Renal Diseases PDF
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Batterjee Medical College
Muhammad Reihan
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This document is a presentation on renal diseases, covering topics such as pathophysiology, epidemiology and complications. It provides a comprehensive overview for medical professionals.
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Renal diseases Name: Muhammad Reihan Designation: Associate professor Department: Medicine Learning Objectives Knowledge & Skill understanding Relate pathophysiological basics and Apply the evidence-based approach etiology of renal diseases...
Renal diseases Name: Muhammad Reihan Designation: Associate professor Department: Medicine Learning Objectives Knowledge & Skill understanding Relate pathophysiological basics and Apply the evidence-based approach etiology of renal diseases in management of renal diseases Describe epidemiology, manifestations, complications of renal diseases Defined as a significant loss of renal function in both kidneys to the point where less than 15% of normal GFR remains. A glomerular filtration rate (GFR) test is a blood test that checks how well your kidneys are working Renal failure Introduction for acute and chronic renal failure Renal failure may occur as; Acute and rapidly progressing process Chronic form in which there is a progressive loss of renal function over a number of years. Acute renal failure is potentially reversible. Chronic failure can lead to permanent renal failure. Chronic renal failure is the end result of progressive kidney damage and loss of function. Stages of Chronic Renal Failure Chronic renal failure is often classified into four progressive stages based on the loss of GFR. Stages of Chronic Renal Failure Diminished renal reserve Renal insufficiency Renal failure End-Stage Renal Disease Causes of chronic renal failure Diabetes (the most common cause of chronic kidney disease in developed countries) Chronic infections Renal obstruction (prolonged) Exposure to toxic chemicals, toxins or Drugs (aminoglycoside antibiotics) Hypertension Nephrosclerosis (atherosclerosis of the renal artery) Polycystic kidney disease Symptoms of chronic renal failure Anemia Dry skin Poor appetite Vomiting Bone pain Metallic taste in mouth Uremic Stomatitis - Soft tissue changes Urea secreted in saliva Urease enzyme produced by oral microflora Liberates free ammonia Damages oral mucosa Oral manifestations of chronic renal failure - Uremic Stomatitis Soft tissue changes Painful plaques and crusts on; ✓ Buccal mucosa ✓ Dorsum of tongue ✓ Flor of mouth With gray pseudo membrane exudate and painful ulcers. Oral manifestations of chronic renal failure - Uremic Stomatitis Soft tissue changes Bleeding diathesis; Petechiae and ecchymosis Irritation and chemical injury of mucosa (ammonium compounds) Xerostomia, unpleasant taste Burning mouth Uriniferous breath odour Uremic Stomatitis - Soft tissue changes Ulcers secondary to ✓ Anemia ✓ Viral infection ( immunosuppressed) Gingival hyperplasia ✓ Cyclosporine ✓ Nifedepine (CCB) Uremic Stomatitis – Hard tissue changes Hard tissue changes Staining in teeth (iron supplements) Reduced caries (urea in saliva) Delayed teeth eruption Enamel hypoplasia Tooth Mobility The oral manifestations of oxalosis can include alveolar bone resorption and external root resorption, leading to: Increased tooth mobility Pain Open bite Oral manifestation in hyperparathyroidism Tooth appear more radiopaque in background of osteoporotic bone Loss of trabeculaions of bone Ground glass appearance Total or partial loss of lamina dura Loss of cortical outlines of inferior alveolar sinus , cortex of mandible Pulpal calcifications Oral manifestation in hyperparathyroidism Multilocular radiolucency Arterial and oral calcification Treatment of chronic renal failure Careful management of fluids and electrolytes Restriction of dietary protein intake Treat anemia Renal dialysis Renal transplantation Post-streptococcal Glomerulonephritis (PSGN) Etiology Cause : Group A beta hemolytic streptococci (GAHS)-serotype 12,4,1 Impetigo Strep. throat Pathogenesis Throat/skin infection by GAHS (serotype 12,4,1 ) Antibodies to streptococcus (anti-streptolysin O) are formed in the circulation. Antigen- antibody circulating immune complexes are deposited at glomerular basement membrane Pathogenesis Nephritic syndrome is an inflammatory process Hematuria with acanthocytes RBC casts in urine Proteinuria (< 3.5 g/24 h) Hypertension Oliguria Azotemia NephrItic syndrome indicates glomerular Inflammation Poststreptococcal glomerulonephritis Usually affects children 3–12 years of age and elderly patients Clinical features Occurs weeks after group A β-hemolytic streptococcal infections o Pharyngitis/tonsillitis (most common): 1–2 weeks after infection o Skin infections: 3–4 weeks after infection Periorbital and peripheral edema Hypertension Tea- or cola-colored urine Usually self-limiting in children May lead to rapidly progressive glomerulonephritis (RPGN) → renal insufficiency in adults Signs and symptoms Investigations Urine analysis Serology Throat swab Renal functions Treatment Mainly supportive care, restriction of fluid and sodium Diuresis within 7-10 days after onset of symptoms 10 days of systemic antibiotic with penicillin V AMBOSS References & Harrison’s Principles of Internal Medicine 20th edition further reading ISBN-13: 978-1259644030 Thank You