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Lecture

Clinical Models of Altered Fluid.docx

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Department
Nursing
Course Code
NURS 2090
Professor
Heather Helpard

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Clinical Models of Altered Fluid, Electrolyte and Acid-Base Balance Cirrhosis Pathophysiology - Altered fluid balance due to Reduced local blood flow  The diseases that lead to cirrhosis do so because they injure and kill liver cells, and the inflammation and repair that is associated with the dying liver cells causes scar tissue to form. The liver cells that do not die multiply in an attempt to replace the cells that have died. This results in clusters of newly-formed liver cells (regenerative nodules) within the scar tissue.  Normally, blood from the intestines and spleen is pumped to the liver through the portal vein. However, cirrhosis blocks the normal flow of blood through the liver. This can lead to swelling of the liver. Blood from the intestines, is then forced to find a new way around the liver through new vessels. Some of these new blood vessels called "varices" which form primarily in the stomach and esophagus become quite large. These varices may rupture due to high blood pressure (portal hypertension) and thin vessel walls, causing bleeding in the upper stomach or esophagus. **by finding a new way around liver, that blood is not filtered and toxins accumulate.  Portal hypertension- is a state of increased pressure on the liver. 1. HTN promotes movement of fluid out of capillaries (into the interstitum) - the movement of fluid exceeds the ability of the lymphatic system to recirculate fluid to the systemic circ (leading to accumulation) 2. Increased vascular resistance triggers vasodilation to decrease resistance (↑BP) and ↑BF, which eventually results in ↓BF and ↓BP 3. A drop in BP makes the body want to increase BV. So it holds onto water + Na **Portal HTN increases pressure & permeability- this promotes transport of fluid to the abdominal cavity  Leads to Kidney impairment + vasoconstriction (impaired water excretion and leads to dilutional hyponatremia – low sodium due to excess fluids) **vasoconstriction leads to hepatorenal syndrome  ↑ renin + aldosterone contribute to fluid imbalance.  Hepatocyte damage – necrosis of the liver cells, which results in inflammation and increased scar tissue. This leads to poor blood flow to the liver.  Can be caused by: alcohol, malnutrition, toxins, viral hepatitis  As liver function decreases, fewer proteins such as albumin are produced resulting in fluid accumulation in the legs (edema) or abdomen (ascites). Clinical Manifestations  Ascites- excess fluid that accumulates in the peritoneal cavity and creates SOB (Right ↑ quadrant pain) **enters the 3 space which can’t be used.  Increased hydrostatic pressure- (CHF) pushes fluid to the ISF  Decreased colloid osmotic pressure- (malnutrition) this is what pulls the fluid back from the vascular area, so decreased OSM is bad!  Increased capillary permeability-which allows fluid to leak out (due to inflammation)  Bruising and bleeding- when the liver slows production of proteins (albumin) for clotting  Itching due to increased bile deposits in the skin  Decrease in mental functioning, personality changes, coma and respiratory depression (due to increased toxins in the body, that the liver can no longer remove)  Na retention + water  Renal failure (+ oliguria and ↑ creatinine)  Jaundice occurs and gallstones because insufficient levels of bile reach the gallbladder. Diagnostic Criteria  Physical exam  Body weight  Abdominal girth measurement- must do this regularly to see growth of fluid  Laboratory analysis (all liver enzymes are elevated: ALK, ALT, GGT, Bilirubin, Creatine) o Ascitic fluid analysis o ↑ PT time o ↓ hemoglobin, hematocrit, electrolytes o ↓Vitamin A, C, K o Creatine levels can indicate kidney damage Treatment  Paracentesis- taking the fluid out of ascities, looks yellow and is done for comfort. Must make sure not to take too much or it will fill back up faster.  Diuresis  IV- albumin to expand plasma volume in individuals that have a lrg volume of fluid removed.  DONT GIVE SODIUM!!! Makes it worse! Renal Tubulopathy Pathophysiology:  Genetic mutations in renal
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