Tubulointerstitial Nephritis and Infections of the Lower Urinary Tract
By the end of the course, students will be able to:
Urinary Tract Infection
- Diagram the gross anatomy of the lower urinary tract (renal pelvis, ureter, urinary bladder, urethra)
- Investigate the histology of the lower urinary tract
- Analyze the major pathogenic organisms that cause urinary tract infections (UTIs) and the host factors favoring UTIs
- Investigate the host defense mechanisms against UTIs
- Describe the pharmacologic principles of treating UTIs including regimens for complicated UTIs
- Examine the pathogenesis of cystitis and prostatitis
- Discuss the treatment of cystitis and prostatitis
- Assess the gross and microscopic pathology of the acute and chronic pyelonephritis
Nephrolithiasis and Renal Stone Formation
- Discuss the pathophysiology of renal stone formation.
- Examine how renal stones may contribute to UTIs.
- Discuss treatment for existing renal stones and for prevention of renal stone formation.
Tubulointerstitial Nephritis (TIN)
- Define TIN as a disease that affects the both the interstitium and the tubules
- Diagram the structures and composition of the normal interstitium
- Describe the mechanisms of reduction of renal function secondary to tubulointerstitial nephritis which includes tubule obstruction, interstitial inflammation and fibrosis, changes in vascular resistance, loss of tubuloglomerular feedback and chronic ischemic atrophy
- Examine the mechanisms of tubulointerstitial injury by immune response genes, antibody mediated immunity, cell mediated immunity, cytokine and amplification process, fibrogenesis and atrophy
- Assess the role of tubule epithelial cells in the recruitment of interstitial infiltrating cells. Release of chemoattractant cytokines, pro-inflammatory cytokines, expression of cell surface markers and of matrix proteins
- Evaluate common causes of acute and chronic TIN, including drugs, infections, metabolic disorders, immunological disorders and toxins
- Examine the pathogenesis of chronic TIN, including pathways leading to chronic TIN, loss of the “repair control” system, consequences of cytokine release, fibrosis, loss of cell function, and ischemia