Author Question: Explain the pathophysiology of esophageal varices and portal hypertension as it relates to liver ... (Read 58 times)

Starlight · **on:** Aug 2, 2018

Explain the pathophysiology of esophageal varices and portal hypertension as it relates to liver disease and Mr. N's bleeding.

Question 2

Explain the variance between the two sets of labs. In your explanation, tell how the various enzymes are used to distinguish between MI, liver disease, pulmonary disease, etc.

momo1250 · **Reply #1 on:** Aug 2, 2018

Answer to Question 1

Mr. N's cirrhosis has advanced to the point of having extensive fibrotic material that is restricting blood flow through the liver. This results in back pressure, and blood is shunted to collateral veins, which include the small veins that surround the esophagus, causing them to enlarge to the point of rupturing. The ruptured veins bleed directly into the esophagus and produce blood in the gut.

Answer to Question 2

LDH: normally, serum contains more LDH2 than LDH1 . Damage to tissues rich in LDH1 causes the ratio to reverse. This reversal is an important diagnostic finding that occurs whether or not total LDH is elevated. In MI, the LDH1 to LDH2 ratio returns to normal within a week, even though total LDH may remain elevated.

The different fractions of LDH are found in different concentrations in various tissues. If those tissues are damaged to the point of cellular rupture, the enzymes are released into the blood and become elevated. By knowing which tissues are high in the various enzymes, tissue damage can be determined by analyzing the serum. For example: the heart and RBC are rich sources of LDH1 and LDH2; the brain is a source of LDH1, LDH2, and LDH3; the kidneys, LDH3 AND LDH4, etc. The fractions of CPK vary in the same manner with CPK2 being elevated with MI. ALT levels are only slightly elevated with MI but very sensitive to liver damage. AST may be elevated 5 x normal with MI.