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What is the diagnosis?

• Second most common (10-15% of all) hematological cancer.

• Responsible for 15-20% of deaths from hematological cancer and about 2% of all deaths from cancer.

• In myeloma, neoplastic plasma cells accumulate in the bone marrow and produce a monoclonal protein that is detected in the blood or urine (or both); this causes organ or tissue impairment

Multiple myeloma

Smith. Multiple myeloma. BMJ 2013;346:f3863

Symptomatic myeloma - All three criteria needed for diagnosis:• Monoclonal plasma cells in marrow ≥10%• Monoclonal protein in serum or urine (unless non-secretory;

if so, need ≥30% monoclonal plasma cells in bone marrow)• Evidence of myeloma related organ or tissue impairment:

– Hypercalcaemia (>10.5 mg/dL (2.6 mmol/L) or upper limit of normal)

– Renal insufficiency (serum creatinine >2 mg/dL (176.8 µmol/L)– Anemia: haemoglobin <100 g/L or 20 g below normal range– Lytic bone lesions, osteoporosis, or pathological fractures

International Myeloma Working Group diagnostic criteria


Screening tests• Full blood count• Serum urea and creatinine• Erythrocyte sedimentation rate or plasma

viscosity• Serum calcium and albumin measurement• Immunoglobulins and serum electrophoresis• Measurement of urinary Bence Jones protein• Radiography of symptomatic areas

Investigations for diagnosing myeloma

Bone marrow aspirate and trephine, with plasma cell phenotyping• Immunofixation of serum and urine• Measurement of serum free light chains• Skeletal survey

Tests to establish the diagnosis


• MULTIPLE MYELOMA [purely Osteolytic ]• METASTATIC CARCINOMA: 80% of primary tumors in patients presenting

with metastatic bone disease:– Prostate (mainly osteoblastic)– Breast cancer in females– Thyroid – Lung – Kidney – Pancreas

• LANGERHANS HISTIOCYTOSIS- is a rare histiocytic disorder– Most commonly characterized by single or multiple Osteolytic bone lesions

demonstrating infiltration with histiocytes with "bean-shaped" nuclei on biopsy with or without histiocytic infiltration of extra skeletal lesions ( mostly skin, lungs and central nervous system)

• Lymphomas

Differential diagnosis for osteolytic bone lesions

http://www.uptodate.com

ACD 08.21

What is the diagnosis>

Renal infarction• The major causes of renal infarction include atrial fibrillation and renal artery injury, such as

dissection. Renal infarction may also result from a hypercoagulable state. Often, no underlying cause is found. (See 'Etiology and pathogenesis' above.)

• Clinical manifestations of acute renal arterial occlusion include flank pain accompanied by nausea and vomiting, fever, and, sometimes, an acute elevation in blood pressure. (See 'Clinical presentation' above.)

• In patients suspected of having renal infarction, we recommend obtaining the following tests (see 'Diagnosis' above):

• ●White blood cell count, serum creatinine concentration, lactate dehydrogenase (LDH), aminotransferases, urinalysis, urine culture, and electrocardiogram (to assess for atrial fibrillation).

• ●A noncontrast spiral computed tomography (CT) to exclude nephrolithiasis and, if negative, a contrast-enhanced spiral CT to evaluate for infarction. Magnetic resonance imaging (MRI) using gadolinium may also be used, although the use of gadolinium has been associated with nephrogenic systemic fibrosis among patients with significantly-impaired renal function, and its use may be contraindicated among such patients. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced renal failure".)

ACD 08.22

Patient is admitted to hospital

4 days later, he cannot wake up. What is the diagnosis?

Posterior circulation stroke• Careful history taking is needed to identify patients with posterior circulation

stroke, who may present with recurrent, stuttering, or progressive symptoms, which may include altered level of awareness.

• Helpful clinical signs: presence of homonymous visual field deficits, eye movement abnormalities, Horner’s syndrome, or gait ataxia

• Investigate posterior circulation transient ischemic attack symptoms urgently to avoid preventable disability or death.

• Use rapid access transient ischaemic attack services or stroke specialist assessment if available, and use magnetic resonance imaging in the acute phase, especially if the diagnosis is unclear, because this modality has high sensitivity for identifying ischemic lesions

• Consider transferring patients at risk of deterioration in the acute phase of posterior circulation ischemic stroke to a neuroscience center because they may need urgent neurosurgery for mass effect or hydrocephalus

Posterior circulation ischemic strokeBMJ 2014; 348 doi: http://dx.doi.org/10.1136/bmj.g3175

ECG time

What is the diagnosis? What artery?

http://www.ebmedicine.net/

Copyright © The American College of Cardiology. All rights reserved.

2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial InfarctionJ Am Coll Cardiol. 2013;61(4):e78-e140. doi:10.1016/j.jacc.2012.11.019

Reperfusion therapy for patients with STEMI. The bold arrows and boxes are the preferred strategies. Performance of PCI is dictated by an anatomically appropriate culprit stenosis. *Patients with cardiogenic shock or severe heart failure initially seen at a non–PCI-capable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset (Class I, LOE: B). †Angiography and revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy. CABG indicates coronary artery bypass graft; DIDO, door-in–door-out; FMC, first medical contact; LOE, Level of Evidence; MI, myocardial infarction; PCI, percutaneous coronary intervention; and STEMI, ST-elevation myocardial infarction.

WHY MY PATIENT HAD AN MI? HE’S ONLY 35.

Etiology of CAD in young adults

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