By R. Douglas Collins MD FACP
- Case shows in quiz format
- New Appendix C together with information for a extra complete background and actual exam and distinct exam innovations for universal Symptoms
- New part "Diseases inside a ailment" (Stroke, Pneumonia, CHF, COPD, Cirrhosis, Peptic Ulcer, Pulmonary Fibrosis, Pericarditis, Myocardopathy, UTI, Renal Calculus, Gall Stones, Hemorrhoids, Thrombophlebitis, Malabsorption Syndrome, Fractures, Diabetes)
- Newer diagnostic assessments corresponding to Troponin for MI's and D-Dimer for Pulmonary Emboli
- Solution website containing totally searchable text
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Extra resources for Differential Diagnosis in Primary Care
Karger AG, Basel Introduction Cardiac disease is often associated with worsening renal function and vice versa. The coexistence of cardiac and renal disease significantly increases mortality, morbidity, and the complexity and cost of care [1, 2]. Syndromes describing the interaction between the heart and the kidney are recognized, but have never Table 1. Definition and classification of the CRS CRS general definition: Disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other Acute CRS (Type 1) Acute worsening of cardiac function leading to renal dysfunction Chronic CRS (Type 2) Chronic abnormalities in cardiac function leading to renal dysfunction Acute Renocardiac Syndrome (Type 3) Acute worsening of renal function causing cardiac dysfunction Chronic Renocardiac Syndrome (Type 4) Chronic abnormalities in renal function leading to cardiac disease Secondary CRS (Type 5) Systemic conditions causing simultaneous dysfunction of the heart and kidney been clearly defined and classified.
Rarely, decreased renal perfusion may also occur as a result of an outflow problem such a renal vein thrombosis or abdominal compartment syndrome which is a symptomatic organ dysfunction that results from an increase in intra-abdominal pressure. Abdominal compartment syndrome leads to AKI and acute oliguria mainly by directly increasing renal outflow pressure, thus reducing renal perfusion. Other possible mechanisms decreasing renal perfusion pressure include direct parenchymal compression and arterial vasoconstriction mediated by stimulation of the sympathetic nervous and renin-angiotensin systems (renin-mediated arterial vasoconstriction) by the fall in cardiac output related to decreased venous return.
J Am Soc Nephrol 2006;17:2034–2047. 16 Ronco C, Cruz DN, Ronco F: Cardiorenal syndromes. Curr Opin Crit Care 2009;15:384–391. Claudio Ronco, MD Department of Nephrology, Dialysis & Transplantation International Renal Research Institute San Bortolo Hospital Viale Rodolfi 37 I–36100 Vicenza (Italy) Tel. it 38 Ronco Pathophysiology Ronco C, Costanzo MR, Bellomo R, Maisel AS (eds): Fluid Overload: Diagnosis and Management. Contrib Nephrol. Basel, Karger, 2010, vol 164, pp 39–45 Oliguria and Fluid Overload Thomas Rimmelé и John A.