Kidney Functions and Nephron Structure

The process of moving water and small solutes from the blood in the glomerulus into Bowman's space.

The transfer of substances from the tubular lumen back into the capillaries.

The process of moving substances from the capillaries into the tubular lumen for excretion.

The major site for reabsorbing glucose, amino acids, sodium, and water, as well as secreting hydrogen ions and organic acids/bases.

A part of the nephron responsible for concentrating urine through a countercurrent mechanism.

The descending limb of the loop of Henle is permeable to water, allowing it to be reabsorbed.

The ascending limb of the loop of Henle actively reabsorbs sodium and chloride ions, while being impermeable to water.

The combination pill contains synthetic forms of estrogen and progesterone, which work by mimicking the effects of these natural hormones.

The movement of fluid and solutes from the blood in the glomerulus into Bowman's space. This is the first step in urine formation.

The pressure that drives fluid from the blood into Bowman's space. It's the difference between glomerular hydrostatic pressure and the opposing pressures (plasma osmotic pressure and Bowman's capsule pressure).

A state of decreased sodium retention and increased potassium levels, often associated with Addison's disease. It disrupts the balance of electrolytes.

The phase of digestion triggered by the sight, smell, taste, or thought of food. It primes the digestive system for action.

This phase is triggered when food reaches the stomach. It involves stomach distension and the presence of proteins and peptides.

The final phase of digestion, triggered by the presence of chyme in the small intestine, especially fatty or acidic chyme. It involves the release of hormones like CCK and secretin.

A hormone released from G cells in the stomach that stimulates acid production by parietal cells, leading to increased gastric motility.

A hormone released from the small intestine that stimulates the release of bile and pancreatic enzymes. Essential for lipid digestion.

Pepsin, an enzyme essential for protein digestion, requires an acidic environment (low pH) to function optimally. When stomach pH increases, pepsin activity slows down, inhibiting protein breakdown.

Trypsin, another digestive enzyme, operates in the alkaline environment of the small intestine. It's less affected by changes in stomach pH because it works in a different part of the digestive tract.

The pancreas releases insulin to regulate blood glucose levels. When blood glucose rises after a high-carbohydrate meal, insulin stimulates glucose uptake by cells and glycogen storage, lowering blood glucose. As blood sugar falls, insulin secretion declines.

When blood glucose levels drop during fasting, the pancreas releases glucagon. Glucagon promotes glycogen breakdown and glucose production (gluconeogenesis), raising blood glucose levels. As blood sugar rises, glucagon secretion decreases.

In Type I diabetes, the pancreas does not produce insulin, leading to uncontrolled blood glucose levels. The body relies on glucagon to raise sugar, but that's not enough to compensate.

Insulin resistance occurs when body cells fail to respond to insulin, despite its presence. This leads to high blood glucose levels and the pancreas compensates by producing more insulin.

Vasopressin (ADH) is a hormone that promotes water reabsorption in the kidneys. It binds to receptors in the collecting duct, causing insertion of aquaporin-2 channels. These channels allow water to move from the urine into the bloodstream.

Hydration status affects how much water is reabsorbed in the kidneys. When dehydrated, ADH release increases, prompting more water reabsorption and concentrated urine. When well-hydrated, ADH release decreases, promoting less water reabsorption and dilute urine.

With low ADH levels, aquaporins are absent, reducing water reabsorption. Urine volume: High (dilute urine). Urine concentration: Low.

With high ADH levels, more aquaporins are inserted, enhancing water reabsorption. Urine volume: Low (concentrated urine). Urine concentration: High.

ACE inhibitors block the conversion of angiotensin I to angiotensin II. Effects: Decreased vasoconstriction. Reduced aldosterone secretion, leading to lower sodium reabsorption and water retention. Lower blood pressure.

Low blood pressure or volume sensed by juxtaglomerular cells. Low sodium concentration in the distal tubule sensed by the macula densa. Sympathetic nervous system activation.

Blood Pressure: Vasoconstriction increases systemic resistance, raising blood pressure. Sodium Balance: Stimulates aldosterone secretion, promoting sodium reabsorption in the distal tubule and collecting duct. Enhances sodium and water reabsorption, increasing blood volume and pressure.

Chloride is often co-transported with sodium, and its movement establishes osmotic gradients. Water follows chloride and sodium through osmosis.

Cholera toxin causes excessive chloride secretion into the intestinal lumen via CFTR channels. Disruption: Water follows chloride, leading to massive water loss in the form of diarrhea. Severe dehydration occurs due to osmotic imbalances.

Essential for maintaining cell integrity, fluid distribution, and proper organ function. Imbalances in the intestine or kidney can lead to dehydration, edema, or other complications.

The network of capillaries in the kidney that filters blood plasma into Bowman's capsule, initiating urine formation.

The arteriole that carries blood away from the glomerulus, regulating blood flow and filtration pressure.

Capillaries surrounding the tubules of the nephron in the cortex, involved in reabsorbing valuable substances and secreting waste.

Capillaries that extend into the medulla, crucial for maintaining the concentration gradient necessary for urine formation.

The volume of filtrate produced by the kidneys per minute, a key indicator of renal function.

When blood glucose levels rise, it acts as a signal to stop further glucagon release from the pancreas. This is a negative feedback loop, ensuring blood glucose levels don't become too high.

Exercise causes an increase in muscle glucose uptake, leading to a decrease in plasma glucose levels. Glucagon and epinephrine help maintain blood glucose levels despite this decrease.

Stress triggers the release of cortisol, which promotes gluconeogenesis (creating glucose from non-sugar sources) and proteolysis (breaking down proteins). This impacts blood glucose levels.

During exercise, both glucose and fatty acids are used as primary fuel sources. Anaerobic metabolism also occurs, producing lactate.

When fasting, the body primarily relies on fatty acids and ketones for energy. This is a metabolic adaptation to conserve glucose for vital organs.

Type 1 diabetes results from a lack of insulin. This causes hyperglycemia (high blood sugar), increased lipolysis (fat breakdown), and ketogenesis (ketone production).

Type 2 diabetes is characterized by insulin resistance, leading to impaired glucose uptake and chronic hyperglycemia. The body doesn't respond properly to insulin.

Insulin excess can lead to hypoglycemia (low blood sugar). This can cause confusion, weakness, or even coma due to insufficient glucose for brain function.