Rheumatology Flashcards
(247 cards)
1
Q
What is the definition of Juvenile Idiopathic Arthritis (JIA)?
A
JIA is arthritis of unknown origin that begins before age 16 and persists for at least 6 weeks, after excluding other causes.
2
Q
What is the epidemiology of JIA?
A
Affects 1 in 1,000 children; most common pediatric rheumatic disease; higher prevalence in females, especially oligoarticular type.
3
Q
What are the ILAR subtypes of JIA?
A
Systemic JIA, Oligoarticular JIA, Polyarticular JIA (RF-positive), Polyarticular JIA (RF-negative), Psoriatic arthritis, Enthesitis-related arthritis, Undifferentiated arthritis.
4
Q
Describe the key features of systemic JIA.
A
Daily spiking fever, evanescent rash, arthritis, hepatosplenomegaly, serositis, lymphadenopathy.
5
Q
What distinguishes oligoarticular JIA?
A
Affects ≤4 joints in the first 6 months; often knees and ankles; may progress to extended oligoarthritis.
6
Q
What complications are associated with oligoarticular JIA?
A
Chronic anterior uveitis (especially in ANA-positive females), joint contractures, leg-length discrepancy.
7
Q
What is polyarticular JIA, and how is it subclassified?
A
Involves ≥5 joints in the first 6 months. Subtypes: RF-positive (resembles adult RA), RF-negative (less aggressive, better prognosis).
8
Q
What is Enthesitis-Related Arthritis (ERA)?
A
Seen in older boys; involves lower limb joints and entheses; associated with HLA-B27; may progress to ankylosing spondylitis.
9
Q
What is psoriatic arthritis in JIA?
A
Arthritis associated with psoriasis, dactylitis, nail pitting, or family history of psoriasis.
10
Q
What are the laboratory findings in JIA?
A
Elevated ESR/CRP, anemia of chronic disease, thrombocytosis, ANA (especially in oligoarticular), RF (in polyarticular), anti-CCP (may be positive in RF+).
11
Q
How is uveitis screened in JIA?
A
Regular slit-lamp exams every 3–12 months, depending on subtype, age, ANA status, and disease duration.
12
Q
What is the first-line treatment of mild JIA?
A
NSAIDs (naproxen, ibuprofen); intra-articular corticosteroids in oligoarticular disease.
13
Q
What are indications for starting DMARDs in JIA?
A
Polyarticular/systemic types, inadequate response to NSAIDs/steroids, high disease activity or risk of joint damage.
14
Q
What is the role of methotrexate in JIA?
A
First-line DMARD for moderate-to-severe disease; effective for joint and eye involvement; given weekly, usually subcutaneously.
15
Q
What biologics are used in JIA?
A
Anti-TNF (etanercept, adalimumab), IL-1 inhibitors (anakinra), IL-6 inhibitors (tocilizumab), abatacept, rituximab for refractory cases.
16
Q
What is Macrophage Activation Syndrome (MAS)?
A
Life-threatening complication of systemic JIA marked by fever, cytopenias, elevated ferritin, liver dysfunction, and coagulopathy.
17
Q
How is MAS managed?
A
High-dose IV corticosteroids, cyclosporine, anakinra; supportive ICU care for organ dysfunction.
18
Q
What imaging studies are used in JIA?
A
Radiographs (joint space narrowing, erosions), MRI (synovitis, bone marrow edema), ultrasound (effusion, synovial hypertrophy).
19
Q
What are poor prognostic factors in JIA?
A
Polyarticular/systemic subtype, RF/anti-CCP positivity, early erosions, persistent active disease, hip/cervical spine involvement.
20
Q
What are non-pharmacologic treatments for JIA?
A
Physical/occupational therapy, exercise, nutritional support, psychosocial support, school accommodations.
21
Q
What is Systemic Lupus Erythematosus (SLE)?
A
SLE is a chronic autoimmune disease characterized by the production of autoantibodies and multi-system involvement.
22
Q
What is the typical age of onset for pediatric SLE?
A
Most commonly presents in adolescents, especially females aged 12–16 years.
23
Q
What are common initial symptoms of SLE in children?
A
Fever, fatigue, arthralgia, malar rash, photosensitivity, and weight loss.
24
Q
What are the 2019 EULAR/ACR criteria for SLE classification?
A
Positive ANA ≥1:80 plus additive weighted criteria from 7 domains with a total score ≥10.
25
What are criteria for diagnosis of SLE according to 2019 EULAR/ACR SLE criteria?
Mnemonic: SOAP BRAIN MD
Each letter helps you remember one of the 11 ACR criteria for diagnosing pediatric SLE.
S - Serositis (pleuritis or pericarditis)
O - Oral ulcers (usually painless)
A - Arthritis (non-erosive, 2 or more joints)
P - Photosensitivity
B - Blood disorders (anemia, leukopenia, or thrombocytopenia)
R - Renal disorder (protein in urine or cellular casts)
A - ANA positive (antinuclear antibodies)
I - Immunologic abnormalities (anti-dsDNA, anti-Sm, antiphospholipid)
N - Neurologic symptoms (seizures or psychosis)
M - Malar rash (butterfly-shaped facial rash)
D - Discoid rash (raised, red, scarring skin lesions)
Diagnosis: 4 or more of these = SLE diagnosis (ACR criteria).
Tip: Pediatric SLE often shows renal, neurologic, and hematologic features more prominently than in adults.
26
Which antibodies are specific for SLE?
Anti-dsDNA and anti-Smith (anti-Sm) antibodies.
27
What antibodies are associated with neonatal lupus?
Anti-Ro/SSA( congenital heart block ) and Anti-La/SSB ( rash ) antibodies.
28
What is the significance of low complement levels in SLE?
Low C3 and C4 suggest active disease and consumption due to immune complex deposition.
29
What is the most common renal manifestation of SLE?
Proteinuria and microscopic hematuria due to lupus nephritis.
30
Which class of lupus nephritis is most severe?
Class IV (diffuse proliferative glomerulonephritis) is the most severe and common in pediatric SLE.
31
What are common hematologic manifestations in SLE?
Anemia of chronic disease, leukopenia, lymphopenia, and thrombocytopenia.
32
What are mucocutaneous signs of SLE?
Malar rash, discoid rash, photosensitivity, oral/nasal ulcers, and alopecia.
33
What neuropsychiatric symptoms can occur in SLE?
Seizures, psychosis, cognitive dysfunction, headaches, and mood disorders.
34
What cardiac and pulmonary manifestations are seen in pediatric SLE?
Pericarditis, myocarditis, pleuritis, pulmonary hemorrhage, and pulmonary hypertension.
35
What is the role of hydroxychloroquine in SLE?
Reduces flares, improves survival, protects against organ damage, and is recommended for all patients.
36
What is the treatment for moderate-to-severe SLE flares?
High-dose corticosteroids, immunosuppressants (e.g., cyclophosphamide, mycophenolate mofetil).
37
What biologic therapies are used in SLE?
Belimumab (anti-BAFF) and rituximab (anti-CD20) for refractory disease.
38
How is lupus nephritis managed?
Induction with corticosteroids plus MMF or cyclophosphamide, followed by maintenance with MMF or azathioprine.
39
What are the risks in pregnancy with SLE?
Flares, preeclampsia, intrauterine growth restriction, neonatal lupus, and congenital heart block.
40
What is the prognosis of pediatric SLE?
Improved with early diagnosis and treatment; prognosis depends on renal and CNS involvement.
41
What is Henoch-Schönlein Purpura (HSP)?
HSP is a small-vessel vasculitis characterized by IgA deposition, commonly affecting the skin, joints, GI tract, and kidneys.
42
What is the typical age and gender affected by HSP?
Most common in children aged 3–15 years, with a slight male predominance.
43
What often precedes the onset of HSP?
Upper respiratory tract infections, particularly streptococcal or viral.
44
What are the four classic features of HSP?
1) Palpable purpura, 2) Arthritis/arthralgia, 3) Abdominal pain, 4) Renal involvement.
45
What is the hallmark skin lesion in HSP?
Palpable purpura, typically on the lower extremities and buttocks.
46
What joints are commonly affected in HSP?
Knees and ankles; arthritis/arthralgia is usually transient and non-deforming.
47
What GI symptoms are associated with HSP?
Colicky abdominal pain, vomiting, GI bleeding, and intussusception.
48
What renal findings may occur in HSP?
Hematuria, proteinuria, and sometimes nephritic or nephrotic syndrome.
49
How is HSP diagnosed?
Clinically based on characteristic symptoms; skin or renal biopsy shows IgA deposition.
50
What lab tests are helpful in HSP?
Normal platelets and coagulation profile, elevated ESR/CRP, hematuria/proteinuria on urinalysis.
51
What is the role of biopsy in HSP?
Skin biopsy: leukocytoclastic vasculitis with IgA deposits; renal biopsy for severe nephritis.
52
What are differential diagnoses for HSP?
ITP, meningococcemia, other vasculitides (e.g., PAN, SLE), HUS, and serum sickness.
53
What is the natural course of HSP?
Usually self-limiting within 4–6 weeks; recurrence occurs in ~30% of cases.
54
How is HSP managed?
Supportive care with hydration and analgesia; corticosteroids for severe GI or renal involvement.
55
When are corticosteroids indicated in HSP?
Severe abdominal pain, renal involvement, orchitis, or CNS manifestations.
56
What complications can occur in HSP?
GI bleeding, intussusception, nephrotic/nephritic syndrome, and chronic kidney disease.
57
What is the prognosis of HSP?
Good in most children; renal prognosis determines long-term outcome.
58
How is renal involvement monitored in HSP?
Regular urinalysis and blood pressure monitoring for at least 6–12 months.
59
What findings on renal biopsy indicate poor prognosis in HSP?
Crescentic glomerulonephritis and high-grade proteinuria.
60
Can HSP recur?
Yes, recurrence occurs in up to 30% of children, often within months of the initial episode.
61
What is Kawasaki Disease?
An acute febrile illness of early childhood characterized by systemic vasculitis of medium-sized arteries, especially the coronary arteries.
62
What age group is primarily affected by Kawasaki Disease?
Children aged 6 months to 5 years, with a peak incidence at 9–12 months.
63
What are the diagnostic criteria for Kawasaki Disease?
Fever ≥5 days plus ≥4 of the following: conjunctival injection, oral mucosal changes, peripheral extremity changes, rash, cervical lymphadenopathy.
64
What is incomplete (atypical) Kawasaki Disease?
Cases with prolonged fever and fewer than 4 clinical criteria but with supporting lab or echocardiographic findings.
65
What are the key mucocutaneous features of Kawasaki Disease?
Strawberry tongue, red cracked lips, diffuse erythema of oral cavity, polymorphous rash, erythema and edema of hands and feet, periungual desquamation.
66
What is the most serious complication of Kawasaki Disease?
Coronary artery aneurysms, which may lead to thrombosis, stenosis, or myocardial infarction.
67
What are the phases of Kawasaki Disease?
Acute (1–2 weeks), subacute (2–4 weeks), and convalescent (weeks to months).
68
What lab findings are supportive of Kawasaki Disease?
Elevated ESR/CRP, leukocytosis, normocytic anemia, thrombocytosis (in subacute phase), elevated liver enzymes, sterile pyuria.
69
What imaging is essential in Kawasaki Disease?
Echocardiography to assess for coronary artery abnormalities.
70
When should echocardiography be performed in Kawasaki Disease?
At diagnosis, at 1–2 weeks, and again at 6–8 weeks after onset.
71
What are echocardiographic signs of coronary artery involvement in Kawasaki Disease?
Z-score-based dilatation or aneurysm, perivascular brightness, lack of tapering, thrombus formation.
72
What is the first-line treatment for Kawasaki Disease?
IVIG 2 g/kg given once plus high-dose aspirin (30–50 mg/kg/day).
73
What is the role of aspirin in Kawasaki Disease?
High-dose aspirin during the acute phase for anti-inflammatory effect, followed by low-dose aspirin for antiplatelet effect until normalization of coronary arteries.
74
What if a child with Kawasaki Disease is IVIG-resistant?
Consider repeat IVIG, corticosteroids, or biologics like infliximab.
75
What is the risk of coronary aneurysm without treatment?
Approximately 25%; reduced to <5% with timely IVIG administration.
76
What is the role of corticosteroids in Kawasaki Disease?
Adjunctive treatment in high-risk patients or IVIG-resistant cases; may reduce coronary artery complications.
77
How is risk stratification for coronary aneurysms done?
Using Z-scores adjusted for body surface area; aneurysms classified as small (<5), medium (5–10), or large/giant (>10).
78
What long-term follow-up is needed for Kawasaki Disease?
Regular cardiology follow-up with echocardiography; ECG and stress testing for patients with persistent aneurysms.
79
What are indications for anticoagulation in Kawasaki Disease?
Large or giant coronary aneurysms; may require warfarin or LMWH in addition to aspirin.
80
What infections must be ruled out before Kawasaki Disease diagnosis?
Scarlet fever, adenovirus, measles, Epstein-Barr virus, toxic shock syndrome.
81
What is Juvenile Dermatomyositis (JDM)?
A rare autoimmune inflammatory myopathy affecting skin and muscles in children, characterized by proximal muscle weakness and pathognomonic skin rash.
82
What is the typical age of onset of JDM?
Most commonly affects children aged 5–10 years, with a female predominance.
83
What is the most common presenting symptom of JDM?
Symmetrical proximal muscle weakness, especially in the shoulders and hips.
84
What are the classic skin findings in JDM?
Heliotrope rash (purple discoloration of eyelids) and Gottron papules (scaly erythematous plaques over knuckles).
85
What other dermatologic signs are associated with JDM?
Shawl sign, V-sign, nailfold capillary abnormalities, calcinosis, and photosensitivity.
86
What laboratory findings support a diagnosis of JDM?
Elevated muscle enzymes: CK, aldolase, AST, ALT, LDH; elevated ESR and ANA positivity.
87
What autoantibodies are seen in JDM?
Anti-Mi-2, Anti-NXP2, Anti-TIF1-γ, and Anti-MDA5 antibodies.
88
What imaging is useful in JDM diagnosis?
MRI of muscles showing edema and inflammation is the preferred non-invasive modality.
89
What is the role of muscle biopsy in JDM?
Confirms diagnosis with evidence of perifascicular atrophy and inflammatory infiltrates.
90
What is electromyography (EMG) used for in JDM?
Shows myopathic changes with short-duration, low-amplitude motor unit potentials and fibrillations.
91
What is the first-line treatment of JDM?
High-dose corticosteroids (oral or IV) combined with methotrexate.
92
What steroid-sparing agents are used in JDM?
Methotrexate, azathioprine, mycophenolate mofetil, and IVIG.
93
When is IVIG indicated in JDM?
Used in moderate to severe disease, steroid-resistant cases, or when rapid response is needed.
94
What is calcinosis in JDM and when does it occur?
Deposition of calcium in skin and soft tissues, occurring in chronic or inadequately treated cases.
95
How is calcinosis managed in JDM?
Difficult to treat; options include bisphosphonates, diltiazem, surgical excision, and aggressive immunosuppression.
96
What are potential complications of untreated JDM?
Dysphagia, respiratory failure, GI vasculopathy, calcinosis, and contractures.
97
What supportive therapies are recommended in JDM?
Physical therapy, sun protection, calcium and vitamin D supplementation, and monitoring for growth and nutrition.
98
What is the prognosis of JDM?
Good with early aggressive treatment; some patients may have chronic or relapsing disease.
99
What is the role of nailfold capillaroscopy in JDM?
Non-invasive tool to detect capillary dropout and dilatation, useful for diagnosis and monitoring.
100
What is the typical pattern of muscle involvement in JDM?
Symmetric proximal muscle weakness (e.g., difficulty climbing stairs, rising from a chair, combing hair).
101
What is pediatric systemic vasculitis?
A group of disorders characterized by inflammation of blood vessels, classified based on vessel size: small, medium, or large vessel vasculitis.
102
What are the major categories of pediatric vasculitis by vessel size?
Large vessel: Takayasu arteritis; Medium vessel: Kawasaki disease, Polyarteritis nodosa; Small vessel: HSP, ANCA-associated vasculitis.
103
What is Takayasu arteritis?
A large-vessel vasculitis affecting the aorta and its major branches, more common in adolescent females.
104
What are the clinical features of Takayasu arteritis?
Constitutional symptoms, limb claudication, bruits, blood pressure discrepancies, absent pulses.
105
What imaging is used to diagnose Takayasu arteritis?
MRI/MRA, CT angiography, or conventional angiography showing arterial stenosis, occlusion, or aneurysms.
106
How is Takayasu arteritis treated?
High-dose corticosteroids, immunosuppressants (methotrexate, azathioprine), and biologics (tocilizumab).
107
What is Polyarteritis Nodosa (PAN)?
A necrotizing vasculitis of medium-sized arteries, causing multisystem involvement without glomerulonephritis or ANCA positivity.
108
What are key features of PAN?
Fever, weight loss, myalgia, hypertension, renal involvement (microaneurysms), neuropathy, skin nodules.
109
What is the gold standard for diagnosing PAN?
Tissue biopsy or angiography showing aneurysms and stenoses of medium-sized arteries.
110
What infections are associated with PAN?
Hepatitis B virus in some cases; consider screening before immunosuppression.
111
How is PAN treated?
High-dose corticosteroids; cyclophosphamide for severe disease; treat underlying infections if present.
112
What is ANCA-associated vasculitis (AAV)?
A group of small vessel vasculitides including Granulomatosis with polyangiitis (GPA), Microscopic polyangiitis (MPA), and Eosinophilic granulomatosis with polyangiitis (EGPA).
113
What antibodies are associated with AAV?
C-ANCA (PR3) in GPA, P-ANCA (MPO) in MPA and EGPA.
114
What are the features of GPA in children?
Chronic sinusitis, epistaxis, hematuria, pulmonary hemorrhage, and renal involvement.
115
What is the role of biopsy in AAV?
Confirms diagnosis by showing necrotizing vasculitis with minimal immune deposits (pauci-immune).
116
How is AAV treated?
Induction: corticosteroids + cyclophosphamide or rituximab; Maintenance: azathioprine or methotrexate.
117
What are complications of untreated vasculitis?
Organ damage, hypertension, renal failure, stroke, ischemia, aneurysm rupture.
118
How is disease activity monitored in vasculitis?
Clinical assessment, ESR/CRP, renal function, urinalysis, and imaging as needed.
119
What are red flag signs in pediatric vasculitis?
Unexplained systemic illness, skin rash with systemic signs, hypertension, hematuria, or mononeuritis multiplex.
120
Why is early recognition of vasculitis important?
To initiate immunosuppressive therapy promptly and prevent irreversible organ damage.
121
What are autoinflammatory syndromes?
Inherited or acquired disorders of the innate immune system characterized by recurrent episodes of systemic inflammation without high-titer autoantibodies or antigen-specific T cells.
122
What is the most common periodic fever syndrome in children?
PFAPA syndrome (Periodic Fever, Aphthous stomatitis, Pharyngitis, Adenitis).
123
What are the clinical features of PFAPA?
Regular episodes of high fever lasting 3–6 days with aphthous ulcers, sore throat, and cervical adenitis.
124
At what age does PFAPA typically present?
Usually before 5 years of age; symptoms often resolve by adolescence.
125
How is PFAPA diagnosed?
Clinical diagnosis; labs show elevated inflammatory markers during episodes, normal in between; no specific genetic marker.
126
How is PFAPA treated?
Single-dose corticosteroids (prednisolone), cimetidine, or tonsillectomy in refractory cases.
127
What is Familial Mediterranean Fever (FMF)?
An autosomal recessive autoinflammatory disorder caused by mutations in the MEFV gene, characterized by episodic fever and serositis.
128
What are the symptoms of FMF?
Recurrent fever, abdominal pain, pleuritis, arthritis, and erysipelas-like skin lesions.
129
What is the long-term complication of FMF?
Amyloidosis leading to renal failure, especially in untreated cases.
130
How is FMF treated?
Lifelong colchicine to prevent attacks and amyloidosis.
131
What is TRAPS (TNF receptor-associated periodic syndrome)?
An autosomal dominant disorder caused by mutations in the TNFRSF1A gene, presenting with prolonged fever, myalgia, and migratory rash.
132
What distinguishes TRAPS from other periodic fevers?
Longer duration of fever (up to 3 weeks), periorbital edema, and poor response to colchicine.
133
What is the treatment for TRAPS?
Anti-TNF agents (etanercept), IL-1 inhibitors (anakinra), and corticosteroids.
134
What is Hyper IgD syndrome (HIDS)?
A mevalonate kinase deficiency leading to recurrent fevers, abdominal pain, lymphadenopathy, and elevated IgD levels.
135
How is HIDS treated?
IL-1 inhibitors (anakinra or canakinumab) and statins (in some cases).
136
What is CAPS (Cryopyrin-Associated Periodic Syndromes)?
A spectrum of disorders caused by mutations in the NLRP3 gene, including FCAS, Muckle-Wells syndrome, and CINCA/NOMID.
137
What are features of FCAS (familial cold autoinflammatory syndrome)?
Urticarial rash, fever, and arthralgia triggered by cold exposure.
138
What are features of Muckle-Wells syndrome?
Urticarial rash, sensorineural hearing loss, arthralgia, and risk of amyloidosis.
139
What is CINCA/NOMID?
The most severe form of CAPS presenting in infancy with rash, chronic meningitis, bony overgrowth, and developmental delay.
140
What is the mainstay of treatment for CAPS?
IL-1 inhibitors (anakinra, canakinumab), which significantly improve symptoms and prognosis.
141
What is juvenile scleroderma?
A rare autoimmune connective tissue disease in children characterized by skin thickening and fibrosis; includes localized and systemic forms.
142
What are the two main types of juvenile scleroderma?
Localized scleroderma (morphea and linear) and systemic sclerosis (systemic scleroderma).
143
What is localized scleroderma?
The most common type in children, affecting only the skin and underlying tissues without internal organ involvement.
144
What are the subtypes of localized scleroderma?
Morphea, linear scleroderma (en coup de sabre), generalized morphea, pansclerotic morphea, and deep morphea.
145
What is linear scleroderma?
A subtype of localized scleroderma with linear bands of skin thickening, often affecting limbs or the face (en coup de sabre).
146
What are complications of linear scleroderma?
Joint contractures, limb length discrepancy, facial asymmetry, and neurologic involvement if affecting the face/scalp.
147
What are the features of systemic sclerosis in children?
Skin tightening, Raynaud phenomenon, digital ulcers, telangiectasia, and internal organ involvement (GI, pulmonary, cardiac, renal).
148
What autoantibodies are seen in systemic sclerosis?
ANA (positive in >90%), anti-Scl-70 (anti-topoisomerase I), anti-centromere antibodies, anti-RNA polymerase III.
149
What is Raynaud phenomenon?
Vasospasm of digital arteries causing triphasic color change (white-blue-red), often triggered by cold or stress.
150
What GI manifestations are seen in systemic sclerosis?
Dysphagia, reflux, hypomotility, constipation or pseudo-obstruction.
151
What pulmonary manifestations occur in systemic sclerosis?
Interstitial lung disease, pulmonary fibrosis, and pulmonary arterial hypertension.
152
What cardiac issues can occur in juvenile systemic sclerosis?
Arrhythmias, pericarditis, myocardial fibrosis, and heart failure.
153
What renal complication is serious in systemic sclerosis?
Scleroderma renal crisis: sudden-onset hypertension, renal failure, and microangiopathy.
154
How is scleroderma renal crisis treated?
Prompt use of ACE inhibitors (e.g., captopril), even if serum creatinine is rising.
155
What is the main treatment for localized scleroderma?
Methotrexate with or without corticosteroids; topical treatments for limited disease.
156
What is the treatment approach for systemic sclerosis?
Immunosuppressants (mycophenolate, cyclophosphamide), vasodilators (for Raynaud’s), supportive care for organ systems.
157
What is the role of phototherapy in localized scleroderma?
UVA1 phototherapy can reduce skin thickness in morphea.
158
How is disease activity monitored in juvenile scleroderma?
Skin scores (modified Rodnan), PFTs, echocardiogram, BP monitoring, and autoantibody titers.
159
What are poor prognostic factors in juvenile systemic sclerosis?
Early internal organ involvement, diffuse skin involvement, male sex, and presence of anti-Scl-70.
160
What is the prognosis of localized vs systemic scleroderma?
Localized: good with treatment; Systemic: guarded, depends on extent of organ involvement and response to therapy.
161
What is the Definition in Perthes Disease?
Idiopathic avascular necrosis of the femoral head
162
What is the Age in Perthes Disease?
4–10 years
163
What is the Sex in Perthes Disease?
♂ > ♀ (4:1)
164
What is the Laterality in Perthes Disease?
Unilateral (85%)
165
What is the Risk Factors in Perthes Disease?
Low birth weight, passive smoking, trauma
166
What is the Presentation in Perthes Disease?
Painless limp, hip/knee pain, limited abduction/internal rotation
167
What is the Onset in Perthes Disease?
Insidious
168
What is the Physical Exam in Perthes Disease?
Trendelenburg gait, decreased ROM
169
What is the Radiographs in Perthes Disease?
Increased density, fragmentation, flattening of femoral head
170
What is the Best Imaging Tool in Perthes Disease?
X-ray + MRI (early AVN)
171
What is the Complications in Perthes Disease?
Femoral head deformity, early osteoarthritis
172
What is the Management in Perthes Disease?
Conservative if <6 y/o, surgery in older kids
173
What is the Prognosis in Perthes Disease?
Variable; worse with older age, lateral involvement
174
What is the Definition in SUFE?
Displacement of femoral head epiphysis from neck
175
What is the Age in SUFE?
10–16 years (pubertal)
176
What is the Sex in SUFE?
♂ > ♀ (2:1)
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What is the Laterality in SUFE?
Bilateral in 20–40%
178
What is the Risk Factors in SUFE?
Obesity, endocrine disorders (hypothyroid, GH)
179
What is the Presentation in SUFE?
Limp, hip/knee pain, external rotation deformity
180
What is the Onset in SUFE?
Sudden or gradual
181
What is the Physical Exam in SUFE?
Limited internal rotation, obligatory external rotation
182
What is the Radiographs in SUFE?
Posterior-inferior displacement of epiphysis
183
What is the Best Imaging Tool in SUFE?
Frog-leg lateral view X-ray
184
What is the Complications in SUFE?
Avascular necrosis, chondrolysis, deformity
185
What is the Management in SUFE?
Immediate surgical fixation (in situ pinning)
186
What is the Prognosis in SUFE?
Depends on stability and early treatment
187
What is the Definition in DDH?
Abnormal development of hip joint (acetabulum ± femoral head)
188
What is the Age in DDH?
Birth to 1 year (infancy)
189
What is the Sex in DDH?
♀ > ♂ (6:1)
190
What is the Laterality in DDH?
Usually unilateral (left hip more affected)
191
What is the Risk Factors in DDH?
Breech, family history, oligohydramnios
192
What is the Presentation in DDH?
Asymmetrical thigh/gluteal folds, limited abduction, positive Barlow/Ortolani
193
What is the Onset in DDH?
Congenital or early infancy
194
What is the Physical Exam in DDH?
Limited hip abduction, leg length discrepancy
195
What is the Radiographs in DDH?
Shallow acetabulum, subluxation or dislocation
196
What is the Best Imaging Tool in DDH?
Ultrasound in newborns; X-ray after 4–6 months
197
What is the Complications in DDH?
Hip dislocation, gait issues, early arthritis
198
What is the Management in DDH?
Pavlik harness (<6 months), closed/open reduction (>6 months)
199
What is the Prognosis in DDH?
Good if diagnosed early; late diagnosis → poor outcome
200
What is the Definition in Septic Arthritis?
Infection of the joint space, usually bacterial
201
What is the Age Group in Septic Arthritis?
Any age, peak in <5 years
202
What is the Onset in Septic Arthritis?
Sudden, acute
203
What is the Fever in Septic Arthritis?
High-grade
204
What is the Pain in Septic Arthritis?
Severe, constant, worse with motion
205
What is the Weight Bearing in Septic Arthritis?
Unable to bear weight
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What is the Joint Involvement in Septic Arthritis?
Monoarticular (hip, knee)
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What is the Lab Findings in Septic Arthritis?
↑ WBC, ESR, CRP; positive blood culture
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What is the Ultrasound in Septic Arthritis?
Effusion present; often purulent
209
What is the Joint Aspiration in Septic Arthritis?
Turbid fluid, high WBC, positive gram stain/culture
210
What is the Kocher Criteria in Septic Arthritis?
Helps differentiate from transient synovitis; includes fever >38.5°C, non–weight bearing, ESR >40, WBC >12,000
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What is the Treatment in Septic Arthritis?
Urgent surgical drainage + IV antibiotics
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What is the Prognosis in Septic Arthritis?
Serious; may lead to joint destruction if delayed
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What is the Definition in Transient Synovitis?
Self-limiting inflammation of the hip joint
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What is the Age Group in Transient Synovitis?
3–8 years (usually boys)
215
What is the Onset in Transient Synovitis?
Subacute, often post-viral
216
What is the Fever in Transient Synovitis?
Low-grade or absent
217
What is the Pain in Transient Synovitis?
Mild to moderate, improves with rest
218
What is the Weight Bearing in Transient Synovitis?
May limp but often can bear weight
219
What is the Joint Involvement in Transient Synovitis?
Usually hip, transient
220
What is the Lab Findings in Transient Synovitis?
Mildly ↑ or normal ESR/CRP; normal WBC
221
What is the Ultrasound in Transient Synovitis?
Effusion present but clear
222
What is the Joint Aspiration in Transient Synovitis?
Clear/yellow fluid, low cell count, sterile
223
What is the Kocher Criteria in Transient Synovitis?
Typically does not fulfill Kocher criteria
224
What is the Treatment in Transient Synovitis?
Supportive care, NSAIDs, rest
225
What is the Prognosis in Transient Synovitis?
Excellent; resolves within days to weeks
226
What is the Definition in Rickets?
Metabolic bone disease due to defective mineralization of growing bone
227
What is the Etiology in Rickets?
Vitamin D deficiency, phosphate/calcium metabolism disorders
228
What is the Age of Onset in Rickets?
6 months to 2 years
229
What is the Leg Deformity in Rickets?
Bilateral genu varum (bow legs)
230
What is the Systemic Features in Rickets?
Yes – delayed milestones, hypotonia, craniotabes, rachitic rosary
231
What is the Physical Exam in Rickets?
Widened wrists, frontal bossing, Harrison sulcus
232
What is the X-ray Findings in Rickets?
Cupping, fraying, and widening of metaphyses (esp. wrist, knees)
233
What is the Lab Findings in Rickets?
Low vitamin D, low calcium/phosphate, ↑ ALP, ↑ PTH
234
What is the Associated Risk Factors in Rickets?
Malnutrition, exclusive breastfeeding, lack of sun
235
What is the Treatment in Rickets?
Vitamin D and calcium supplementation
236
What is the Prognosis in Rickets?
Good with early treatment
237
What is the Definition in Blount Disease?
Growth disorder of the medial proximal tibial physis leading to bowing of legs
238
What is the Etiology in Blount Disease?
Unknown; associated with early walking, obesity, African ancestry
239
What is the Age of Onset in Blount Disease?
1–3 years (infantile type), adolescence (late-onset type)
240
What is the Leg Deformity in Blount Disease?
Progressive genu varum (asymmetrical in early stages)
241
What is the Systemic Features in Blount Disease?
No systemic features
242
What is the Physical Exam in Blount Disease?
Prominent bowing of tibia with medial beaking
243
What is the X-ray Findings in Blount Disease?
Medial beaking and downward slope of proximal tibial metaphysis
244
What is the Lab Findings in Blount Disease?
Normal labs (no metabolic abnormality)
245
What is the Associated Risk Factors in Blount Disease?
Early walking, obesity, family history
246
What is the Treatment in Blount Disease?
Bracing (early), surgery for severe or progressive cases
247
What is the Prognosis in Blount Disease?
Good with early recognition; untreated cases may lead to permanent deformity
