Fick’s principle states that the total uptake (or release) of a substance by peripheral tissues is equal to the product of the blood flow to the peripheral tissues and the arterial– venous concentration difference (gradient) of the substance. It is used to measure the cardiac output, and the formula is Cardiac output = oxygen consumption divided by arteriovenous oxygen difference. Assuming there are no shunts across the pulmonary system, the pulmonary blood flow equals the systemic blood flow. The arterial and venous blood oxygen content is measured by sampling from the pulmonary artery (low oxygen content) and pulmonary vein (high oxygen content). Peripheral arterial blood is used as a surrogate for the pulmonary vein.

The description of the patient here fits the diagnosis of obstructive jaundice or cholestasis, which results in conjugated hyperbilirubinemia. Cholestasis occurs due to impairment of bile flow, which can be anywhere from the liver cell canaliculus to the ampulla of Vater. Causes can be divided into intrahepatic and extrahepatic.

– Intrahepatic causes include hepatitis, drug toxicity, alcoholic liver disease, primary biliary cirrhosis, cholestasis of pregnancy and metastatic cancer.

– Extrahepatic causes include common duct stone, pancreatic cancer, benign stricture of the common duct, ductal carcinoma, pancreatitis and sclerosing cholangitis.

There is absence of bile constituents in the intestine, which causes spillage in the systemic circulation. Symptoms include pale stools, dark urine, pruritus, malabsorption leading to steatorrhea and deficiency of fat-soluble vitamins. Chronic cases can result in osteoporosis or osteomalacia due to vitamin D deficiency and Ca2+ malabsorption. Cholesterol and phospholipid retention produces hyperlipidaemia despite fat malabsorption (although increased liver synthesis and decreased plasma esterification of cholesterol also contribute); triglyceride levels are largely unaffected. The lipids circulate as a unique, low-density lipoprotein called lipoprotein X.

Polycythaemia is a condition that results in an increase in the total number of red blood cells (RBCs) in the blood. It can be due to myeloproliferative syndrome or due to chronically low oxygen levels or rarely malignancy. In primary polycythaemia/polycythaemia vera the increase is due to an abnormality in the bone marrow, resulting in increases RBCs, white blood cells (WBCs) and platelets. In secondary polycythaemia the increase occurs due to high levels of erythropoietin either artificially or naturally. The increase is about 6-8 million/cm3 of blood. A type of secondary polycythaemia is physiological polycythaemia where people living in high altitudes who are exposed to hypoxic conditions produce more erythropoietin as a compensatory mechanism for thin oxygen and low oxygen partial pressure.

As most of the coagulation factors are synthesized in the liver, liver diseases like hepatitis or cirrhosis will depress the coagulation system. Vitamin K deficiency can also decrease the production of vitamin K dependent coagulation factors VII, XI, X and prothrombin.

A stretch reflex is a monosynaptic reflex that causes muscle contraction in response to stretching within that muscle. The sensory apparatus in a muscle that are sensitive to stretch are the muscle spindles. The patellar (knee jerk) reflex is an example. In upper motor neuron lesions, the stretch reflexes tend to be brisk due to loss of inhibitory signals on gamma neurons through the lateral reticulospinal tract.

The oxygen-haemoglobin dissociation curve plots saturated haemoglobin against the oxygen tension and is usually a sigmoid plot. Each molecule of haemoglobin can bind to four molecules of oxygen reversibly. Factors that can influence the binding include: pH, concentration of 2,3-diphosphoglycerate (2,3-DPG), temperature, type of haemoglobin molecules, and presence of toxins, especially carbon monoxide. Shape of the curve is due to interaction of bound oxygen molecules with the incoming molecules. The binding of first molecule is difficult, with easier binding of the second and third molecule and increase in difficulty with the fourth molecule – partly as a result of crowding and partly as a natural tendency of oxygen to dissociate.

Left shift of curve indicates haemoglobin’s increased affinity for oxygen (seen at lungs). Right shift indicates decreased affinity and is seen with an increase in body temperature, hydrogen ions, 2,3-diphosphoglycerate (DPG), carbon dioxide concentration and exercise. Under normal resting conditions in a healthy individual, the normal position of the curve is at a pH of 7.4. A shift in the position of the curve with a change in pH is called the Bohr effect. Left shift occurs in acute alkalosis, decrease in p(CO2), decrease in temperature and decrease in 2,3-DPG. The fetal haemoglobin curve is to the left of the adult haemoglobin to allow for oxygen diffusion across the placenta. The curve for myoglobin is even further to the left. Carbon monoxide has a much higher affinity for haemoglobin than oxygen does. Thus, carbon monoxide poisoning leads to hypoxia.

Jaundice can occur due to any of the possible causes and treatment depends upon diagnosing the correct condition. Mild hyperbilirubinemia with normal levels of aminotransferase and alkaline phosphatase is often unconjugated (e.g., due to haemolysis or Gilbert’s syndrome rather than hepatobiliary disease). Moderate or severe hyperbilirubinemia along with increased urinary bilirubin (bilirubinuria), high alkaline phosphatase or aminotransferase levels suggest hepatobiliary disease. Hyperbilirubinemia produced by any hepatobiliary disease is largely conjugated. In this case, other blood tests include hepatitis serology for suspected hepatitis, prothrombin time (PT) or international normalised ratio (INR), albumin and globulin levels, and antimitochondrial antibody levels (suspected primary biliary cirrhosis). Low albumin and high globulin levels suggest chronic rather than acute liver disease. In cases where there is only a an elevation of alkaline phosphatase, γ-glutamyl transpeptidase (GGT) levels should be checked – the levels of which will be found high in hepatobiliary disease, but not in bone disorder which can also lead to elevated alkaline phosphatase levels. In diseases of hepatobiliary origin, aminotransferase elevations > 500 units suggest a hepatocellular cause, whereas disproportionate increases of alkaline phosphatase (e.g., alkaline phosphatase > 3 times normal and aminotransferase < 200 units) suggest cholestasis. Because hepatobiliary disease alone rarely causes bilirubin levels > 30 mg/dl, higher levels are suggestive of a combination of severe hepatobiliary disease and haemolysis or renal dysfunction. Imaging is best for diagnosing infiltrative and cholestatic causes of jaundice. Liver biopsy is rarely needed, but can be of use in intrahepatic cholestasis and in some types of hepatitis.

PR interval extends from the beginning of the P-wave until the beginning of the QRS complex. The normal duration of the PR interval is 0.12-0.20 s. It can be prolonged in first degree heart block, and reduced in Wolff-Parkinson-White syndrome.

Gastric blood flow is increased by vagal stimulation, gastrin, histamine and acetylcholine as they stimulate gastric section and the production of vasodilator metabolites. Acetylcholine and histamine also have a direct action on the gastric arterioles. Similarly, gastric blood flow is reduced by inhibitors of secretion – catecholamines, secretin and vasopressin.

Fick’s principle states that, VO2 = (CO × CAO2) – (CO × CVO2) where VO2 = oxygen consumption, CO = cardiac output, CAO2 = oxygen concentration of arterial blood and CVO2 = oxygen concentration of venous blood. Thus, CO = VO2/CAO2– CVO2, CO = 500/0.24–0.16, CO = 500/0.8, CO = 6.25 l/min. Cardiac output is also given by product of stroke volume and heart rate. Thus, stroke volume = cardiac output / heart rate = 6.25/70 × 1000 stroke volume = 90 ml approximately.