Symptom Finder - Functional Changes
Functional Changes
Functional changes take place because of an alteration in the physiology or biochemistry of an organ system. Consequently, a differential diagnosis can be best developed by using physiology or biochemistry. For example, a 24-year-old black woman presents with a 2-day history of jaundice and anorexia. Jaundice results from an elevation in the bilirubin level in the blood. Using pathophysiology, one can appreciate that an increased serum bilirubin may result from increased production of bilirubin as occurs in hemolytic anemia or decreased excretion of bilirubin by a diseased liver or obstructed biliary tree. Now, one can translate these categories into a list of possibilities using common causes as follows:
1. Increased production: sickle cell anemia, hereditary spherocytosis, acquired hemolytic anemia
2. Decreased excretion by a diseased liver: viral hepatitis, toxic hepatitis, cirrhosis
3. Decreased excretion due to bile duct obstruction: biliary cirrhosis, common duct stone, neoplasm
This list may be abbreviated, but it would provide the clinician with a basis for a meaningful interview of the patient and a logical laboratory workup. Thinking of increased production, one would ask about other symptoms of sickle cell anemia, such as joint pain, cramps, and the fever
of sickle cell crisis. Thinking of bile duct obstruction, one would ask about previous attacks of right upper quadrant pain with fever and nausea or
vomiting to substantiate a diagnosis of cholecystitis or common duct stone. In the workup, one would not forget to order a serum haptoglobin level to exclude hemolytic anemia or sickle cell preparation. One would also consider a gallbladder sonogram if the hepatitis profile were normal.
Now, for a more extensive list of possibilities, a second step can be taken to develop functional changes like jaundice using etiologic categories. The mnemonic MINT can be applied as follows:
M—Malformation would help recall congenital bile duct atresia and hereditary hemolytic anemias.
I—Inflammation would bring to mind viral hepatitis, amebic abscess, lupoid hepatitis, and acquired hemolytic anemia.
N—Neoplasm would suggest hepatoma, carcinoma anywhere along the biliary tree, and metastatic carcinoma.
T—Toxins would remind one of chlorpromazine, carbon tetrachloride, alcoholic cirrhosis, and so on.
A third step can be taken to develop a table as has been done in the other categories of symptoms or signs previously discussed.
Functional changes take place because of an alteration in the physiology or biochemistry of an organ system. Consequently, a differential diagnosis can be best developed by using physiology or biochemistry. For example, a 24-year-old black woman presents with a 2-day history of jaundice and anorexia. Jaundice results from an elevation in the bilirubin level in the blood. Using pathophysiology, one can appreciate that an increased serum bilirubin may result from increased production of bilirubin as occurs in hemolytic anemia or decreased excretion of bilirubin by a diseased liver or obstructed biliary tree. Now, one can translate these categories into a list of possibilities using common causes as follows:
1. Increased production: sickle cell anemia, hereditary spherocytosis, acquired hemolytic anemia
2. Decreased excretion by a diseased liver: viral hepatitis, toxic hepatitis, cirrhosis
3. Decreased excretion due to bile duct obstruction: biliary cirrhosis, common duct stone, neoplasm
This list may be abbreviated, but it would provide the clinician with a basis for a meaningful interview of the patient and a logical laboratory workup. Thinking of increased production, one would ask about other symptoms of sickle cell anemia, such as joint pain, cramps, and the fever
of sickle cell crisis. Thinking of bile duct obstruction, one would ask about previous attacks of right upper quadrant pain with fever and nausea or
vomiting to substantiate a diagnosis of cholecystitis or common duct stone. In the workup, one would not forget to order a serum haptoglobin level to exclude hemolytic anemia or sickle cell preparation. One would also consider a gallbladder sonogram if the hepatitis profile were normal.
Now, for a more extensive list of possibilities, a second step can be taken to develop functional changes like jaundice using etiologic categories. The mnemonic MINT can be applied as follows:
M—Malformation would help recall congenital bile duct atresia and hereditary hemolytic anemias.
I—Inflammation would bring to mind viral hepatitis, amebic abscess, lupoid hepatitis, and acquired hemolytic anemia.
N—Neoplasm would suggest hepatoma, carcinoma anywhere along the biliary tree, and metastatic carcinoma.
T—Toxins would remind one of chlorpromazine, carbon tetrachloride, alcoholic cirrhosis, and so on.
A third step can be taken to develop a table as has been done in the other categories of symptoms or signs previously discussed.
