Cellular Respiration and Metabolism

Cell Metabolism

• The cell cannot tolerate accumulation of pyruvate, so it shifts pyruvate into other pathways, converting it to Acetyl-CoA, which is used in the TCA cycle and fatty acid synthesis.
• There is no feedback inhibition of triacylglycerol synthesis, making it an overflow pathway for many metabolites, occurring in many cells, even in those not supposed to store them.

Anaerobic Glycolysis

• Impaired TCA or lack of oxygen leads to anaerobic glycolysis, producing lactate.
• Anaerobic glycolysis occurs to regenerate NAD+ and secrete lactate, generating ATP, but is not very efficient.
• It occurs in strenuous or rapid exercise, or in poisoning cases, such as cyanide poisoning, and can lead to tissue acidification with lactic acid, causing muscle cramps.

Gluconeogenesis

• Gluconeogenesis is the process of synthesizing glucose from pyruvate and other metabolites (lactate, TCA cycle intermediates), providing glucose in times of fasting.
• The liver performs gluconeogenesis to support the body.
• Acetyl-CoA cannot be converted to glucose, so none of the carbons in a fatty acid can be converted into pyruvate, and therefore, glucose cannot be made from fatty acids.
• However, ATP generated from fatty acid breakdown can be used to fuel gluconeogenesis.
• Ethanol inhibits gluconeogenesis, leading to hypoglycemia if not eaten in a long time.

Glucogenic vs. Ketogenic

• Glucogenic molecules can be converted to glucose.
• Glucogenic molecules include growth hormone, lactate, and TCA cycle intermediates.

Assessment Tools

• Growth charts reflect the optimal growth of a healthy population and are useful for assessing growth patterns over time.
• Weight is a primary indicator of over/under nutrition, and is an acute indicator.
• Length/height is a slower indicator of nutritional changes, and is a chronic indicator.
• Body Mass Index (BMI) is calculated by dividing weight in kg by height in m2, and is useful in children over 2 years old.

Dietary Intake

• Dietary intake is assessed by asking who, what, where, when, how, how much, and why.
• Pathophysiology of altered gastric mucosal barrier involves decreased prostaglandin production, decreased mucus and HCO3, and decreased submucosal blood flow.

H. Pylori

• H. Pylori is a slow-growing, highly motile, gram-negative, spiral-shaped bacteria that produces urease, protecting it in the acid environment of the stomach.
• Prevalence of H. Pylori infection depends on age, SES class/hygiene, country of origin, and genetic factors.
• Infection is usually acquired in childhood, and chronic non-atrophic gastritis is associated with a 4-fold increased risk of developing an ulcer.

Management of Diarrhea

• Empiric management of diarrhea includes loperamide (Imodium), Lomotil, bulking agents, and Cholestyramine.
• Loperamide acts directly on intestinal muscles to inhibit peristalsis and prolong transit time, reducing fecal volume and electrolyte loss.
• Lomotil is a combination of atropine and diphenoxylate, which inhibits excessive GI motility and propulsion.
• Bulking agents include psyllium (Metamucil) and wheat dextran (Benefiber), which absorb and retain water, increasing stool bulk.
• Cholestyramine is an oral bile acid sequestrant, indicated in patients who develop diarrhea post-cholecystectomy.