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PBL Cases Flashcards

1
Q

What are some differentials fo common causes of knee pain in children and what are some factors to differentiate them?

A
  • Muscle contusion (which would improve in ~3 weeks)
  • SCFE
  • Patellofemoral syndrome in girls
  • Rheumatoid arthritis (juvenile)
  • Osteochondritis dissecans (also has palpable hard mass after fragmentation of bone and/or cartilage)
  • Osteoid osteoma (benign, better with NSAIDS)
  • Fractures (which would improve in 0-5 days)
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2
Q

What is the natural history of the slipped capital femoral epiphysis (SCFE)? What age group and population is this commonly found in?

A
  • Natural History: when the femoral neck slips down the physeal plate due to shearing force
    • Common in boys who are in puberty and obese
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3
Q

What is the treatment and clinical presentation of Slipped Capital Femoral Epiphysis (SCFE)?

A
  • Treatment: pin the neck back into place
  • Clinical Presentation: knee pain because of the abnormal gait to avoid pain at the hip (15 percent of patients)
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4
Q

Why do you do a hip exam when a juvenile presents with knee pain?

A
  • When a juvenile presents with knee pain, the risk of SCFE is reason to perform hip exam
    • SCFE decreased ROM of hip, abnormal gait, Trendelenburg exam to see if the hips are aligned
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5
Q

What are 4 large risk factors for devleoping bone tumors?

A
  • Risk Factors
    • Paget’s Disease
    • Radiation
    • Retinoblastoma (Rb mutation)
    • Li-Fraumeni syndrome (germline p53 mutation)
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6
Q

What chromosomes are often abnormal in osteosarcomas and what genes may be affected?

A
  • Osteosarcoma: chromosomal abnormalities in 1, 6, 9, 10, and 13
    • Rb mutation
    • p53 mutation
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7
Q

What is the most common mutation that causes Ewing Sarcoma?

A

Pneumonic: (11+22)=33 (Patrick Ewing’s Number)

  • Ewing’s Sarcoma: t(11;22)
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8
Q

What are common sites of metastasis to bone?

A

Pneumonic: BLT w/KP M (BLT with kosher pickle and mayo)

  • Carcinoma metastases
    • Common sites: Breast, Lung, Thyroid, Kidney, Prostate, and Melanoma
    • Age ranges: adults
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9
Q

Compare the radiographic presentation in Osteosarcoma vs Ewing’s sarcoma.

A

Osteosarcoma: Sunburst pattern, blastic (sclerotic), periosteal Codmans triangle

Ewing’s: Onion-skin appearance, lytic, periosteal Codmans triangle

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10
Q

What part of the bone are osteosarcoa and ewing sarcoma generally located at?

A

Osteosarcoma mainly on metaphysis of long bones and ewing’s on diaphysis.

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11
Q

Compare and contrast the histology of osteosarcoma and ewing’s sarcoma.

A

Osteosarcoma: Pleomorphic spindle cells with abnormal, irregular osteoid formation

Ewing: Small, round, blue cells

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12
Q

What is the treatment plan for osteosarcoma vs Ewing sarcoma?

A

Osteosarcoma: Surgery, chemotherapy (neo-adjuvant and adjuvant)

Ewing: Surgery, chemotherapy (neo-adjuvant and adjuvant), AND Radiation

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13
Q

Describe the natural history of bone tumors. What are the general initial sites and what are the most common metastasis sites?

A
  • Common site of initial tumor growth and metastasis
  • Initial site – distal femur, proximal tibia, proximal humerus, middle and proximal femur, and other bones
  • Metastasis – lungs is the most common. Metastasis through blood because bone is highly vascularized
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14
Q
  • Why is surgical resection alone insufficient to cure a patient who has no known metastatic disease at the time of presentation of a primary bone tumor (osteosarcoma)?
A

You are worried about micro-metastases

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15
Q

What is the value of assessing percent tumor necrosis in the main resection specimen?

A
  • Percent tumor necrosis: the percentage of dead tumor cells with 70-90% considered good response to neo-adjuvant chemotherapy
  • A good indicator of prognosis
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16
Q
  • Why is it important to employ a multi-disciplinary approach to patients with these tumors?
A
  • Tumors involve worries of death
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17
Q

Define degenerative disc disease and what the general epidemiology of it is.

A
  • Degenerative disc disease: thinning of the vertebral disc due to a loss of water causing compression of spinal nerves in the transverse foramen and spinal cord (aka radiculopathy)
  • Epidemiology: process of aging and may be exacerbated by injury, trauma, infection, heredity, and tobacco use
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18
Q

What are some distinguishing symptoms for tumor, infection, mechanical LBP, and inflammatory LBP?

A
  • Distinguishing Symptoms for Tumor: Constant, unrelenting night pain and weight loss
    • Ages > 50
  • Distinguishing Symptoms for Infection: Constant, unrelenting night pain and weight loss, fevers, chills and sweats
    • Ages > 0
  • Symptoms for Mechanical LBP: Discomfort relieved with rest, worse with activity
  • Symptoms for Inflammatory LBP: Discomfort relieved with activity, worse with rest
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19
Q

What motor, sensory, and reflex loss can occur with the herniation of the three lowest motion segments of the lumbosacral spine?

A
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20
Q

Indicate the imaging that you would use for the following conditions:

  • Osteoporotic compression fracture
  • A suspected metastatic tumor of the thoracolumbar spine
  • Spinal stenosis
  • Sciatica both during the initial evaluation and when unresponsive to conservative therapy
  • Mechanical low back pain
A
  • Osteoporotic compression fracture: XR
  • A suspected metastatic tumor of the thoracolumbar spine: XR
  • Spinal stenosis: MRI
  • Sciatica both during the initial evaluation and when unresponsive to conservative therapy: None, then MRI when unresponsive
  • Mechanical low back pain: None – physical exam until pain lasts 6 weeks with XR
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21
Q

Define cauda equina. What is cauda equina syndrome and what symptoms does one experience from this?

A
  • Cauda equina: a bundle of spinal nerves extending from the end of the spinal cord around L1 and L2
  • Cauda equina syndrome: results from a sudden reduction in the volume of the lumbar spinal canal that causes compression of multiple nerve roots and leads to muscle paralysis
  • Symptoms: urinary incontinence/retention (S2-S4), bilateral motor weakness, perianal numbness
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22
Q

Compare and contrast the mechanism of action of Aspirin and NSAIDs.

A
  • Aspirin is an irreversible inhibitor of COX1/2
  • NSAIDs are reversible inhibitors of COX1/2
    • Adverse effects: GI ulcers, renal dysfunction, and increased bleeding risk
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23
Q

What is the initial treatment plan of simple mechanical LBP for an adult?

A
  • NSAIDs
  • XR if pain persists for 6 weeks
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24
Q

What is spondylolysis? What is aggravated and relieved by? Who do you normally find it in?

A
  • Spondylolysis is a unilateral or bilateral defect in the pars interarticularis
    • Aggravated by hyperextension of the back
    • Relieved by forward flexion
    • Often found in competitive athletes like gymnasts, figure skaters, and wrestlers
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25
Q

What is spondylolisthesis and what is it aggravated by?

A
  • Spondylolisthesis occurs secondary to spondylolysis
    • Bilateral pars interarticularis fracture causing a forward slippage of the vertebral body
    • Aggravated by hyperextension of the back
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26
Q

What are the sites of metastatic cancer involving the spine?

A
  • BLT w/KP, M – Breast, Lung, Thyroid, Kidney, Prostate, Melanoma
    • Spine is secondary site to these tumors
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27
Q

What are some mechanisms of injury for osteoporotic compression fractures?

A
  • Mechanisms: MVA, fall from great height, post-menopause women falling
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28
Q

What is spinal stenosis and what does it cause? What symptom of spinal stenosis must be differentiated from another common lower leg pain? How can you differentiate this?

A
  • Narrowing of the lumbar spinal canal with subsequent compression of the nerve roots
  • Causes neurogenic claudication in the legs
    • Different from peripheral vascular disease (PVD) because PVD gets better at rest
    • Forward flexion expands spinal canal and relieves pain
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29
Q

Describe some key findings that would cause you to refer a patient with joint pain to rheumatologist.

A
  • Duration of symptoms lasting longer than 6 weeks:
    • Ulnar deviation
    • Morning stiffness
    • Extra-articular manifestations (periodontal disease and Rheumatoid nodules)
  • Family history of autoimmune diseases
30
Q

Compare and contrast rheumatoid arthritis and osteoarthritis in every aspect possible. Some things to think about:

  • Etiology
  • Inflammation?
  • Predisposing factors?
  • Presentation
  • Joint findings
  • Non-affected joints
A
31
Q

What are 3 cell populations and 2 cytokines involved in the inflammatory response in rheumatoid arthritis?

A
  • Cytokines: TNF-alpha and IL-1 – inflammatory and fever causing cytokines
  • Cell populations: macrophages, T cells, B cells – immune response
32
Q

What is the physiology of how the autoimmune attack in rheumatoid arthritis works? Go into some depth.

A
  • CD4 T helper cells react with arthritogenic agent, perhaps microbial or self-antigen
  • Adaptive immunity attacks citrullinated peptides in cartilage or in the mouth
  • Release of cytokines
    • TNF-alpha and IL-1 → synovitis → hyaline cartilage damage
    • RANKL→ stimulates bone resorption
  • Inflammation of the joint causes pain, warmth, swelling, morning stiffness
33
Q

Recognize some medications that can be provided to rheumatoid arthritis patients. What are the main classes (7)? What are some of the meds in each one of these classes. Recognize some side effects.

A
34
Q

Distinguish immune vs infectious etiologies on the basis of the time course of symptom onset.

A

Infectious: Faster onset (weeks), shorter duration, asymmetrical/one joint, Lyme/Gonococcal

Autoimmunity: Insidious, longer (months-years), symmetrical/multiple joints. Anything longer than 6 weeks - suspect

35
Q

Assess how a patient’s past history of a hematologic disorder is relevant to the described presentation.

IN TERMS OF ITP**

A

Thrombocytopenia is a feature of lupus. Your platelets are attacked by your immune system. ITP is often the first sign of SLE in children. These patients have demonstrable antibodies against some components of the blood or other tissues. This results in a positive Coombs Test and may result in anemia. The abnormally regulated immune system in ITP can also lead to production of autoantibodies against self (ANA).

36
Q

Describe the criteria for diagnosing systemic lupus erythematosus.

A
37
Q

Describe how autoimmune diseases are likely to appear in families.

A
  • Family history of autoimmune disease (i.e. thyroid disease) makes it more likely for one to be affected by an autoimmune disease
  • HLA involvement (66% heritability with lupus - one of the highest of any autoimmune disease): Genetic abnormalities may create a tendency for autoimmune response, which are then triggered by additional factors, such as viruses or sunlight (environmental stimulus)
38
Q

List and categorize by organ or system the physical exam findings of systemic lupus erythematosus.

skin, msk, cv, gi, pulm, opto, renal, neuro, heme

name a few symptoms per organ system

A
  • Cutaneous: Malar rash over cheeks, discoid rash, alopecia, photosensitivity, Raynauds
  • MSK: Arthritis is non-erosive, but you can still get the typical deformities (Swan neck, ulnar deviation)
  • CV: Vasculitis of small vessels, sometimes large vessel involvement (pancreas, coronary, pulmonary, hepatic, mesenteric, and renal), pericarditis
  • GI: Nausea, vomiting, abdominal pain
  • Pulm: Pleuritis, Shrinking lung syndrome (pulling in from the pleural sack, causing lung volume to shrink), fibrosis
  • Opto: Conjunctivitis
  • Renal: Glomerulonephritis
  • Neuro: cerebritis, strokes
  • Heme: Hemolytic anemia, thrombocytopenia, neutropenia, NH lymphoma
39
Q

Compare and contrast three types of treatments for systemic lupus erythematosus.

A
  • Corticosteroids (Prednisone): Useful topically for rash or PO when there is a flare-up
  • Hydroxychloroquine: Minimal side effects (especially when compared to prednisone), but make sure to get yearly eye exams due to possible deleterious side effect (rare). Good when there is no major organ involvement and long-term maintenance of mild-moderate disease
  • Biologics: targets B cells to reduce the amount of antibodies produced. More severe disease, chronic, advanced, not responding to other treatments. Side effects: increased susceptibility to infection. No live vaccines for you!
    • Rituximab, Belimumab
  • Immunosuppressants: For lupus nephritis (kidney involvement)
40
Q

describe 4 lab values for lupus

A
  • ANA: If you test positive at 1:80 (sensitive - good for screening), you also get 1:640 (specific - for diagnosis). Cardinal test. Most SLE patients will have positive ANA at some point in disease
  • Anti-SM & Anti-dDNA: Also useful for confirmation of diagnosis. Very specific for lupus. If you have these, you have lupus
  • CH50: Tests complement pathway; defect in C3 or C4 is indicator for lupus
  • Coombs Test: Tests levels of antibodies or complement bound to RBC. Positive indicates hemolytic anemia
41
Q

Describe the shave and punch biopsy methods including the methods and portions of the skin that will be sampled.

A
  • Different types of biopsy:
    • Shave- scraping the lesion with a razor blade
    • Punch - excise a whole from the lesion with the entire depth
  • Excision- removing the entire lesion such as Mohs
42
Q

Describe the meaning of the term ‘SPF’.

UVA vs UVB?

A
  • SPF = sun protection factor; mostly protects against UVB light, which is the most damaging UV light
    • “Broad-spectrum” tells protection against both UVA and UVB
  • UVB = burn, targets DNA; UVA = aging, targets Keratinocytes (deeper penetration)
43
Q

Select methods of protection from ultraviolet light damage.

A
  • Dermatologists recommend using a SPF15 or SPF30 sunscreen
  • Time of day (10am-3pm) correlates with more rays
  • Other protective measures:
    • Clothes with SPF factor
    • Wide-brimmed hat, sunglasses
    • Loose fitting clothes with tight weave, darker colors
    • Shade
44
Q

Apply ethical considerations to solicited advice on a person who is not a patient.

A
  • Criteria for providing unsolicited advice (according to Mosley)
    • Serious impending risk to health
    • The physician should be fairly certain of diagnosis
    • Condition could remain untreated if physician did not give advice
    • A reasonable person who would want to be aware
    • Treatment is available for this condition
45
Q

Basal Cell Carcinoma

Genetics:

Etiology:

Metastatis:

A

Genetics:

Hedgehog pathway: PTCH 1/2 gene mutations

P53 mutations

Etiology: Sun exposure

Metastatis:Locally invasive, but almost never metastasis

46
Q

Melanoma

Genetics:

Etiology:

Metastatis:

A

Genetics:

Activating mutation in BRAF kinase, S-100 (somatic mutation)

Germline familial mutations include CDKN2A, CDK4 and MC1R

Etiology: Sun exposure, dysplastic nevi (mole), fair-skinned people

Metastatis:Breslow’s Depth correlates with risk of metastasis

47
Q

Squamous Cell Carcinoma

Genetics:

Etiology:

Metastatis:

A

Genetics:Actinic Keratosis is main precursor

Etiology:Sun exposure, arsenic exposure, XR radiation, immunosuppression, inflammation/wounds/scarring

Metastatis:Metastasis rare

48
Q

Basal Cell Carcinoma

Apperance, Histology, Disrubtion?

A

Apperance:Waxy, pink, pearly nodules, commonly with telangiectasis (arborized capillaries), rolled borders, central crusting or ulceration, with slight erosion/scab

Histology:Occurs above lower lip to forehead

Disrubtion:Palisading nuclei - elongated basal cells perpendicular to the surface of skin

49
Q

Melanoma

Apperance, Histology, Disrubtion?

A

Apperance:

  • Asymmetry
  • Border irregularity
  • Color variation
  • Diameter > 6mm
  • Evolution over time

Histology:Specific features include consumption of the epidermis, pagetoid (upward spreading) spread of melanocytes, nests of melanocytes with variable size and shape

Disrubtion:

Men - back

Women - legs

50
Q

Squamous Cell Carcinoma

Apperance, Histology, Disrubtion?

A

Apperance:Ulcerated, scaling papule, plaque, or nodule

Histology:Keratin pearls

Disrubtion:Face, lower lip, ears, hands

51
Q

Vismodegib

A

PTCH 1/2 therapy

52
Q

vermurafenib

A

BRAF kinase inhibitor

53
Q
A

Basal Cell Carcinoma

54
Q
A

Melanoma

55
Q
A

Squamous Cell Carcinoma

56
Q

What are the three main arteries that provide blood supply to the femoral neck?

A
  • Blood Supply
    • Profunda femoris
      • Medial circumflex femoral artery (runs posterior)
      • Lateral circumflex femoral artery (runs anterior)
    • Descending branch of the obturator artery
57
Q

What are the 6 main femur fractures?

A
  • Femur fractures
    • Femoral neck fracture – possible for avascular necrosis
      • Sub-capital
      • Transcervical
    • Intertrochanteric fracture
    • Subtrochanteric fracture
    • Lesser trochanteric fracture
    • Greater trochanteric fracture
58
Q

What are the 4 stages of secondary bone healing? Provide a general timeline of each one.

A
  • Secondary Bone Healing
    • Inflammation (0 – 5 days)
    • Repair – Soft Callus (5 – 21 days)
    • Repair – Hard Callus (21 days – 4 months)
    • Remodeling
59
Q

What occurs in the inflammation stage of secondary bone healing?

A
  • Inflammation (0 – 5 days)
    • Begins at impact and lasts until cartilage formation occurs
    • Correlates with pain and swelling
    • Events in Phase
      • Hematoma
      • Fibroblasts form granulation tissue replacing hematoma
      • Osteoclasts remove necrotic tissue
60
Q

What occurs in the repair - soft callus stage of secondary bone healing?

A
  • Repair – Soft Callus (5 – 21 days)
    • Stage ends when fracture fragments are no longer clinically moveable
    • Events in Phase
      • Increased vascularity and cellularity
      • Recruitment of mesenchymal stem cells
      • Fibrocartilaginous callus bridges fracture site
61
Q

What occurs in the repair - hard callus stage of secondary bone healing?

A
  • Repair – Hard Callus (21 days – 4 months)
    • Begins when soft callus is completed
    • Ends with clinical and radiographic union (bones look united with no air in between)
    • Events in Phase
      • Blood supply is fully returned
      • Endochondral ossification (creation of bone through cartilage replacement)
        • Calcification of cartilage
62
Q

What occurs in the remodeling stage of secondary bone healing?

A
  • Remodeling
    • Conversion of woven bone to lamellar bone
    • Diameter of callus is reduced to normal
63
Q

What are the differences between primary and seconadary bone healing?

A
  • Primary bone healing requires rigid stabilization with or without compression of the bone ends. Unlike secondary bone healing, this rigid stabilization suppresses the formation of a callus in either cancellous or cortical bone
  • Secondary bone healing undergoes endochondral bone ossification
64
Q

Describe the lesion in dermatologic morphologic terminology.

A
  • Over the sacrum on top of the gluteal cleft, there is a broad lesion topped with a yellow film surrounded by a erythematous base
  • Non-blanchable, skin erythema with yellow plaque
65
Q

What are the 4 stages of secondary skin healing? What are the timelines and what generally occurs in each stage?

A
  • Secondary Skin Healing
    • Hemostasis/Coagulation (stopping blood)
      • Immediate
      • Platelet cells aggregate to the site to clot
    • Inflammation (destroying necrotic tissue)
      • 0-5 days
      • Neutrophils and macrophages to clear any bacteria or infection
    • Proliferation (wound closure)
      • 4-42 days
      • Angiogenesis with fibroplasia (type III collagen forms)
    • Maturation (restore function)
      • 42 days for 1 year
      • Type III collagen gets remodeled to type I collagen; collagen cross linking for strengthening of the skin
66
Q

What three factors can impede skin from healing and why?

A
  • Pressure – decreased blood flow
  • Infection – decreased immune response and glucose availability
  • Poor nutrition – decreased calcium and vitamin C
67
Q

What are three factors that contribute to the developmenet of a pressure ulcer?

A
  • Immobility
  • Poor nutrition
  • Diabetes (neuropathy)
68
Q

What are the 4 stages of pressure ulcers and describe what the appearance of each ulcer is. Provide a treatment for each type as well.

A
  • Grade 1 – purpura/bruising
    • Use moist bandages
  • Grade 2 – partial erosion/ulceration
    • Use moist bandages
  • Grade 3 – penetrating ulceration to subcutis
    • Irrigation and debridement
  • Grade 4 – penetrating ulceration to ligaments, muscles and bone
    • Surgery with skin grafts
69
Q

What are the patients that are most at risk for osteoporosis and should be evaluated according to the NOF? What are T-scores and what T-scores designate osteoporosis?

A
  • Post-menopause women ≥ 65
  • T-scores – comparing bone density in normal individuals to that of patient through standard deviation
    • T-score ≥ 2.5 designates osteoporosis diagnosis
70
Q

What are 5 drugs uses to treat osteporosis and what are there mechanisms of actions?

A
  • Selective estrogen receptor modulators – act on estrogen receptors to increase calcium deposition in the bone
  • Bisphosphonates – induces apoptosis in osteoclasts preventing resorption of bone
  • Calcitonin – decreases serum calcium levels by inhibiting osteoclasts
  • Teriparatide – PTH analogue; works by transiently activating osteoclast activity to stimulate longer term osteoblast activity resulting in net gain of bone formation
  • RANKL inhibitors – inhibits osteoclast maturation (RANK is major receptor on osteoclasts)
71
Q

What are 3 side effects of bisphosphonates?

A
  • Erosion of stomach lining and esophagus (must sit up without food to take bisphosphonates)
  • Associated with osteonecrosis of the jaw
  • Renal failure

MSDR (7 decks)

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