Nephrotic syndrome
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This document summarizes nephrotic syndrome, including the anatomy and physiology of the nephron, primary causes like minimal change disease and focal segmental glomerulosclerosis, systemic causes such as diabetes and lupus, clinical findings of edema and proteinuria, lab tests to diagnose including urine analysis and blood tests, differential diagnoses, treatments focusing on managing protein loss and edema, and complications involving infection, thrombosis, and acute kidney injury. The summary provides an overview of nephrotic syndrome and how it is diagnosed and treated.
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Chronic kidney disease is defined as glomerular filtration rate below 60 mL/min/1.73m2 or markers of kidney damage. It is staged based on GFR. Common causes include diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and congenital anomalies. Manifestations include electrolyte imbalances, cardiovascular complications, central nervous system effects, peripheral neuropathy, and bone disease like renal osteodystrophy. Treatment depends on stage but may include dialysis, kidney transplantation, and management of complications.
Nephrological assessment
The nephrological assessment is very important nursing procedure help to rule out the provisional diagnosis of patient and their general condition. it also help in certain type of investigation and treatment of patient.
Peripheral Neuropathy
Peripheral neuropathies can affect the cell body, myelin sheath, or axon. When evaluating a patient with neuropathy, the clinician aims to identify where the lesion is located, determine the cause, and prescribe proper treatment. Electrodiagnostic studies and nerve biopsies help classify the neuropathy and diagnose underlying causes like diabetes, autoimmune diseases, toxins, vitamins deficiencies, infections, and malignancies. Cryptogenic neuropathies have no known cause and treatment focuses on managing neuropathic pain symptoms.
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Nephritic vs nephrotic syndrome6npoqoa8qakc (1).pdf
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CHRONIC KIDNEY DISEASE CAUSES, PATHOPHYSIOLOGY, CLINICAL PRESENTATION AND TRE...
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This document provides an overview of leishmaniasis, a protozoal disease caused by Leishmania parasites and transmitted by sand flies. It discusses the history, epidemiology, clinical manifestations, diagnosis and treatment of the disease. Leishmaniasis exists in three main forms - cutaneous, mucocutaneous, and visceral - and causes lesions on exposed parts of the body. Diagnosis involves identification of the parasites in skin smears or cultures. Treatment depends on the form of the disease but commonly involves antimonial drugs administered either topically or systemically. Prevention focuses on controlling sand fly populations through insecticide spraying and treated nets.
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Learning objectives:
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Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Nephrotic syndrome
- 1. By: Intern Maryam Shamal Ghalib Dept. Int. Med , Shah A.Ghazi Hosp
- 2. What to expect? • Anatomy and Physiology of Nephron • Nephrotic Syndrome • Etiology – Primary causes – Systemic causes • Clinical findings – Signs and symptoms – Lab findings • DDX • Treatment • Complications
- 3. NEPHRON- The functional and Structural Unit of Kidney
- 10. Etiology • Primary Causes – Minimal Change Disease – Focal Segmental Glomerular sclerosis – Membrane Nephropathy – Rapidly progressive Glomerulonephritis(<nephritic synd) • Systemic Causes – Diabetes Mellitus - Î Î Î – Systemic Lupus Erythematous – Amyloidosis
- 20. Diagnosis - S&S
- 21. Diagnosis – Lab findings • Urine Analysis (proteinuria, albumin on dipstick, abnorm. Paraproteins on sulfosalycilic acid addition, casts and oval fat bodies on microscopy) • Blood Chemistries (hypoalbuminemia <3g/dL, Hypoproteinemia <6g/dL, Hyperlipidemia, elevate ESR , inc. fibrinogen, dec. vit D, zinc and copper, other tests for complement level, serum and urine protein electrophoresis, antinuclear antibody, serologic test for Hepatitis) • Renal Biopsy
- 22. DDX • Acute/ Chronic Glomerulonephritis (Nephritic Syndrome) • Protein Losing enteropathy • Hepatic Failure • Heart Failure • Protein Malnutrition
- 23. ITIC Vs. OTIS
- 24. OTIC Vs. ITIC
- 26. Treatment • Protein loss (protein intake to balance loss, ACE-I and ARBs) • Edema (Dietary salt Restrictions, diuretic therapy- thiazides and loop diuretics) • Hyperlipidemia (Diet modification and pharmacologic treatment- statins+/- gemfibrozil or fenofibrate/niacin) • Hypercoagulable State (anticoagulant for 3- 6M or indefinite of recurrent RVT/TE)
- 28. Complications • Hypovolemia (Exc. Diuresis, Sev. Hypoalb.) • Ac. Kidney Inj (Exc. Diuresis, ATIN, Superimposed Crescentic GN) • Infection (Dec. Ser. IG, Impaired Synthesis of AB, Dec. Compliment Level, Imm.supp Therapy) • Thyroid Dysfunc. (steroids reduce TSH) • DVT – PE &RVT ( Inc. Coagulation, Aggregation, dec anticoag)
- 29. References • Current Medical Diagnosis and Treatment 2013 • Internet sites (mainly www.pathguy.com)
- 30. THANK YOU ALL