab
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39
Q

What is felty’s syndrome?

A

Felty’s syndrome which usually occurs late in the disease process is manifested by splenomegaly, neutropenia, & + RA factor.

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40
Q

What is caplan’s syndrome?

A

Pulmonary-nodules, interstitial disease, pleural disease, Caplan’s syndrome [sero(+) RA associated with pneumoconiosis]
* Sero (+) that of CRP or RF

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41
Q

What is Juvenile idiopathic arthritis?

A
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42
Q

JIA Epidemiology:
* Who does it affects?
* What is the incidence?
* What is the prevalence?
* What is the female to male ratio?

A
  • Affects all races and geographical locations
  • Incidence: 6-20 cases per 100,000 children
  • Prevalence: 16-150 per 100,000
  • Females to Males ratio: 2>1
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43
Q

JIA etiology:
* What is the exact cause?
* What type of disease is it?
* What is happening in JIA to cause the disease? (MOA)
* What needs to be ruled out before JIA diagnosis?

A
  • Exact Causes of JIA – UNKNOWN
  • Is Autoimmune disease – body attacks itself
  • In JIA, the synovial membrane is recognized by own immune system as a “foreign” invader, which causes immunologic attack in attempt to kill the tissue, hence the inflammatory process.
  • Infection (septic arthritis), cancer, bone disease, Lyme disease and lupus must be ruled out before making a JIA/JRA diagnosis
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44
Q

What are the signs and symptoms of JIA (articular and extra-articular)

A
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45
Q

Diagnosis Criteria of JIA:
* Age?
* Duration of disease?
* What happens to the joints?
* What is the exclusion of?

A
  • Age of Onset <16yo
  • Duration of Disease >6 weeks
  • Arthritis (swelling or effusion, limited ROM, tn or pain, increased warmth) in one or more joints
  • Exclusion of other forms of arthritis
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46
Q

What are the different types of disease defined in the first 6 months with JIA?

A

Type of disease defined in the first 6 months:
* Polyarticular: 5 or more inflamed joints
* Oligoarticular: less than 5 inflamed joints
* Systemic arthritis with presence of fever

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47
Q
A
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48
Q

JIA treatment:
* What is preferred?
* What other therapies are there?
* What do you need to monitor for?

A
  • DMARDs preferred over NSAIDs (2019 ACR guideline)
    * Methotrexate preferred, Alt: Leflunomide or sulfasalazine
    * MTX requires CBC (pancytopenia) and LFT monitoring (cirrhosis and hepatitis)
  • PT/OT
  • Anakinra, TNFs, or abatcept for intractable cases
  • Monitor for growth abnormalities, nutritional deficiencies and school/social impairment.
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49
Q

JIA:
* Who has a poorer prognosis than other children do?

A

Children with systemic JIA who fail to respond adequately to therapy have a significantly poorer prognosis than do children who achieve disease control.

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50
Q

Fibromyalgia Epidemiology:
* What is it?
* What is the prevalence?
* What was it initally termed? More common in who?

A
  • Fibromyalgia (FM) is a common cause of chronic pain and the most common cause of generalized, musculoskeletal pain in women between ages of 20 and 55 years
  • Prevalence is 2-3 percent and increases with age.
  • Initially termed fibrositis, FM is more common in women than men and occurs in both children and adults. It is six times more common in women

The diagnosis may be under-recognized in clinical practice according to some sources, others indicate that those that are diagnosed, only half meet the actual criteria.

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51
Q

Fibromyalgia Etiology:
* What are the issues?

A
  • Alterations in CNS pain processing patterns
  • Sleep, mood, stress and cognitive disturbances.
  • Genetics and environment
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52
Q

What are the different clinical presentations of FM?

A
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53
Q

Fibromyalgia:
* What do you need to rule out?
* How was it previously diagnosed?

A
  • Rule out Differential diagnosis (Hypothyroidism, Hep C, Vitamin D deficiency, inflammatory processes)
  • No specific tests, previously was diagnosed using tender point counting, no longer validated
    * Generalized pain and tenderness, especially if disproportionate to physical findings
    * Negative laboratory results despite widespread symptoms
    * Fatigue as a predominant symptom
  • Clinical diagnosis-> rule out everything before FM
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54
Q

What is the treatment of FM?

A
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55
Q

What is the prognosis for FM?

A
  • Chronic issue
  • Waves often-> pain up and down
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56
Q

Polymyositis (PM) & Dermatomyositis (DM):
* What is it?
* What is it when skin is affected?
* What are other organs?

A
  • Inflammatory CTD of WBC’s attacking healthy striated muscle
    affecting the proximal limbs, neck, pharynx.
  • Skin can be affected = dermatomyositis
  • Other organs - heart, joints, lungs, and GI tract
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57
Q

Polymyositis (PM) & Dermatomyositis (DM):
* Association of malignancy with dermatomyositis suggests what?
* Symmetrical weakness & pain causes what?

A
  • Association of malignancy with dermatomyositis suggests that a tumor may incite myositis as result of an autoimmune reaction directed against a common antigen in muscle & tumor
  • Symmetrical weakness & pain cause classic complaint of difficulty rising from a chair. Patients may eventually have difficulty breathing or swallowing

Tissue is replaced by scar tissue= decrease fxn

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58
Q

PM/DM Epidemiology:
* How many people are affected?
* The incidence of DM is higher in who?
* What is the annual incidence of PM?

A
  • Dermatomyositis (DM) and polymyositis (PM) are relatively uncommon disorders. In a population-based study of the residents of Olmsted County in Minnesota that incorporated data from 1976 to 2007, the estimated annual incidence of all subtypes of DM was approximately 1 per 100,000 persons.
  • The incidence of DM is higher in females compared with males. In the population-based study from Olmsted County, 22 of the 29 patients (76 percent) with DM were female. Individuals of any age can be affected.
  • The annual incidence of PM has been reported to be 0.41 to 0.75 per 100,000 persons
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59
Q

What is the clinical presentation of DM and PM?

A
  • The cardinal manifestation of dermatomyositis (DM) and polymyositis (PM) is gradual skeletal muscle weakness (usually painless), specifically symmetric proximal>distal muscle weakness.
    * Muscle weakness may start suddenly & progress over weeks to months
    * Difficulty raising their arms above shoulders, climbing steps or arising from a sitting position
    * Flexors of neck may be severely affected, causing an inability to raise head from pillow
  • Dysphagia
  • Malar skin rash
  • Polyarthralgias (less pronounced than weakness)
  • Muscle atrophy
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60
Q

What is the DM clinical presentation?

A
  • Heliotrope rash (be careful-> similar to lupus)
  • Reddish-violaceous eruption on upper eyelids, often accompanied by swelling of eyelid
  • Symmetric, erythematous to purplish, scaly, flat papules on extensor surfaces of metacarpophalangeal & interphalangeal joints)
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61
Q

Low yield

What are the classfication of PM and DM?

A
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62
Q

What is the labs for PM/DM diagnosis? What else should be preformed?

A
  • ESR, CPK and aldolase levels are elevated
  • ANA may be positive
  • Autoantibodies—anti-Jo-1 seen in 50% of pts with PM/15% with DM
  • Muscle biopsy should be performed and will show inflammatory changes
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63
Q

What is the treatment plan for PM/DM (4 steps)?

A
  • Step 1-Glucocorticosteroids-Prednisone 1mg/kg/d for 3-4 weeks, then tapered very gradually
  • Step 2- Azathioprine or methotrexate
  • Step 3 IV immunoglobulin over 2-5 days
  • Step 4- Cyclosporine, chlorambucil, cyclophosphamide, or mycophenolate
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64
Q

Prognosis of PM/DM:
* What is the survival rate?
* What is mortality is often associated with?
* What is present in 305 of patients?
* What will have 5% of DM have?

A
  • 5-year Survival is >80%
  • Mortality is often associated with increased chance of malignancy and CV complications
  • Residual weakness is present in 30% of patients following resolution
  • Those with DM, 5% of them will have fulminant progression leading to death-> No treatment works
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65
Q

What are the symptoms/signs of Polymyalgia rheumatica (PMR)

A
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66
Q

PMR Epidemiology:
* Polymyalgia rheumatica (PMR) is almost exclusively a disease of adults over what?
* What is the prevalence of the disease?
* Who is more affected?

A
  • Polymyalgia rheumatica (PMR) is almost exclusively a disease of adults over the age of 50, with a prevalence that increases progressively with advancing age. The peak incidence of PMR occurs between ages 70 and 80.
  • PMR is relatively common. The lifetime risk of developing PMR has been estimated at 2.43 percent for women and 1.66 percent for men and is second only to rheumatoid arthritis (RA) as a systemic rheumatic disease in adults.
  • Women are affected two to three times more often than men. Cases of familial aggregation are recognized
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67
Q

What is the big association with patients with PMR?

A
  • Big association with patients having Giant Cell Arteritis (GCA)
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68
Q

PMR:
* What are the clinical presentation?
* What are the labs?
* When does it occur?
* Can occur in assoication with what?

A
  • Clinical syndrome characterized by aching & morning stiffness in the shoulder girdle, hip girdle, or neck for > 1 month
  • Elevated ESR, & rapid response to low-dose prednisone (15mg qd)
  • Rarely occurs before age 50
  • Can occur in association with giant cell arteritis, which requires treatment with higher doses of prednisone
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69
Q

What are other diagnosis/imaging needed for PMR?

A

ESR levels are markedly elevated. Temporal artery biopsy if suspected GCA.
* Labs to R/O other disorders (RF, ANA,CBC, CPK, SPEP)
* Renal, hepatic, & thyroid function tests

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70
Q

PMR treatment:
* What is it?
* What is the average length of disease?
* When can the disease recur?

A
  • Primarily Low vs high-dose corticosteroids. Usually up to 2 years and slowly tapered.
  • Average length of disease is 3 years
  • Can recur if steroids are tapered too quickly
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71
Q
A
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72
Q

Sjogren Epidemiology:
* What does the estimates of SS depend on?
* How many people are affected?

A
  • Estimates of the incidence and prevalence of Sjögren’s syndrome (SS) vary widely, depending upon the specific classification criteria, study design, and the population examined.
  • Only a small minority (approximately 10 percent) of patients with clinically significant dry eye have SS.
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73
Q

What are the clinical manifestations of Sjogren?

A
  • Constituional- fatigue
  • Sicca symptoms- keratoconjunctivits sicca (KCS) & xerostomia
  • Dryness of other surfaces-nose, vagina, trachea, skin
  • Extraglandular features- arthralgia/arthritis, Raynaud’s, lymphadenopathy, interstitial pneumonitis, vasculitis (usually cutaneous), nephritis, lymphoma
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74
Q

Sjogren’s diagnosis:
* What is the criteria?
* What is considered necessary?

A
  • Criteria: keratoconjunctivits sicca (KCS) xerostomia, (+) serologic features of autoimmunity
    • Postive ANA, Anti SSA/Ro, anti SSB/La
  • Positive lip biopsy considered necessary in some series-should be performed in setting of objective KCS/xerostomia with negative serologies
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75
Q

Sjogren:
* What are the lab levels?
* What biopsy needs to be done?
* What test?
* What does labial salivary gland biopsy show?

A
  • RF is present in over 70%
  • ANA in 60%
  • Anti-Ro (SS-A) antibodies in 60%
  • Anti-La (SS-B) antibodies in 40%
  • Biopsy of lower lip mucosa confirms gland fibrosis and lymphocytic infiltrate (if negative above)
  • Schirmer test (tear production)
  • Labial salivary gland biopsy-demonstrates lymphocytic infiltration and destruction of glandular tissue
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76
Q

What is the schirmer test?

A
  • Small strip of paper applied in conjunctival sac (lower eyelid) and eyes closed for 5 minutes.
  • Moisture is measured after 5 minutes
    * <5mm in 5 minutes is diagnostic for Sjogren’s syndrome
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77
Q

What is the Sjogren’s treatment

A
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78
Q

What is primary and secondary sjogren?

A
  • Primary Sjogren: Usually good, unless severe extraglandular manifestations develop
    * Pediatric patients often do not develop sicca symptoms, therefore often do not seek care until more severe symptoms develop (eye irritation, dental caries, dyspareunia)
  • Secondary Sjogren: depends on primary autoimmune disorder
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79
Q

What is scleroderma aka systemic sclerosis?

A
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80
Q

SS epidemiology:
* What is the female to male ratop?
* What is the peak age?
* How many people affected?

A
  • Female to male 4:1
  • Peak age is between 30-50 years
  • 2.5 million people-worldwide
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81
Q

SS Etiology:
* What is the cause?
* What is the chronic and rare?
* What does it involve?
* Antibodies are produced to what?

A
  • Unknown cause and characterized by deposition of collagen in the skin and less commonly heart, kidney, lungs and stomach.
  • Chronic and rare autoimmune systemic vascular and connective tissue disease
  • Involves immunologic mechanisms leading to vascular endothelial damage & activation of fibroblasts
  • Antibodies are produced to deoxyribonucleoprotein, nucleolar, centromere, & topoisomerase 1 antigens
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82
Q

What are the two different types of SS?

A
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83
Q

What is the clinical presentation of SS?

A
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84
Q

What are the skin changes in SS?

A

Shiny, taut skin seen here in a middle-aged woman who has no facial wrinkles at all is typical of scleroderma.

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85
Q

What are the chemically induced SS-like disorders?

A
  • Toxic-oil syndrome
  • Vinyl chloride-induced disease
  • Bleomycin-induced fibrosis
  • Pentazocine-induced fibrosis
  • Epoxy & aromatic hydrocarbons-induced fibrosis
  • Eosinophilia- myalgia syndrome
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86
Q

SS:
* What are the labs of SS?
* What do you need to watch for?

A
  • ANA is present in 90% with diffuse scleroderma.
  • Anticentromere antibody is associated with CREST Syndrome
  • Anti-SCL-70 antibody is associated with diffuse scleroderma and has poor prognosis
  • Watch for HTN and kidney function decline
    * Renal failure, pulmonary fibrosis and/or pulmonary HTN are leading causes of death
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87
Q

SS (scleroderma and systemic sclerosis):
* Cure?
* What is treatment aimmed for?

A
  • No cure
  • Treatment is aimed at organ-specific disease processes
    * D-penicillamine-controversial benefit to reduce skin thickening & prevent organ involvement
    * Glucocorticoids-indicated for inflammatory myositis or pericarditis
    * Cyclophosphamide-improves lung function & survival in patients with alveolitis
    * Epoprostenol-may improve cardiopulmonary hemodynamics in pts with PHTN
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88
Q

SS Treatment:
* What are PPIs for?
* What are CCBs for?
* What are immunosuppressive drugs for?

A
  • PPIs for GI, ACEI for kidneys, avoidance of triggers
  • CCBs for Raynaud’s phenomenon
  • Immunosuppressive drugs for pulmonary HTN.
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89
Q

SS prognosis:
* Who has a worst outcome?
* Who has a better prognosis?
* What causes death and morbidity in patients with limited cutaneous disease?
* Prognosis worse in patients with who?
* Death occurs most often from what?
* In patients with diffuse cutaneous disease, what is the survival rate?
* In limited cutaneous disease. what is the survival rate?

A
  • Quite variable; males have a worse prognosis
  • Patients with limited cutaneous scleroderma, better prognosis
  • Malabsorption syndrome & primary biliary cirrhosis (PBC) causes of death & morbidity in some patients with limited cutaneous disease
  • Prognosis worse in patients with diffuse cutaneous disease
  • Death occurs most often from pulmonary, cardiac, & renal involvement (CKD)
  • In patients with diffuse cutaneous disease, 5-year cumulative survival rate is ~70% & 10-year is ~55%.
  • In limited cutaneous disease 5-year is ~90% & 10-year is ~75%.
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90
Q

Systemic lupus erythematosus (SLE):
* Characterized by what?

A

Autoimmune disorder characterized by inflammation, positive ANA level and involvement of multiple organs

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91
Q

SLE Epidemiology:
* What is the prevalence of SLE?
* Who is it more common in?
* Triple due to why?
* What are estimated incidence rates?

A
  • The reported prevalence of systemic lupus erythematosus (SLE) in the United States is 20 to 150 cases per 100,000.
  • 90% women, usually of child-bearing age & more common in African Americans
  • Due to improved detection of mild disease, the incidence nearly tripled in the last 40 years of the 20th century.
  • Estimated incidence rates are 1 to 25 per 100,000 in North America, South America, Europe, and Asia
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92
Q

SLE:
* What is there a production of?
* Where are immune complexed deposited?
* What does the depositions leads to?

A
  • Production of autoantibodies with specificity for nuclear antigenic determinants leads to immune complex formation.
  • Immune complexes deposited in glomeruli, skin, lungs, synovium, mesothelium, & other places.
  • Deposition leads to manifestations of disease
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93
Q

What can play a role in SLE?

A
  • Genetics may play a role
  • Environmental/diet/ chemical agents/drugs, UV radiation and infections all play a role
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94
Q

What are the typical drugs that cause drug induced lupus?

A
  • INH
  • Hydralazine
  • Minocycline
  • Methyldopa
  • Chlorpromazine
  • Quinidine
  • Procainamide
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95
Q

Drug-Induced lupus:
* What are the clinical features?
* All patients will have what?
* When will the patients improve?

A
  • Clinical features predominantly constitutional, joint, & pleuropericardial
    * Rare CNS & renal disease
  • All patients have antinuclear antibodies(ANA)
  • Improvement following withdrawal of offending drug
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96
Q

What is the clinical presentation of SLE?

A
  • Constitutional-fatigue, fever, malaise, weight loss
  • Arthritis-inflammatory, symmetric, nonerosive
  • Cardiopulmonary- Pericardial effusions & serous pericarditis, myocarditis, Libman- Sacks endocarditis
  • Nephritis
  • GI-peritonitis, vasculitis
  • Cutaneous-rashes-malar “butterfly” rash, photosensitivity, vasculitis, alopecia, oral ulcers
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97
Q

SLE Clinical Presentation, part two

A
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98
Q

What is the SLE diagnostic criteria?

A
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99
Q

What labs and levels need to be done for SLE?

A
  • CBC, CMP, Urinalysis, ESR, and Serum complement C3 or C4
  • Antibodies of Smith antigen (anti-Smith antibody)
  • Anti-Double-stranded DNA (Anti-dsDNA)
  • ANA is present in 99%
    * But ANA is not specific for SLE
  • Anti-histone antibodies (present in most JRA/JIA/RA/SLE or even drug induced lupus)
  • 50% have + Anticardiolipin Antibody
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100
Q

Anticardiolipin Antibody in SLE:
* How many people have it? What is it associated with?
* How might it manifest?
* How might bleeding may result?
* Confirmation that PTT is prolonged on basis of what?

A
  • Approximately 50% have an anticardiolipin antibody, which is associated with a prolonged PTT & false-positive serologic tests for syphilis.
  • This so-called lupus anticoagulant may be manifested by thrombocytopenia, venous or arterial clotting, & recurrent fetal loss
  • Although thrombotic problems are most common, if antibody is associated with hypoprothrombinemia, severe thrombocytopenia, or antibodies to clotting factors (usually VIII or IX), bleeding may result.
  • Confirmation that PTT is prolonged on basis of a lupus anticoagulant may be proved by failure of normal plasma to correct defect

Clotting ot bleeding issue

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101
Q

What is the SLE treatment?

A
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102
Q

What is Behcet’s syndrome?
* What is the major risk factor?

A

Behçet’s syndrome, a recurrent disease of unknown cause, is characterized by painful oral and genital ulcers, eye inflammation, arthritis, central nervous system symptoms, thrombophlebitis/vasculitis, fever, and abdominal symptoms.
* HLA-B51 is a major risk facto

HLA-B27 for AS

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103
Q
  • How do you diagnosis behcet’s syndrome?
  • What is detected in biopsy?
A
  • (1)Requires the presence of recurrent oral ulcers + 2 of following
    * Recurrent genital ulcerations
    * Eye lesions
    * Skin lesions or a positive pathergy test (inflammatory reactivity to scratches or intradermal saline).
  • Neutrophil infiltration is detected in biopsy specimens from oral aphthous ulcers and erythema nodosum and pathergy lesions
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104
Q

What is the treatment of Behcet’s treatment?
* What are also signs/symptoms?

A

Anti-TNF drugs and/or colchicine, dapsone, azathioprine, apremilast, thalidomide, MTX, cyclosporine, biologics like infliximab

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105
Q

Mixed Connective Tissue Disease (MCTD):
* Syndrome characterized by what?
* What is there high titers of?
* Overlap syndromes are what?

A
  • Syndrome characterized by a combination of clinical features seen in SLE, SSC, Polymyositis & RA
  • High titers of ANA’s to nuclear ribonucleoprotein (RNP)
  • Overlap syndromes are diseases that fulfill diagnostic criteria for two rheumatic diseases.
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106
Q

MCTD:
* What are the clinical manifestations?

A
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107
Q

MCTD:
* What is the laboratory evaluation?
* What is the treatment?

A

Laboratory Evaluation
* High-titer ANA’s
* Very high titers of antibody to RNP
* +RF in 50% of pts

Treatment
* Little published data
* Treat based upon manifestations with similar approach to that used if feature occurred in other CTD’s

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108
Q

What is Polyarteritis Nodosa?
* What does it excludes?
* What are unususal findings that should clue into PN?

A
  • Necrotizing vasculitis of medium or small arteries
  • Excludes glomerulonephritis or vasculitis in arterioles, capillaries or venules
  • Unusual findings, such as infarcts in odd places such as liver or testes, should heighten suspicion
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109
Q

Polyarteritis Nodosa:
* What is the incidence? What can decrease this?
* What is the prevalence?
* What is the etiology?

A
  • Incidence of 0.7/100,000
    * Decreased concomitantly with HBV vaccination
  • Prevalence 50/100,000
  • Etiology – HBC/HCV, rarely HIV, parvovirus B19, EBV, deficiency of ADA2 (adenosine deaminase)
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110
Q

What is the PN’s clinical presentation?

A
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111
Q

PN Diagnosis/imaging:
* What needs to be done?
* What is elevated?
* What is positive and negative
* Urine?
* What might be present sometime?

A
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112
Q
  • What is the PN prognosis if untreated?
  • What is death usually from?
A
  • If untreated, prognosis is poor: 10-20% survival rate at 5 years
  • Death usually results from gastrointestinal issues (infarcts or perforation) or CV issues (Intractable HTN causing damage across the body)
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113
Q
  • What is gout?
  • What will go into the synovial fluid?
  • Who is affected from gout ?
A

Gout (monosodium urate [MSU] crystal deposition disease or Podagra) is a systemic disease characterized biochemically by extracellular fluid urate saturation, which is reflected in the blood by hyperuricemia, with serum or plasma urate concentrations exceeding 6.8 mg/dL (approximately 400 micromol/L); this level of urate is the approximate limit of urate solubility.
* Altered purine metabolism and subsequent sodium urate crystal
precipitation into Synovial fluid.
* Seen with patient consuming lots of meat/beer/seafood

1ST MTP JOINT

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114
Q

What are the stages of gout?

A
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115
Q

Gout:
* When does gout tend to occur?
* What is both incidence and prevalence of diease?

A
  • Gout tends to occur earlier in life in men than women and is rare in childhood.
  • Both the incidence and prevalence of the disease appear to be increasing since at least the late 1970s in the United States, where the prevalence is likely to exceed 3 percent of adults, and worldwide
116
Q

What is the pathogenesis of gout?

A
117
Q

What is overproduction and underexcretion of gout?

A
118
Q

What is gout’s clinical presentation?

A
119
Q
  • How do you diagnosis gout?
  • What is suspicious but not diagnostic?
  • What are th characteristic erosions?
A
120
Q

Gout treatment:
* What needs to change?
* What can help?
* What cannot be taken (Pharm)?
* What is the pharm txt?

A
  • Lifestyle changes and Diet changes
  • Elevation and rest
  • No Thiazide (>25mg) diuretics or ASA (both compete with uric acid excretion)
  • Pharm:
    * NSAIDs for pain
    * How I remember it: A for C and C for A
121
Q

What is the acute txt? What is the prevention of recurrence?

A
122
Q

Gout treatment:
* How does Allopurinol and colchicine work?
* What are NSAIDs for?
* What are steroids for?

A
123
Q

What is pseudogout

A

AKA: Calcium pyrophosphate crystal deposition disease (CPPD)

124
Q

Pseudogout Epidemiology:
* How many people are affected?
* Why has an estimate of the prevalence of clinically significant CPPD disease has been more difficult to attain?
* What si the average age of diagnosis of CPPD?

A
  • Calcium pyrophosphate crystal deposition (CPPD) has been estimated to affect 4 to 7 percent of the adult populations, especially among persons of advanced age.
  • However, an estimate of the prevalence of clinically significant CPPD disease has been more difficult to attain, because the available prevalence estimates have relied primarily upon radiographically detected cartilage calcification rather than clinical evaluation, and also because prevalence data concerning patients less than about 60 years of age are not available.
  • The average age at diagnosis of CPPD disease in one study was 72 years
125
Q

Pseudogout:
* What is the etiology?
* What is the pathology?

A

Etiology
* Unknown, but thought to be secondary to elevated levels of calcium or inorganic pyrophosphate

Pathology
* CPPD crystals are found in the joint capsule and fibrocartilaginous structures associated with neutrophil infiltration and erosion

126
Q

Pseudogout Clinical Presentation:
* What joints are affected?
* What is the clinical presentation?

A
  • Large peripheral joints more affected than Gout; Knee, wrist and elbow and lower extremity
  • Painful, red, swollen but no tophi
127
Q

Pseudogout Diagnosis/Imaging:
* What is shown under the microscope?
* What does x-ray show?

A
  • Rhomboid-shaped crystals that are positively birefringent
  • X-rays show fine, linear calcification in cartilage
128
Q

What is pseudogout treatment?

A
  • NSAIDs, colchicine, steroid injections
  • HCTZ: Can increase Calcium concentration
  • Prognosis is good, but tends to relapse
129
Q

Synovitis:
* What is it?
* What should it be considered as a cause of?
* What is treatment directed towards?

A
  • Inflammation of synovial membrane (very common in kids)
  • Should be considered as a cause of joint pain, has many etiologies
    * Inflammatory from OA/RA/overuse/infection etc.
  • Treatment is directed towards the cause, so work them up for RA/infection etc.
    * NSAIDs, DMARDs, steroids, PT
    * Surgical synovectomy in rare cases
130
Q

What is the difference from Tendonitis vs tendinopathy vs tenosynovitis

A
  • Tendinitis is inflammation of a tendon. Tenosynovitis is tendinitis accompanied by inflammation of the protective covering around the tendon (tendon sheath).
  • Tendinopathy (weakening of the tendon) leading to rupture
131
Q

Septic Arthritis: aka Bacterial Arthritis:
* What is it?
* What should you expect?

A
  • Is an inflammation of synovial membrane with purulent effusion into the joint capsule, due to infection
  • Expect a nontraumatic joint pain with systemic symptoms
    * Exactly why General ROS is important to ask everyone
132
Q

Septic arthritis:
* What is the prevalence of bacterial arthritis?
* Who is most likely to develop septic?
* 50% is what age?
* Male and female ratio?
* What is the most commonly affected joint?

A
133
Q

Fill in for most common joints for septic arthritis

A
134
Q

Septic arthritis:
* What is the most common pathogen?
* What is the most common pathogen for children?
* What is the most common pathogen for children and young adults with sickle cell anemia?
* What is the most common pathogen for young adults for sex (+)?
* What is the most common pathogen cause for young adults (<35)?

A
  • ~ 75% of non-GC pyroarthroses due to gram + cocci with S. aureus most common pathogen
  • Hemophilus influenzae
    * PEAK AGE INCIDENCE -Children
  • Salmonella
    * PEAK AGE INCIDENCE -Children & young adults with sickle cell anemia
  • Neisseria gonorrhea
    * PEAK AGE INCIDENCE -Young adults
    * Most common cause of an acute septic arthritis in young adults
  • GC infection common cause of septic arthritis in young adults(<35)
135
Q

What are the risk factors of septic arthritis?

A
  • Bacteremia
  • Intravenous drug abuse (IVDA)
  • Skin Infection
  • Diabetes
  • RA
  • HIV
  • Age>80yo
  • Recent joint procedure or surgery
  • Presence of prosthetic device
  • Or any other state causing immunocompromised status
136
Q

Septic arthritis:
* What are the systemic and localized symptoms?

A

Systemic
* Fevers
* Chills
* Malaise

Localized
* Joint pain and tn
* Edema
* Erythema
* Inflammation/warmth
* Decreased ROM

137
Q

Septic arthritis:
* What does the CBC show?
* What is positive?
* What is a modality of choice?
* Presence?
* What will the synovial fluid have?
* Gram stain?
* Culture?
* What should the x-ray assess?

A
138
Q

Septic Arthritis Treatment
* If gram stain is positive, what should you treat it with?
* How do you drain the joint?

A

If gram stain is positive, vancomycin should be initiated IV. If gram stain is negative, a third generation cephalosporin should be used.
* 2 weeks of IV antibiotics (vancomycin and ceftriaxone)
* Oral antibiotics covering pathogen based on culture and sensitivity for another month afterwards

Arthrotomy or joint drainage by arthrocentesis
* Post-surgical artificial joints have to be removed

139
Q

Septic Arthritis:
* What sometimes follows?
* DDx includes what?

A
  • Osteoarthritis sometimes follows
  • DDx includes reactive arthritis, rheumatoid arthritis, Lyme disease, gout and psuedogout
140
Q

Disseminated Gonococcal Infection (DGI):
* Accounts for how much of infectious arthritis?
* Results from what?
* Who is affected?
* What will the patients usually not have?
* Who is at greater risk?

A
  • Accounts for 70% of episodes of infectious arthritis in persons < 40
  • Results from bacteremia arising from GC infection or, from asymptomatic gonococcal mucosal colonization of urethra, cervix, or pharynx
  • 2/3 of patients women & symptoms of bacteremia often begin during menses
  • Most women or men with DGI do not have symptoms of urogenital, anorectal, or pharyngeal GC
  • Women greatest risk during menses or during pregnancy & overall are 2-3 x more likely than men to develop DGI & arthritis
141
Q

What does the DGI Clinical manifest as?

A
  • Syndrome of fever, chills, rash, & articular symptoms
  • Small numbers of papules that progress to hemorrhagic pustules develop on trunk & extensor surfaces of distal extremities
  • Migratory arthritis & tenosynovitis of knees, hands, wrists, feet, & ankles
  • Cutaneous lesions and articular findings believed to be consequence of an immune reaction to circulating gonococci and immune complex deposition in tissues
142
Q

DGI Laboratory Findings:
* What does synovial fluid have?
* What is negative and positive?

A
  • Synovial fluid may be difficult to obtain from inflamed joints & usually contains only 10,000 to 20,000 leukocytes/ L.
  • C/S synovial fluid are consistently negative, & blood cultures + in < 45% of patients.
143
Q

True Gonococcal Septic Arthritis:
* Less common then what?
* What is usually involved?
* What does the labs show?
* What should be obtained and why?

A
  • Less common than DGI & always follows disseminated infection, which is unrecognized in 1/3 of patients
  • A single joint, such as hip, knee, ankle, or wrist, usually involved
  • Synovial fluid, which contains >50,000 leukocytes/ L, can be obtained; gonococcus is only occasionally evident in gram-stained smears, & C/S of synovial fluid + in <40%
  • C/S & gram-stained smears of skin lesions occasionally are positive
  • Because it is difficult to isolate gonococci from synovial fluid & blood, specimens for culture should be obtained from potentially infected mucosal sites
144
Q

What is the treatment for DGI and gonococcal spetic arthritis?

A
  • Ceftriaxone (1 g IV or IM every 24 h) to cover possible penicillin-resistant organisms
  • Once local & systemic signs are resolving, 7-day course of therapy can be completed with PO cefixime (400 mg bid) or ciprofloxacin (500 mg bid)
  • Suppurative arthritis usually responds to needle aspiration of involved joints & 7 to 14 days of AB treatment
145
Q

Reactive arthritis AKA Reiter’s Syndrome:
* What is the classic triad?
* What are the incidence ranges?
* Immune response associated to what?

A

Classic Triad
* Conjunctivitis (cant see)
* Urethritis (cant pee)
* Arthritis (cant climb a tree)

Incidence ranges from 0.6 to 3.1 cases per 100,000, depending upon the organism

Immune response associated to GU or GI organisms
* Chlamydia is the most common causative agent
* Campylobacter, Salmonella, and Shigella are common pathogens

146
Q

Reiter’s Diagnosis/Imaging
* What is positive?
* What does the x-ray show?
* What is negative?

A
  • Up to 80% are HLA-B27 positive. What was the other condition we discussed recently?
  • X-ray show evidence of permanent and progressive joint disease.
  • Synovial fluid culture is negative because chlamydia will not grow
147
Q

What is the treatment of reiter’s

A
  • No specific treatment other than ABX for confirmed infection
  • NSAIDs, topical or systemic steroid based on symptom severity
    * DMARDs if NSAIDs contraindicated or ineffective
  • 30% develop chronic symptoms
148
Q

What is the prognosis of Reiter’s

A
  • Typically is self-limited, unless its caused by an infection
  • Typical resolution is 3-12 months with high recurrence
    * Even higher in those with + HLA-B27
149
Q

Infections in Prosthetic Joints:
* What is the percentages of complications?
* How is it acquired?
* Less commonly develope when?
* What is presentation? Most common pathogens?

A
  • Complicates 1 to 4% total joint replacements
  • Majority acquired intraoperatively or immediately postoperatively as a result of wound breakdown or infection
  • Less commonly, develop later after joint replacement from hematogenous spread or direct inoculation
  • Presentation may be acute, with fever, pain, & local signs of inflammation, especially in infections due to S. aureus, pyogenic streptococci, & enteric bacilli
150
Q

Prosthetic Joints:
* What needs to be done for diagnosis?
* What is present?
* What is usually yielded?
* What do you need to use?

A
  • Needle aspiration of joint
  • Synovial fluid pleocytosis with a predominance of PMN’s
  • C/S & Gram’s stain usually yield responsible pathogen
  • Use of special media for unusual pathogens such as fungi, atypical mycobacteria, & Mycoplasma may be necessary if routine & anaerobic cultures are negative
151
Q

What is the treatment for prosthetic joints?

A
  • Surgery & high doses parenteral antibiotics, x 4 to 6 weeks because bone usually involved
  • In most cases, prosthesis must be replaced to cure infection.
  • Implantation of a new prosthesis best delayed for several weeks or months because relapses of infection occur most commonly within this time frame. ; In some cases, reimplantation not possible
152
Q

What is psoriatic arthritis?

A
153
Q

Psoriatic Arthritis Etiology:
* 30% of psoriasis patients will develop what?
* Prevalence increases with what?
* What is a strong association?
* What is presence that increases risk of PA?

A
  • Exact cause is unknown
  • 30% of psoriasis patients will develop psoriatic arthritis
    * Prevalence increased with AIDS or Immunodeficiency
    * Strong familial association (mom to daughter and dad to son)
  • HLA-B27 presence increases risk of PA development (among other autoimmune diseases)
154
Q

Clinical Presentation of Psoriatic Arthritis:
* For the skin, what is more commonly affected?
* When can the skin lesions develop?
* May lead to what?
* What can they have?

A

Among the skin lesions, DIP joints are more commonly affected
* Skin lesions may develop after the arthritis
* May lead to sausage-shaped deformities, which are not present in patients with RA
* Once can have arthritis mutilans (destruction of multiple hand joints with telescoping of the digits

155
Q

Clinical Presentation of Psoriatic Arthritis:
* What joints can be involved?
* What can develop and cause pain?

A
  • Asymmetric involvement of large and small joints, including the sacroiliacs and spine, is common
  • Enthesopathy (inflammation at tendinous insertion into bone—eg, Achilles tendinitis, patellar tendinitis, elbow epicondyles, spinous processes of the vertebrae) can develop and cause pain
156
Q

PA Diagnosis/Imaging:
* How you do diagnosis this?

A
  • Diagnosis is Clinical with exclusion of other causes of arthritis elbow
  • RF is necessary to r/o PA
    * In some cases RF is positive, but the anticyclic citrullinated peptide antibodies (anti-CCP) are negative (which are highly positive in RA)
157
Q

What is the treatment for PA?

A
  • Aside the topical therapy for dermatological psoriasis, PA is treated with DMARDs (MTX) and/or TNF-alpha antagonists biological agents
  • Very similar to RA management
    * Hydroxychloroquine may cause exfoliative dermatitis and worsen the derm presentation, thus worsening the PA
158
Q

Enteropathic Arthritis:
* What is it associated with?
* When can arthritis occur?
* What joints are affected?
* When do attacks usually subside?

A
  • Peripheral & axial arthritis associated with Ulcerative Colitis or Crohn’s disease
  • Arthritis can occur after or before onset of intestinal symptoms
  • Peripheral arthritis episodic, asymmetric, & most frequently affects knee & ankle
  • Attacks usually subside within several weeks & characteristically resolve completely without residual joint damage
159
Q

Enteropathic Arthritis:
* What are the clincial findings?
* What does the labs show?

A

Clinical Findings
* Enthesitis
* Achilles tendonitis & plantar fasciitis
* Axial involvement as spondylitis &/ or sacroiliitis (often symmetric)

Lab
* RF negative
* X-Rays peripheral joints usually normal
* Axial involvement often indistinguishable from AS

160
Q

What is the treatment of enteropathic arthritis?

A
  • Directed as underlying IBD
  • NSAIDs may alleviate joint symptoms
  • Sulfasalazine may benefit peripheral arthritis
161
Q

Intestinal Bypass Arthritis:
* When does this develop?
* Possibly related to what?
* Symptoms may be relieved by what?

A
  • Some develop arthritis-dermatitis following intestinal bypass surgery
  • Possibly related to bacterial overgrowth
  • Symptoms may be relieved by NSAID’s, suppression of bacterial overgrowth with tetracycline or other antibiotics, or surgical
    reanastomosis of bypassed segment
162
Q

Whipple’s Disease:
* What is it characterized by?
* What are the symptoms?

A
  • Characterized by arthritis in up to 90% of pts that usually precedes appearance of intestinal symptoms
  • Polyarticular, symmetric, transient but may become chronic
  • GI & joint manifestations respond to antibiotic therapy
163
Q

Neuropathic Joint Disease:
* What is it also called?
* What it is?
* Usually begins as what?
* What are the joint effusions?
* What can radiographs show?

A
  • AKA Charcot’s Joint
  • Severe destructive arthropathy in joints
    deprived of pain & position sense
  • Usually begins in single joint but may spread to involve other joints
  • Joint effusions are usually noninflammatory but can be hemorrhagic
  • Radiographs can reveal either bone resorption or new bone formation with bone discoloration & fragmentation
164
Q

Neuropathic Joint Disease:
* What are the etiologies?
* What is the treatment?

A

Etiologies
* Diabetic neuropathy
* Tabes dorsalis -> untreatedsyphilis
* Syringomyela
* Amyloidosis
* Spinal cord or peripheral nerve injury

Treatment
* Stabilization of joint
* Surgical fusion may improve function

165
Q

Hypertrophic Osteoarthropathy:
* What is it?
* Most commonly seen in who?
* What are the two forms?
* Symptoms include what?
* What does x-rays show?

A
  • Syndrome consisting of periosteal new bone formation, digital clubbing, & arthritis
  • Most commonly seen in association with CA lung but occurs with chronic lung or or none liver disease, CHD, lung, or liver disease in children
  • Idiopathic & familial forms
  • Symptoms include burning & aching pain most severe in distal extremities
  • X-rays show periosteal thickening with new bone formation of distal ends of long bones
166
Q

Ehlers-Danlos Syndrome:
* What is it?
* What does mild trauma cause?
* How do you diagnosis it?
* What is txt?

A
  • Autosomal dominant CTD characterized by varying degrees of joint hypermobility, skin extensibility, and tissue fragility.
    * Mild trauma causes gaping wounds, hard to place sutures as they rip the skin, dehiscence later is very common as well
  • Dx: Clinical
    * Genetic testing reveals Type 5 collagen mutation
    * Gorlin’s sign (tongue to nose) and Metenier’s sign (upper eyelide eversion)
  • Tx: Supportive
167
Q

Osteogenesis Imperfecta (Brittle Bone Disease):
* What is it?
* How is it diagnosised?
* What is the txt?

A
  • Hereditary Collagen disease leading to bone fragility, hearing loss, blue sclera and joint hypermobility
  • Diagnosis is clinical supported by genetic testing
    * COL1A1andCOL1A2genes
  • Tx: hGH, bisphosphonates, and cochlear implants

Life expectancy according to Cleveland clinic is 72yo for a male

168
Q

OM Epidemiology:
* What is the incidence of OM?
* Some countries have noticed an increase dt to what pathogen?
* What are common sites?

A
  • The incidence of osteomyelitis ranged from approximately 1 in 5000 to 7700 children in developed countries and 1 in 500 to 2300 children in developing countries.
  • Some countries have noted a decrease in the incidence over time, whereas others, including the United States, have noted an increase, particularly with the emergence of community-associated methicillin- resistant Staphylococcus aureus.
  • Metaphyses of long bones(tibia, femur, humerus) & vertebrae most frequently involved sites
169
Q

OM Etiology:
* What is the most common pathogen in all age groups?
* What is the most common pathogen in 1m to 24 mo olds?
* What pathogens are the most common in children with sickle cell anemia?
* What pathogens are the most common in neonates?
* What are the most common pathogens for drug abusers and foor injuries?

A
  • Staph. aureus is the most common cause in ALL age groups
  • Strep. pneumoniae is most common in kids 1m-24mo old
  • Salmonella and Staph. aureus are the most common causes in
    children with sickle cell anemia
  • Group B strep and E.coli are most common in neonates
  • Pseudomonas aeruginosa and MRSA are most common in drug
    abusers and foot injuries
170
Q

OM:
* How is it classifed?
* What is chronic and acute OM?
* When does nonhematogenous OM occur?
* What is hematogenous OM caused by?

A
  • Osteomyelitis may be classified based on the duration of illness (acute versus chronic) and the mechanism of infection (hematogenous versus nonhematogenous).
  • Acute osteomyelitis typically presents with a symptom duration of a few days or weeks. Sequestra (pieces of necrotic bone that separate from viable bone) are absent.
  • Chronic osteomyelitis is characterized by long-standing infection over months or years. Sequestra are usually present; they form as a result of bone ischemia and necrosis in the context of blood vessel compression due to elevated medullary pressure associated with bone marrow inflammation. Sequestra can be seen radiographically. The presence of a sinus tract is pathognomonic of chronic osteomyelitis.
  • Nonhematogenous osteomyelitis can occur as a result of contiguous spread of infection to bone from adjacent soft tissues and joints or via direct inoculation of infection into the bone (as a result of trauma or surgery).
  • Hematogenous osteomyelitis is caused by microorganisms that seed the bone in the setting of bacteremia.
171
Q

Acute OM Clinical Presentation ?

A
172
Q

OM:
* What will x-ray show? How long does it take?
* What is sensitive but not specific?

A
  • X-ray will usually show bone resorption (osteolytic patchy lesions)
    * Takes approximately 2 weeks from onset of infection to start destroying the bone and appear on plain radiography
  • Bone scans are sensitive but not specific
173
Q

OM:
* What is increased?
* What needs to be done?
* What takes awhile for the xray?
* What is best?

A
  • CBC (Increased WBC’s), CRP, ESR
  • Blood culture
  • Bone biopsy
  • Late sequestra take several weeks to months to appear on X-ray
  • MRI is best
174
Q

What is the treatment for OM? (chronic v acute)
* What may need to be done?

A
  • Acute: 6-8 weeks for antibiotics (IV) via PICC line
  • Chronic: 1-24 months of IV and oral antibiotics
  • Immobilization and surgical drainage may be indicated
  • Wound attention
  • Surgical debridement
175
Q

Treatment of Acute Osteomyelitis:
* What is used for s.aureus or empirical therapy?
* What is used for pseudomonas?
* What is used for enterobacter?
* What is used for other gram negative bacillary infections?

A
176
Q

What is the prognosis for acute and chronic OM?

A

Acute
* Responds to treatment after several weeks (typically 6)

Chronic
* May persist for years with exacerbations and remissions

177
Q

Osteosarcoma:
* Most common in who?
* What is the incidence?
* What is the peak age?
* What is the most common sites?

A
  • The most common malignant bone tumor in children and adolescents
  • Incidence of 4.4 per million
  • Peak age 10-20 y/o – highest during growth spurts
  • Distal femur most common site, followed by proximal tibia and then proximal humerus.
178
Q

Osteosarcoma Clinical Presentation & Diagnosis:
* What is present first?
* What may we abserve?
* What do you start with?
* stage with _

A
  • Most will have pain before tumor is noticeable (might come in for knee pain but PE is normal) -> dull pain but worst at night)
  • You may observe dilated veins in overlying skin (dt tumor blood supply)
  • Start with plain radiographs
  • Stage with MRI
179
Q

What is this?

A

Osteosarcoma

180
Q

Treatment & Prognosis of osteosarcoma
* What happens before advent of multidrug chemotherapy?
* What is the surivial rate?
* What does amputation reserved for?
* What are emerging as limb saving options?

A
  • Before advent of multidrug chemotherapy – radical amputation lead to 80% dying from disseminated pulmonary disease
  • Currently, with a combo of chemotherapy and surgical treatment, 5 year survival approaches 70%
  • Amputation is reserved for the exceptional or recurrent tumors
  • Endo-prosthetics are emerging as limb saving options
181
Q

Ewing Sarcoma:
* how common?
* Incidence?
* What does it have high rates of?
* What age groups?
* If found in a child less than 5, what is the likely diagnosis?
* More common in who?
* Most commonly found where?

A
182
Q

What are the radiographic Features of ES?

A
  • Central lytic tumor of the diaphyseal-metaphyseal bone
  • Extensive permeative destruction on the cortical bone
  • As it breaks through the periosteum, it has an “onionskin”, or multi –layered appearance.
  • “Hair on end” appearance
  • may be mistaken for osteomyelitis
183
Q

What is this?

A

ES

184
Q

What is the treatment and prognosis of ES?

A
  • If locally resectable and treated with chemotherapy, 5 year survival rate is 70%
  • If at presentation, the patient has nonlocalized disease/advanced metastatic disease, the survival rate is 30%
185
Q

Rhabdomyosarcomas:
* What does it constitute as?
* How many cases per year?
* Can manifest where? Most typical?
* Common or rare?
* What is the age range?
* Very uncommon in who?

A
186
Q

Clinical Presentation of Rhabdomyosarcomas:
* Dependent on what?
* What will orbital RMS present with?
* What may be mistreated as URI?

A
  • Dependent on location
  • Orbital RMS may present with pain in eye, orbital swelling, bulging of eye.
  • Tumors of the sinus, nose, pharynx may be mistreated as URI’s for weeks or months
187
Q

Rhabdomyosarcoma Treatment and Prognosis:
* Depends on what?
* Tyically what?
* What is prognosis?

A
  • Depends on location
  • Typically surgical, resection
  • Prognosis dependent on location and extent of insult
187
Q

Multiple Myeloma:
* Most common what?
* Accounts for what?
* What is the most common age?
* What is the triad?
* What is it considered?

A
  • Most common primary tumor of bone
  • Accounts for 45% of all malignant bone tumors
  • 90% occur in patients over 40 years old
  • Triad of osteolytic ”punched-out” lesions “multifocal”, neoplastic proliferation of atypical plasma cells and and a monoclonal gammopathy
  • Considered a hematologic malignancy
188
Q

What is this?

A

Punched out lesions of multiple myeloma

189
Q

MM Clinical Presentation and Diagnosis:
* What is on plain radiograph?
* Increased what?
* What is unexplained?
* What level is high
* What may occur?

A
  • Bone pain with lytic lesions on plain radiograph
  • Increased serum protein
  • Unexplained anemia chronic bone
  • Hypercalcemia
  • Acute renal failure may occur
190
Q

Paget’s Disease of Bone:
* What is it? What is often involved?
* What is a predisposition?
* Most patients are what?
* What is a rare complication?

A
191
Q
  • What is used for dx of pagets?
  • What may be elevated and what is normal?
  • What is the txt?
A
  • Bone scan or plain xray is sufficient to Dx
    * ALP may be elevated but Calcium and Phosphate is normal
  • Tx: Biphosphonates, calcitonin is secondary
    * If osteosarcoma noted, surgical removal and palliative care is advised.
192
Q

What does paget look like under x-ray

A
193
Q

Benign Bone Tumors:
* Frequently what?
* Usually detected when?
* What can be used to diagnosed?
* What does the tumor boarders look like?
* What type of zone?

A
  • Frequently asymptomatic
  • Usually detected incidentally
  • Easily diagnosed with plain radiography
  • Well circumscribed with evidence of host bone response
  • Sclerotic margins or dense osteoblastic reactive zone
194
Q

Pseudotumor – Cystic Bone Lesions:
* What is the most common cause of in children?
* Who does it occur in? (age)
* Male to female ratio?
* How many cases a year?
* Most common where?
* Typically asymptomatic until what occurs?

A
195
Q

What is this?

A

Pseudotumor-cystic bone lesions

196
Q

What is the bone cyst treatment

A
  • Upper extremity – conservative
  • Lower extremity – aspiration and injection with bone marrow or
    corticosteroid
  • Series of 3-5 Injections occur every 2-3 months

Can add cement to fill in

197
Q

Giant Cell Tumor of the Bone:
* many types of tumors contain what?
* True “giant cell tumors” comprise of how many benign tumors?
* Frequently occurs when?
* What is the male to female ratio?
* Where is it most common?
* usually what? What does it lead to?
* May cause what?

A

Cystic bone lesions is common in prox humerus and femur

198
Q

How does giant call tumors appear as?

A

Giant Cell Tumors appear lytic and involve the epiphyseal- metaphyseal end of long bones, may contact cartilage, but rarely enters joints

199
Q

What is the treatment of giant cell tumor?

A
  • Aggressive curettage, followed by high speed burring, followed by phenol, hydrogen peroxide and bone cement
  • If tumor involves expendable bone (fibula) – gross resection
200
Q

What are the 4 types of soft tissue injuries?

A
  • Sprain – involves stretched or torn ligament
  • Strain – Musculotendinous unit injury
  • Contusions – bruise
  • Laceration – skin integrity disruption
201
Q

Low yield

What are the 5 types of lacerations?

A

1.Split-Spitting of skin and underlying tissues occur when there is compression/crushing, of the affected tissues between 2 hard objects (usually over scalp, chin, eye brow and cheek.
2.Stretch-Caused by overstretching of the skin to produce by blunt tangential impact
3.Avulsion (Shearing)-Caused by shearing force delivered at an acute angle to detach a portion of traumatized surface.
4.Tears-Caused by impact by or against the irregular or semi-sharp objects such as the handle of the car. Typically seen in open fractures.
5.Cut-caused by heavy and sharp-edged instruments.

202
Q
  • In any fracture, dislocation or traumatic injury, you MUST ensure what?
  • EVERY known or suspected fracture/dislocation MUST be what?
A
  • In any fracture, dislocation or traumatic injury, you MUST ensure that there is a distal intact neurovascular supply
  • EVERY known or suspected fracture/dislocation MUST be immobilized until cleared or appropriately treated
203
Q

List the terms:
* Reduction:
* Non-union:
* Malunion:
* External fixation:
* Open Reduction Internal Fixation:
* Fracture/Dislocation:

A
  • Reduction – the action of re-aligning fractured pieces of bone or placing a dislocated joint back into correct anatomical position
  • Non-union – failure of the fractured ends to bond, heal back together
  • Malunion – healing occurs but not in correct anatomical position
  • External fixation – the use of an external brace to maintain alignment during healing
  • Open Reduction Internal Fixation (ORIF) – surgical procedure with use of plates, rods, screws, pins, staples.
  • Fracture/Dislocation – a fracture associated with dislocation
204
Q

Non-union and Malunion:
* What are factors that contribute malunion and non-union?

A
  • Factors influencing non-union – smoking, venous stasis disease,
    atherosclerosis, malnutrition
  • Factors contributing to malunion – poor skill of clinician, inadequate blood flow, loss of reduction
205
Q

What is this a example of?

A

Non-union

206
Q

What is this an example of?

A

Malunion

most common: clavicle

207
Q

What is the treatment for malunion and non-union?

A
  • Pain control, return of MSK function
  • May splint, cast, apply traction, surgically fixate or replace (joints)
  • Deformed bone transmits abnormal forces to the joints below and above
  • Primary goals – correction of deformity and return to function
208
Q

What is this?

A

External fixation

Used for open fractures

209
Q

Traction:
* What is it used with?
* Historically, using traction to heal what?
* What bones carry the highest risk of fat embolus?

A
  • One of the oldest forms of treatment
  • Used with long-bone fractures
  • Historically, using traction to heal long-bone fractures had many potential risks and complications – DVT, infection, decubiti, PE,
    pneumonia
  • Remember – long bone fractures carry highest risk of fat embolus development
210
Q

What is dislocation and subluxation?
* What are common sites?
* What is the treatment?
* Dislocations that reduce spontaneously require what?
* If associated fractures or soft tissue injuries, then what?
* Always assess what?

A

ORIF: Open reduction and internal fixation (ORIF)

211
Q

What are orthopedic emergencies?

A
  • Knee dislocation – vascular compromise (NOT patella dislocation)
  • Traumatic amputation
  • Spinal fracture
  • Any open fracture
212
Q

Open Fractures:
* Any bleeding should be what?
* What does happen after adequate stabilization of patient?
* What should happen 4-8hr after inital trauma?
* What needs to be given?
* Confirm what?
* What should be done to preserve function?

A
213
Q

Reassess Frequently:
* Always conduct what?
* When do you repeat?

A
  • ALWAYS Conduct a thorough neurological and peripheral vascular exam of injured limb
  • Repeat this exam as you wait on radiography, consult, casting
  • Repeat after immobilization
  • Repeat post op
  • Repeat on daily rounds
214
Q

Fracture Treatment:
* What should you try to reduce?
* What does the patient have to do?
* What do you give as needed?
* What can you give local?
* Do not give what?
* Immobilize or not?

A
215
Q

Fracture Reduction:
What are the short term benefits?

A

*alleviates pain
* relieve tension on nerves and vessels
* eliminating risk of conversion to open
* restores circulation to pulseless ext

216
Q
A
217
Q
A
218
Q
A
219
Q
A
220
Q
A
221
Q

What do you need to educate your patient on with a split or cast?

A
  • Elevate injured limb – above the level of the heart. This is only effective in a recumbent or semi-recumbent position
  • Instruct patients to wiggle toes, fingers if not covered with cast or splint
  • Monitor fingers and toes for loss of sensation, excessive swelling or cyanosis
  • Report any significant increase in pain
  • If any of the signs/symptoms above appear – instruct them to go to ED or seek immediate follow up with physician
222
Q

Complications of Fractures:
* What is hemorrhage?
* Pelvic fractures can cause what?
* What is neurologic injury from?
* What is neurapraxia?
* What is vascular injury?

A
  • Hemorrhage – rich vascular supply, potential for large blood loss, shock, death
  • Pelvic Fractures can cause large vascular compromise and DIC (disseminated intravascular coagulation)
  • Neurologic injury – from traction or pressure on a peripheral nerve or nerve plexus – may be temporary or perm.
  • “Neurapraxia” – contusion to nerve
  • Vascular Injury – this an orthopedic emergency and requires a vascular surgeon in the OR with Ortho.
223
Q

When does compartment syndrome happen?
* What compromises circulation?
* What happens if untreated?
* What is the most common site?

A
  • ACS occurs when the pressure in a muscle compartment rises sufficiently to cause tissue ischemia leading to muscle or nerve damage. Impending ACS occurs when tissue pressure has begun to increase and tissue perfusion is reduced but is not sufficient to cause muscle or nerve damage.
  • Increased pressure within the limb compromises circulation
  • If untreated – necrosis of muscle and neurologic injury
  • Most common site – anterior compartment of lower leg

  • This is an emergent condition requiring early recognition
  • Always consider Compartment Syndrome when pain increases or seems out of proportion to known injury
224
Q

What are the risk factors of compartment syndrome?

A
225
Q

What is the clinical presentation of compartment syndrome?

A
226
Q

What is the hourly changes with compartment syndrome?

A
227
Q

What is the treatment of compartment syndrome

A
228
Q

What are delayed/late complications of bone fractures? What are the signs/symptoms?

A

Long bone fractures carry an increased risk of fat embolus originating from marrow (especially large bones)
* Typically will occur in first 3 days after injury
* Tachypnea
* Pulmonary edema
* Confusion
* Petechial Rash-> does not blench so when press on, it does not go away

229
Q

What are the complications from immobilization dt fracture

A
  • DVT
  • Infection
  • PE
  • Muscle atrophy
  • Psychiatric disorders

* Geriatric age increases risk of these complications

230
Q

Fracture Blisters:
* why does it occur?
* What should you try to do?
* Appears as early as?
* Usually _ fluid, hemorrhagic then what happens?

A
  • Occur on overlying skin due to swelling
  • Try to keep intact, clean, antibiotic ointment or silver sulfadiazine
    dressing
  • Appear as early as 6 hours post injury
  • Usually clear fluid – if hemorrhagic, worse prognoses, indicating detachment between the epidermal and dermal layers
231
Q

Spine Injury:
* Likely the most what?
* How many spinal cord injuries?
* What are the common age and sex?
* When is it common in geriatric patients?
* When is it common in younger patients?

A
232
Q

Epidemiology of spine injury:
* How many compression fracture?
* How many traumatic spinal fractures
* How many spinal cord injury?
* Estimated cost of SCI is what?

A
233
Q

What is spondylolysis and spondylolisthesis?

A
  • Spondylolysis – fracture of the pars interarticularis
  • Spondylolisthesis – a vertebra shifts due to instability
234
Q

What are the three types of spinal fractures?

A
  • Traumatic
  • Pathologic
  • Degenerative
235
Q

With a spinal cord injury, what can you obtain?

A

CT but ideally an MRI

236
Q

What is this?

A

Traumatic Spondylolisthesis ”vertebral vertebrae slip”

237
Q

What is this?

A

Burst fracture

238
Q

What is this?

A

compression fracture

239
Q

What is this?

A

Degenerative Spondylolisthesis

240
Q

What is Scotty (or Scottie) Dog sign?

A

a NORMAL appearance of the lumbar spine when seen on oblique view

241
Q

What is A “collar” on the Scotty Dog?

A

A “collar” on the Scotty Dog = Pars defect or fracture
*Remember, a “Scotty” shows up on the
oblique view

242
Q

PARS Defect and Fracture:
* PARS defects are what?
* Occurs in up to _
* What is the highest risk?
* What is the treatment?

A
  • PARS defects are small stress fractures resulting from over-use, typically in a young athlete, results from repetitive hyperextension.
  • Occurs in up to 30%
  • Sports with highest risk – football (offensive line), gymnastics, diving, weight lifting, wrestling, dancing, volleyball
  • Treatment – rest, good nutrition, strengthening and stretching, prevent overextension
243
Q

Vertebral Compression Fracture:
* One of the most freq manifestations of what?
* What type of pain?
* usually no what?
* Loss of what?
* No what?
* These are considered what?
* What collapses?

A
244
Q

What is this?

A

Dowager’s Hump with Compression FX

245
Q

Vertebral Compression Fracture:
* What is the diagnosis?
* What is key?
* What is initial txt?
* When should surgery happen?
* What are red flags?

A
  • Diagnosis - radiography
  • Prevention of Osteoporosis is Key
  • Initial treatment is analgesic therapy and bracing – this should last for up to twelve months, especially if effective in reducing pain
  • Surgical – If neurologic deficits or significant spinal cord compression evident – anterior decompression and fusion, posterior segmental instrumentation and fusion
  • Red Flags – neurological compromise – watch for bladder dysfunction
246
Q

Compress fracture

Recalcitrant pain with Conservative Mngt
Failure:
* Stabilization of fracture via what?
* What are the two most popular procedures?
* What is the difference between the two procedures?

A
  • Stabilization of fracture via percutaneous application of cement into the fracture.
  • Two most popular procedures – kyphoplasty (minor) and vertebroplasty (burst/major)
  • Safe and effective
  • Difference between the two procedures – a balloon is used to create more space within the compressed vertebra, allowing for some remodeling and increased injection of cement
247
Q

Rib Fractures:
* When do they occur?
* Fractured ribs may heal how?
* What can happen? What will need to be done?

A
  • Fractured ribs (also known as cracked ribs), usually occur as a result of blunt chest wall trauma or lifestyle injuries that range from cycling to football.
  • Fractured ribs may heal on their own without treatment.
  • However, some patients have rib fractures in which bone fragments can damage major blood vessels, or structures like the lung, liver, kidneys or spleen.
  • In these cases, rib fractures usually require treatment.
248
Q

Symptoms of a rib fracture may include pain with the following actions:

A

1.Taking a deep breath
2.Pressing on the injured area
3.Bending or twisting your body

249
Q

What are the factors may increase your risk of a having a rib fracture?

A

1.Osteoporosis – this disease decreases the density of your bones, making your rib more sensitive to fractures.
2.Playing sports
3.Having an area of cancer in your rib – cancer may weaken the bone, making your rib more sensitive to fractures.

250
Q

What are the three diagnostic tests that you can do with rib fractures?

A
  • X-Ray: Rib fractures are typically diagnosed on chest x-ray with rib series and the severity of the fracture is easily seen.
  • CT Scan: CT scans may show rib fractures that were not visible on an X-ray. Injuries to blood vessels and soft tissues are easier to see on a CT scan than an X-ray.
  • MRI: An MRI can also look at the organs and soft tissues around the ribs to detect damage to these areas.
251
Q

What is the treatment for rib fractures? (nondisplaced, flail)

A
  • Most nondisplaced fractured ribs heal without surgery in one to two months and are treated with non-surgical care that ranges from aggressive pain management to proper ventilation (i.e. incentive spirometer)
  • For patients with displaced fractures, flail segments, or high narcotic requirement surgical treatment with rib plating may be required along with aggressive pain management and proper ventilation.
  • Always watch out for risk of pneumothorax!
252
Q

Clavicle Fracture:
* What is the mechanism?
* What are the signs and symptoms?
* What tests?
* What is treatment?
* Watch out for?

A
  • Mechanism: Fall on shoulder or direct blow to shoulder (football injuries common), middle shaft is common lesion
  • Signs and Symptoms: Tenderness, swelling, and deformity
  • Tests: AP X-ray
  • Treatment: Ice, analgesics, sling, surgery
  • Watch for multiple fractures
253
Q

Clavicle Fractures:
* Strong what?
* Most managed how?
* Out of activity for how long?
* What should be restricted?
* May return to normal activities when?
* Need what to confirm prior to full activity resumed?
* When do you need surgery?

A
254
Q

Humeral Head Fracture:
* What is the mechanism of injury? (old and young)
* What are the S/S?
* What are the tests?
* What is the treatment?

A
  • Mechanism of injury:
    * Elderly (osteopenia)—fall on outstretched hand
    * Young—high energy trauma (e.g. MVA or fall)
  • Signs and Symptoms: Tenderness, swelling, and decreased ROM
  • Tests: X-ray is sufficient
  • Treatment: Ice, analgesics, sling and swath
255
Q

What is this?

A

humeral head fracture

256
Q

Proximal Humerus Fracture:
* Shoulder is what?
* Given the joints capacity to move in nearly every angle, small deformities resulting from fracture are what?
* What are most common? What will it be managed by?
* When should surgery occur?

A
257
Q

How is elbow fracture treated?

A

Unlike the radial head fracture, most other elbow fractures are treated with posterior long arm splint or double sugar tongue splint

258
Q

Radial head/neck fracture:
* Where is it?
* Result from what?
* Typically stable or unstable?
* Often not evident on what?
* Indications for fixation include what?
* What is the txt?
* This is a fracture that is best NOT immobilized due what?

A
259
Q

Hand/Wrist pain mostly likely do to what?

A

Mostly due to OA and RA

260
Q

Distal Radius Fracture:
* What is the typical MOI?
* Common in who?
* What type of deformity?
* What is the txt?

A
  • MOI typically a FOOSH
  • Common in falls in post-menopausal women
  • High impact motor or bike sports
  • “Silver Fork” Deformity – dorsal angulation
  • TX – reduction with splint vs SX based on degree of displacement and/or age of pt. rem
  • Volar or Sugar tongue splint
261
Q
  • What is a boxers fx and the treatment?
  • What is a colles fracture and the treatment?
A

Boxer’s Fracture – distal 3rd of the 5th metacarpal
* Tx with Ulnar Gutter splint, RICE, analgesia

Colles Fracture – distal end of radius with dorsal angulation
* Tx Sugar Tongue Splint, RICE, analgesia

262
Q

Scaphoid fracture:
* When can it occur?
* Clincally characterized by what?

A
263
Q

Scaphoid Fracture:
* Common but can be occult on x-ray when?
* Poor blood supply can lead to what?
* Pain over what?
* What tests might not show anything?
* If suspected, then what do you do?

A
  • Common but can be occult on x-ray in the 1st week
  • Poor blood supply-can lead to avascular necrosis or nonunion of the scaphoid
  • Pain over anatomic snuffbox-common complaint, swelling with bruising
  • AP, lateral, scaphoid views may not see anything. Bone scan or MRI possibly
  • If suspected, appropriate to immobilize with thumb spica cast or splint for 7-10 days, re-eval post
264
Q

Scaphoid Fracture:
* When is it easier to see?
* High risk of what?
* How do you treat?
* Surgery when?

A
  • Easier to see on x-ray at 7-10 day post injury , so re-xray if negative study initially
  • High risk of non-union, necrotizing bone, early onset arthritis
  • Once confirmed and not displaced – cast for 6-8 weeks
  • Surgery indicated if displaced
265
Q

Hip Fractures:
* Global impact?
* Results from what?
* Who is most likely to fracture hip?

A
266
Q

What are the 6 different hip fractures?

A
267
Q

Femur Neck “surgical neck”:
* What is the characteristic of bone?
* Common or uncommon?
* What is the txt?
* If acetabulum intact, what is the txt?
* A non-displace femur neck fracture may be what?

A
  • Thinnest, most fragile part of the femur
  • Very common fracture
  • Surgical – hip replacement
  • If acetabulum intact – only the head portion is replaced, this is called a “hemiarthroplasty”
  • A non-displace femur neck fracture may be “pinned”
268
Q

Intertrochanteric Fracture:
* Where is this?
* What is the txt?

A
  • Area between the greater and lesser trochanters
  • Surgical - plates, screws, rods for fixation
269
Q

Which one has a better result dt blood supply? (Intertrochanteric and displaced femoral neck fracture)

A
270
Q

Femoral Neck Fracture:
* poor what?
* Left untreated causes what?
* Big push on what?
* In elderly patients – risk of what?
* In patients younger than 40, these can be treated with what?

A
  • “Hip” fracture
  • Poor blood supply
  • Left untreated, the femoral head usually necroses – therefore, nearly always surgical
  • Big push on surgery within 24 hours, so you will hear “Hip Alerts”
  • In elderly patients – risk of avascular necrosis very high – hip replacements is the TX of Choice
  • In patients younger than 40, these can be treated with immediate reduction and surgical fixation
271
Q

What is this?

A

A displaced femoral neck fracture

272
Q

Consequences of non-operative mgmt of hip fracture?

A
  • Avascular necrosis of femoral head
  • Unable to ambulate
  • Rarely chosen and if non-surgical treatment is chosen, typically relates to pre-fx debility and quality of life issues
273
Q

Intertrochanteric Hip Fracture:
* Blood supply?
* Not as common as what?
* What is txt?

A
  • Blood supply is intact to the femur head
  • Not as common as femoral neck fracture, but still common
  • Surgical fixation (i.e. hip alert)
274
Q

Pelvic Rami Fracture:
* What are the non weight bearing areas?
* Typically occurs in who? What can be present?
* Does not require what?
* When does admission happen?
* What is pain management?
* What should patients be doing ASAP?
* Refer to who?

A
  • Superior and inferior rami – non-weight-bearing areas
  • Typically occur in geriatric patients, trauma or demineralizing
    conditions
    * Obturator nerve injury can be present
  • Do not require surgery, can not be immobilized
  • Admission generally required in intractable pain only
  • Curtail weight-bearing only for pain management
  • Get patient up and mobilizing as soon as pain is tolerable
  • Refer to Physical Therapy
275
Q

Knee fracture:
* Probably the injury that is the worst of all what?
* What is the txt?
* Recall what if physis is still present?

A
  • Probably the injury that is the worst of all of the possible knee injuries but that is also not uncommon.
  • Surgery and prolonged immobilization is often required
    * Use posterior long leg splint
  • Recall Salter Harris classification if physis is still present
276
Q

Tibial plateau:
* Where?
* What will it require?
* What do you need to provide?

A
  • Proximal end of the tibia, typically intra-articular
  • Will require hospitalization
  • Provide analgesia, ice, splint (knee immobilizer) and call ortho
277
Q

How do you fix tibial plateau?

A
278
Q

Patella Fracture:
* What are the S/S?
* What do you do for txt?

A
279
Q

Distal Tibia Fractures:
* Notorious for having what?
* Very prone to what?
* What can improve the odds of union?
* What do you for short term txt?

A
  • Notorious for having a poor blood supply, particularly at the junction of the middle and distal thirds
  • Very prone to nonunion
  • Good reduction, immobilization and non-weight-bearing improve odds of union.
    * In short-term, immobilize via posterior long leg splint
280
Q

What are the s/s of Ankle Fractures

A
  • Inability to bear weight
  • Pain and swelling
  • Point tenderness
  • Obvious deformity
281
Q
  • Ankle fractures are commonly either what?
  • What is a pott’s fx/dupuytren fx and henderson fx?
  • What should you always evaluate?
A

Fractures are commonly either medial or lateral, but may be complex:
* Bimalleolar fracture—Pott’s fx or Dupuytren fx
* Trimalleolar fracture—Henderson fx (involves medial, lateral, and posterior malleoli of tibia)

  • ALWAYS Evaluate Mortise
282
Q

Ankle Fracture:
* What do you need to ensure?
* use what rules?
* Apply what do patients?
* Provide what?

A
283
Q

What is a Jones Fracture?

A

junction of the metaphysis and diaphysis of the proximal end of the 5th metatarsal

284
Q

What is the tretment for jones fracture?

A
  • The first step of Jones fracture treatment is rest and to prevent movement in the foot.
    * Posterior short leg/boot or post-op shoe non-weightbearing (crutches/walker)
  • Apply ice to the break as well.
  • Jones fracture surgery may be needed to align the bone and help with healing.
  • These fractures will sometimes heal on their own but may take
    months to heal without surgery.
  • Can be occult like Scaphoid fractures, so re-xray them if negative initially
285
Q
A

Clinical Medicine 1 (8 decks)

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