Pathophysiology of HYPERNATREMIA

The fundamental problem is that hypernatremia strictly defined is hyperosmolality, ie, an overall deficit of total body water. This deficit accrues by 2 mechanisms, which are inadequate fluid intake and water loss. Because thirst is a potent mechanism in the response to hyperosmolality, hypernatremia patients either have an inadequate thirst mechanism or have an inability to respond to thirst. If the thirst response to hyperosmolality is impaired, ongoing water losses raise serum sodium concentration. Ongoing water losses include insensible (always) water in excess of solute or renal loss (with a solute diuresis such as hyperglycemia or water diuresis). Increased sodium intake (salt tablets) is a rare cause of hypernatremia in hot, humid weather. The keys to the pathophysiology of hypernatremia include the following: 1. Thirst should lead to water intake. 2. Vasopressin is critical to water reabsorption in the cortical collecting tubule. 3. The CNS is sensitive to changes in osmolality. 4. Water may be lost by renal and extrarenal mechanisms.

PATHOPHYSIOLOGY OF PYELONEPHRITIS 1. (The ascending route from the lower urinary tract is the most common pathway) The infection develops in patchy areas spreading to the cortex with WBC infiltration and inflammation 2. The kidney becomes grossly edematous and localized abcesses may form; tissue damage may occur primarily of the tubules; scar tissue replaces the infected/inflamed area 3. (E. coli is responsible in 85% of the cases; other common pathogens are proteus and klebsiella) 4. The onset of pyelonephritis is typically rapid with chills and fever, malaise and vomiting along with flank pain, costovertebral tenderness, urinary frequency and dysuria 5. As with urinary tract infections, older client may present with behavior changes, confusion, incontinence, or general deterioration

6. Chronic renal failure and end stage renal disease may develop with chronic pyelonephritis; hypertension may develop as the renal tissue is destroyed

PATHOPHYSIOLOGY OF CHRONIC GLOMERULONEPHRITIS Chronic glomerulonephritis is the end stage of glomerular disorders! 1. 2. 3. 4. 5. slow, progressive destruction of glomeruli impairs renal function symmetrical decrease in kidney size kidney becomes granular and roughened eventually nephrons are all destroyed

If theres a need for you to mention acute glomerulonephritis: 1. 2. 3. 4. 5. 6. 7. 8. circulating antigen-antibody immune complexes are formed these are then trapped in the glomerular membrane causes inflammatory response activates complement system to release vasoactive substances and inflammatory mediators edema and iflammatio increase porosity of glomerular capillaries allowing plasma proteins and blood cells to escape into the urine rennin-angiotensin aldosterone (RAA) system is disrupted leads to hypertension