(Calcium and Phosphorus are a part of the CKD objectives)

Transcription

1 Course Objectives Electrolytes and Water: 1. Differentiate the effects of changes in sodium content from changes in water content 2. Describe how the body compensates for volume loss and volume overload 3. Recognize that serum sodium is a reflection of water in comparison to the sodium content of the body, and that disorders of serum sodium concentration usually reflect disorders of excess water or water loss 4. Understand mechanisms by which serum sodium concentration may increase or decrease. What is the pathophysiology of the major causes of hyponatremia and hypernatremia 5. Describe how edema forms. Describe the mechanism of edema formation in nephrotic syndrome, and compare it with mechanisms of edema formation is congestive heart failure and cirrhosis 6. Recognize that there are no normal values for urine chemistries, rather expected values for a particular situation 7. Define polyuria. Differentiate between a solute diuresis and a water diuresis. 8. Outline the pathophysiology of impaired urinary diluting ability and impaired urinary concentrating ability 9. Recall the distribution of potassium throughout the body 10. Describe how potassium is handled by the kidney, and the role of aldosterone in disorders of potassium homeostasis 11. Describe the pathogenesis of the major causes of hypokalemia and hyperkalemia 12. Recognize the clinical consequences of hypokalemia and hyperkalemia (Calcium and Phosphorus are a part of the CKD objectives) Rennke and Denker, Chapters 2-4 (Sodium and Water) o Skip pages Steady State & Role of impaired renal excretion in electrolyte disorders o Skip pages Water Deficit & Concept of free water clearance Videos: Sodium and Water (2 videos on calendar and homepage, 20 mins each by Dr. Simon) Rennke and Denker, Chapter 7 (Potassium) 1

2 Acid- Base Homeostasis: 1. Describe how the body and the kidney in particular maintain acid/base homeostasis 2. Be able to distinguish metabolic and respiratory causes of acid/base disturbances a. Calculate an anion- gap (AG) and explain the significance of an AG 3. Distinguish simple acid/base disturbances from mixed acid/base disorders 4. Outline the compensatory mechanisms for acid/base derangements a. Illustrate the use of Winter s formula 5. Recognize the clinical consequences of acidosis and alkalosis Rennke and Denker, Chapter 5-6 (Acid Base Disorders) o Skip pages Law of mass action & Bicarbonate- carbon dioxide system o Skip pages Regulation of renal acid excretion (Resume at: Metabolic alkalosis on page 142) Hypertension: 1. Understand that the pathogenesis of hypertension is multifactorial and complex 2. Describe the diagnosis and classification of hypertension 3. Identify secondary forms of hypertension 4. Outline the approach to treatment of hypertension and the mechanism of action of various anti- hypertensive medications (e.g. effects of ACEi on glomerular hemodynamics, systemic blood pressure, and electrolytes) 5. Compare and contrast diagnosis and treatment principles of hypertensive urgency and hypertensive emergency Pathogenesis of Hypertension (review article, link on the homepage) Rennke and Denker, read pages (Efficacy of antihypertensive therapy & Reduction in protein excretion) Rennke and Denker, read pages (Hypertension) Lecture slides: Hypertension 10/16 2

3 Glomerular Diseases (an intrinsic/intrarenal cause of AKI and CKD): 1. Compare and contrast the differences between nephrotic syndrome and nephritic syndrome a. Clinical presentation b. Pathogenic mechanism c. Microscopic characterization 2. Organize the major glomerular diseases based on nephrotic vs. nephritic syndromes and based on primary vs. systemic disorders 3. Describe the clinical and histopathologic presentations for each of the major glomerular disease entities. Describe the pathogenic mechanism responsible for glomerular injury. Be sure to review at least the following disease entities. a. Primary Nephrotic i. Minimal Change Disease ii. FSGS iii. Membranous Glomerulonephropathy b. Secondary Nephrotic i. SLE Type V Membranous Lupus ii. Diabetic Nephropathy c. Nephritis i. Post- infection glomerular nephritis ii. SLE lupus nephritis iii. IgA glomerular nephritis iv. Alport s Syndrome v. Goodpastures Disease/Anti- GBM Disease 4. Describe the clinical and histopathologic presentations of rapidly progressive glomerular nephritis (RPGN). List the disease entities that are most commonly associated with RPGN. 5. List the major complications of nephrotic syndrome 6. Compare and contrast the major classes of lupus nephritis. Include the clinical and the histopathologic presentations from above in the comparison. Videos, study guides, and articles from Dr. Krane Rennke and Denker, Chapter 9 (Pathogenesis of glomerular diseases) 3

4 Acute Kidney Injury and Chronic Kidney Disease: 1. Define and diagnose acute kidney injury (AKI) using common diagnostic studies 2. Compare and contrast the differences between the three major categories of acute kidney injury and their pathogenic mechanisms 3. Describe the effects of inhibition of prostaglandins and angiotensin II on glomerular filtration rate in patients with impaired renal perfusion and function 4. List the major risk factors for the development of AKI 5. Identify life- threatening complications of AKI 6. Define chronic kidney disease (CKD) and describe the physiologic changes that occur in progressive stages of CKD that result in the multi- system complications of this disorder 7. Apply common diagnostic studies used to evaluate patients with CKD and its complications 8. Describe the kidney s role in calcium and phosphorus homeostasis, including the role of vitamin D and PTH. 9. Describe abnormalities in calcium and phosphorus metabolism that occur in chronic kidney disease. Outline the compensatory mechanisms that occur in chronic kidney disease as a result of abnormal calcium and phosphorus metabolism Videos, study guides, and articles from Dr. Krane on Tmedweb Rennke and Denker, Chapter 11 (Acute Renal Failure) Rennke and Denker, Chapter 13 (Signs and symptoms of chronic renal failure Includes calcium/phosphorus disorders in CKD) 4

5 Kidney and bladder infections: 1. Compare and contrast the following: urinary tract infection, urinary tract colonization, contamination of urine specimens 2. Explain the pathogenesis of the urinary tract infections (ascending and descending infections) a. Identify the main virulence determinants of uropathogenic Escherichia coli b. Identify host factors that determine susceptibility to urinary tract infections (including nephrolithiasis) 3. Categorize the spectrum of microorganisms that cause urinary tract infections in different clinical settings 4. Describe the different modalities in the diagnosis of urinary tract infections 5. Compare and contrast different clinical presentations of urinary tract infections a. Uncomplicated vs. complicated b. Cystitis (lower) vs. Pyelonephritis (upper) 6. Recognize the histopathology of pyelonephritis (compare and contrast with histopathology of acute interstitial nephritis) 7. Outline treatment principles of both complicated and uncomplicated urinary tract infections, such as: a. Appropriate use of empiric antibiotics b. Antibiograms (know underlying principles for use, we do not expect you to become experts in using it) 8. Describe the pharmacological characteristics of Nitrofurantoin and Fosfomycin, including settings for clinical use (other common antibiotics for treatment of UTIs, such as trimethoprim- sulfamethoxazole and cephalosporins, have been covered in detail elsewhere in MoD) Intro- block lectures: Review UTI- relevant Enterobacteria (E. coli, Proteus), Gram- negative oxidase- positive motile rods (Pseudomonas), Gram- positive cocci (S. saprophyticus), Fungi (Candida) Study guides from Dr. Rajan and Dr. Freytag on Tmedweb Pharm Wiki: Optional in- depth reading: Mims Medical Microbiology (5 th ed): Chapter 20: Urinary Tract Infections (Go through 5

6 Congenital and Interstitial Renal Disease/GU Tract Malignancies/Prostate: 1. Compare and contrast the genetic pattern and clinical presentation of autosomal dominant polycystic kidney disease, autosomal recessive polycystic kidney disease, and multicystic renal dysplasia 2. Recognize the histopathologic appearance of acute and chronic pyelonephritis 3. Describe the clinical presentation, epidemiology, pathogenesis, and related syndromes associated with renal cell carcinoma (RCC) 4. Describe the morphology of the most common type of RCC 5. Differentiate the morphology and clinical presentations of the following common neoplasms of the urinary tract a. Translocation RCC b. Medullary carcinoma c. Angiomyolipoma d. Wilms Tumor (nephroblastoma) 6. Compare and contrast what zones of the prostate are involved in prostatic adenocarcinoma and benign prostatic hypertrophy. Why is this clinically relevant? 7. See additional objectives by Dr. Kidd (on Tmedweb calendar) Lecture 10/23, Dr. Kidd Prostate Self- Study, Dr. Crawford Optional in- depth reading: Robbins and Cotran Pathologic Basis of Disease NOTES: With the exception of antibiotics used in treatment of UTIs (which have been incorporated into this syllabus), the Med Pharm objectives from Dr. Clarkson should also be reviewed GU tract malignancies also have additional objectives (on Tmedweb calendar) 6