پزشکی و سلامتآناتومی و فیزیولوژیبیماری‌هاپرستاری و پیراپزشکی

قالب پاورپوینت رشته پزشکی، آناتومی، فیزیوتراپی

صفحه 1:
A 73-year-old man is evaluated for a 3-year history of progressive weakness. He has a 7- year history of hyperlipidemia and hypertension treated with atorvastatin and lisinopril. On physical examination, vital signs are normal. Symmetric proximal and distal weakness in both arms is noted. Hip flexor strength is diminished, and he has a waddling gait. Otherwise, lower extremity strength is normal. Upper extremity examination is notable for atrophy of the forearm muscles and a weak grip. No muscle tendermess, joint swelling, edema, or rash is observed. Laboratory findings: + Serum creatine kinase (CK): 310 U/L (mildly elevated) + Erythrocyte sedimentation rate (ESR): Normal * Serum aminotransferases: Normal + Thyroid-stimulating hormone (TSH): Normal Question: Which of the following is the most likely diagnosis? (A) Inclusion body myositis (B) Polymyositis (C) Statin myopathy ( D) Systemic lupus erythematosus

صفحه 2:
Case Overview: Clinical Presentation Patient History Physical Findings A 73-year-old man with a 3-year history of progressive Symmetric proximal and distal weakness in both arms, weakness and a 7-year history of hyperlipidemia and diminished hip flexor strength, waddling gait, forearm hypertension treated with atorvastatin and lisinopril. muscle atrophy, and weak grip. No muscle tenderness or joint abnormalities.

صفحه 3:
Laboratory and Diagnostic Findings Creatine 250:U Key Lab Results Mildly elevated serum creatine kinase (CK) at 310 U/L, normal erythrocyte sedimentation rate (ESR), normal serum aminotransferases, and normal thyroid-stimulating hormone (TSH). Significance CK elevation is mild, consistent with IBM rather than other inflammatory myopathies which typically show higher CK levels.

صفحه 4:
Inclusion Body Myositis: Clinical Characteristics Muscle Weakness Typical Patient Profile Pattern Asymmetric involvement of Insidious onset in men over 50 proximal muscles like hip flexors years, with slow progression and distal muscles such as over years leading to falls, finger and wrist flexors. dysphagia, and grip weakness. Laboratory Features Normal or mildly elevated CK, presence of anti-cN-1A antibodies, and characteristic muscle biopsy findings.

صفحه 5:
Histopathologic Features of IBM Key Biopsy Findings Vacuolated muscle fibers with eosinophilic inclusions known as rimmed vacuoles, protein aggregates such as amyloid-B and phosphorylated tau, and endomysial inflammation with CD8+ T-cell infiltration. Diagnostic Importance Biopsy confirms diagnosis especially in atypical cases, distinguishing IBM from polymyositis and dermatomyositis.

صفحه 6:
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صفحه 7:
Pathognomonic Signs and Diagnostic Laboratory and Biopsy * Mildly elevated CK (usually <10x ULN) * Muscle biopsy showing rimmed vacuoles and protein aggregates * EMG with myopathic and chronic neurogenic changes Criteria Clinical Hallmarks + Slow progressive weakness >12 months * Proximal and distal muscle involvement * Finger flexor and quadriceps weakness

صفحه 8:
Management and Prognosis of IBM Treatment Supportive Care Challenges IBM shows poor response Physical therapy to to immunosuppressive maintain muscle strength therapies like steroids or and swallowing IVIG, unlike polymyositis. evaluations to manage dysphagia risks. Statin Consideration Adjust statin therapy if statin-induced myopathy is suspected, although less likely in classic IBM.

صفحه 9:
Comparative Summary of Inflammatory Inclusion Body Myositis Older males, slow progressive proximal and distal weakness, mild CK elevation, poor response to immunotherapy. Polymyositis Proximal weakness, elevated CK, responds well to immunotherapy, associated with other connective tissue diseases. Myopathies Dermatomyositis More common in females, presents with rash, proximal weakness, high CK, and perivascular inflammation.

صفحه 10:
Key Takeaways and Clinical Implications Recognise Clinical Pattern Identify slow, progressive proximal and distal weakness, especially finger flexor involvement in older adults. Confirm Diagnosis Use mildly elevated CK, EMG, and muscle biopsy to differentiate IBM from other myopathies. Manage Supportively Focus on physical therapy and symptom management due to poor response to immunosuppressive treatments.

A 73-year-old man is evaluated for a 3-year history of progressive weakness. He has a 7- year history of hyperlipidemia and hypertension treated with atorvastatin and lisinopril. On physical examination, vital signs are normal. Symmetric proximal and distal weakness in both arms is noted. Hip flexor strength is diminished, and he has a waddling gait. Otherwise, lower extremity strength is normal. Upper extremity examination is notable for atrophy of the forearm muscles and a weak grip. No muscle tenderness, joint swelling, edema, or rash is observed. Laboratory findings: • Serum creatine kinase (CK): 310 U/L (mildly elevated) • Erythrocyte sedimentation rate (ESR): Normal • Serum aminotransferases: Normal • Thyroid-stimulating hormone (TSH): Normal Question: Which of the following is the most likely diagnosis? (A) Inclusion body myositis (B) Polymyositis (C) Statin myopathy ( D) Systemic lupus erythematosus Case Overview: Clinical Presentation Patient History Physical Findings A 73-year-old man with a 3-year history of progressive Symmetric proximal and distal weakness in both arms, weakness and a 7-year history of hyperlipidemia and diminished hip flexor strength, waddling gait, forearm hypertension treated with atorvastatin and lisinopril. muscle atrophy, and weak grip. No muscle tenderness or joint abnormalities. Laboratory and Diagnostic Findings Key Lab Results Mildly elevated serum creatine kinase (CK) at 310 U/L, normal erythrocyte sedimentation rate (ESR), normal serum aminotransferases, and normal thyroid-stimulating hormone (TSH). Significance CK elevation is mild, consistent with IBM rather than other inflammatory myopathies which typically show higher CK levels. Inclusion Body Myositis: Clinical Characteristics Muscle Weakness Pattern Typical Patient Profile Asymmetric involvement of Insidious onset in men over 50 proximal muscles like hip flexors years, with slow progression and distal muscles such as over years leading to falls, finger and wrist flexors. dysphagia, and grip weakness. Laboratory Features Normal or mildly elevated CK, presence of anti-cN-1A antibodies, and characteristic muscle biopsy findings. Histopathologic Features of IBM Key Biopsy Findings Vacuolated muscle fibers with eosinophilic inclusions known as rimmed vacuoles, protein aggregates such as amyloid-β and phosphorylated tau, and endomysial inflammation with CD8+ T-cell infiltration. Diagnostic Importance Biopsy confirms diagnosis especially in atypical cases, distinguishing IBM from polymyositis and dermatomyositis. Differentiating IBM from Other Myopathies Pathognomonic Signs and Diagnostic Criteria Clinical Hallmarks Laboratory and Biopsy • Slow progressive weakness >12 months • Mildly elevated CK (usually <10× ULN) • Proximal and distal muscle involvement • Muscle biopsy showing rimmed vacuoles and protein • Finger flexor and quadriceps weakness aggregates • EMG with myopathic and chronic neurogenic changes Management and Prognosis of IBM Treatment Challenges Supportive Care IBM shows poor response Physical therapy to to immunosuppressive maintain muscle strength therapies like steroids or and swallowing IVIG, unlike polymyositis. evaluations to manage dysphagia risks. Statin Consideration Adjust statin therapy if statin-induced myopathy is suspected, although less likely in classic IBM. Comparative Summary of Inflammatory Myopathies Dermatomyositis Polymyositis Inclusion Body Myositis More common in females, presents Proximal weakness, elevated CK, with rash, proximal weakness, high responds well to immunotherapy, Older males, slow progressive CK, and perivascular inflammation. associated with other connective proximal and distal weakness, mild tissue diseases. CK elevation, poor response to immunotherapy. Key Takeaways and Clinical Implications Recognise Clinical Pattern Identify slow, progressive proximal and distal weakness, especially finger flexor involvement in older adults. Confirm Diagnosis Use mildly elevated CK, EMG, and muscle biopsy to differentiate IBM from other myopathies. Manage Supportively Focus on physical therapy and symptom management due to poor response to immunosuppressive treatments.

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