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14. Homeostasis

Syllabus
9700–2028–2029
Section
14
Level
A2

14.1 Homeostasis in Mammals

Syllabus
9700–2028–2029
Topic
14.1
Level
A2

Homeostasis maintains a functional internal range

Homeostasis is the maintenance of a relatively stable internal environment within limits, despite changes inside or outside the body. A regulated condition can fluctuate around a suitable level; it does not have to remain at one exact value.

This stability matters because:

  • enzymes work effectively only within suitable conditions such as temperature and pH
  • controlled water potential limits harmful net water movement into or out of cells
  • cells receive suitable concentrations of substances needed for metabolism

Homeostasis is dynamic control, not perfect constancy. Small deviations occur, but corrective responses keep conditions inside a functional range.

Negative feedback opposes a detected deviation

A stimulus is a detectable change. It may be internal, such as a change in blood glucose or water potential, or external, such as a change in environmental temperature. Receptors detect the relevant change and send information to a coordination system.

The control pathway is:

  1. a stimulus moves a condition away from its suitable range
  2. a receptor detects the change
  3. a nervous or endocrine coordination system processes the information and sends a signal
  4. effectors—muscles or glands—produce a response
  5. the response opposes the original change, so the deviation becomes smaller

The receptor detects; it does not itself correct the condition. Negative means that the response reduces the deviation, not that the response is harmful.

The liver produces urea by converting toxic ammonia into a soluble waste

Excess amino acids cannot be stored as amino acids. In the liver, deamination removes the amino group and produces ammonia; the remaining carbon skeleton can be used in metabolism, while the nitrogen-containing waste is processed into urea.

Urea pathway boundary:

  1. Excess amino acids are broken down and their amino groups are removed by deamination.
  2. The removed nitrogen forms ammonia, which is very soluble and toxic if it accumulates in the blood.
  3. Liver cells combine ammonia with carbon dioxide to form urea, a less toxic nitrogenous waste.
  4. Urea dissolves in the blood and is transported to the kidneys.
  5. The kidneys remove urea from the blood and it leaves the body in urine; this card does not describe nephron structure or the detailed formation of urine.

Converting ammonia to urea reduces the immediate toxicity of nitrogen waste and makes its transport in body fluids manageable. Water is required to carry dissolved urea and to remove it, so nitrogen excretion has a water-handling cost; the kidney-level details belong to later cards.

Urea is formed in the liver, not made by the kidney from scratch. Deamination is not the same as complete respiration of the carbon skeleton, and this card does not cover ultrafiltration, selective reabsorption or osmoregulation.

Identify the kidney from capsule to pelvis and vessels

On a kidney section, identify structures from outside inward:

  • fibrous capsule: the thin protective outer covering
  • cortex: the outer tissue region beneath the capsule
  • medulla: the inner region, arranged into darker pyramidal areas
  • renal pelvis: the central collecting space leading into the ureter
  • ureter: the tube carrying urine away from the kidney

At the kidney's indented side, identify the renal artery and renal vein. Their branches extend through kidney tissue: artery branches deliver blood for processing, while vein branches collect blood leaving the kidney.

Do not confuse tissue regions with transport routes: cortex and medulla are regions; the renal pelvis and ureter carry urine; renal artery and vein branches carry blood.

Follow the nephron to identify its six required parts

Part to identify Recognition cue
Glomerulus knot-like capillary network inside Bowman's capsule
Bowman's capsule cup-shaped structure surrounding the glomerulus
Proximal convoluted tubule (PCT) first coiled tubule leaving the capsule, in the cortex
Loop of Henle long hairpin loop descending into and returning from the medulla
Distal convoluted tubule (DCT) later coiled tubule in the cortex before the collecting duct
Collecting duct straighter, wider duct receiving fluid from nephrons and passing through the medulla

Trace the route in this order: Bowman's capsule receives filtrate from the glomerulus, then PCT → loop of Henle → DCT → collecting duct. On a simplified diagram, continuity of the tubule is more reliable than its exact drawn shape.

The glomerulus is the capillary network; Bowman's capsule is the cup around it. They form one renal corpuscle region but are not the same structure.

Urine formation begins with filtration, then selective recovery

Two linked processes begin urine formation:

  1. Ultrafiltration in Bowman's capsule: high pressure forces water and small dissolved substances from glomerular blood into the capsule. Blood cells and most plasma proteins remain in the blood.
  2. Selective reabsorption in the proximal convoluted tubule: useful substances such as all glucose and amino acids, together with required ions and much water, move from the filtrate back into the blood.

The filter separates mainly by particle size, not usefulness. Selective reabsorption then recovers substances the body needs, so useful small molecules can enter the filtrate first and still be returned to the blood.

At this syllabus point, explain urine formation only through ultrafiltration at Bowman's capsule and selective reabsorption in the PCT. Do not replace either stage with the claim that the kidney simply removes waste.

Bowman's capsule filters; the PCT selectively reabsorbs

Region and feature Functional consequence
Glomerular afferent arteriole wider than efferent arteriole creates high hydrostatic pressure for ultrafiltration
Fenestrated capillary endothelium allows plasma water and small solutes to leave the capillary
Basement membrane acts as a fine filtration barrier, restricting large proteins
Podocyte filtration slits provide final narrow pathways into Bowman's capsule
PCT epithelium one cell thick with microvilli short diffusion distance and large surface area for reabsorption
PCT cells with many mitochondria and basal infoldings supply ATP and membrane area for active transport
Close capillary network around PCT rapidly carries reabsorbed substances away and maintains gradients

In the PCT, sodium ions are actively transported and cotransport helps return glucose and amino acids to the blood. Water follows by osmosis. In a healthy person, all filtered glucose and amino acids are reabsorbed here, along with required ions and much water.

Cells and most plasma proteins are too large to cross the normal filtration barrier. Microvilli increase surface area; they do not generate the pressure that drives ultrafiltration.

ADH increases collecting-duct water permeability when blood water potential falls

Osmoregulation keeps the water potential of body fluids within a functional range. When blood water potential falls, osmoreceptors detect the change and the ADH pathway makes the collecting duct more permeable to water, allowing more water to be recovered.

ADH control chain:

  1. A fall in blood water potential is detected by osmoreceptors in the hypothalamus.
  2. Nerve impulses stimulate the posterior pituitary gland to release antidiuretic hormone (ADH) into the blood.
  3. ADH reaches the kidney and binds to receptors on collecting-duct cells.
  4. Signalling causes aquaporin-containing vesicles to add water-permeable channels to the luminal membrane, increasing collecting-duct water permeability.
  5. Water moves from the filtrate through aquaporins into the surrounding medullary tissue fluid and blood down a water-potential gradient.
  6. The filtrate loses water and becomes a small volume of concentrated urine, reducing water loss.

When blood water potential is high, less ADH is released and fewer aquaporins remain in the collecting-duct membrane. Less water leaves the filtrate, so a larger volume of dilute urine is produced. The medullary gradient supplies the osmotic pull; ADH changes permeability so the existing gradient can act rather than directly pumping water or creating the gradient.

This card is the ADH/osmoregulation control chain, not the general nephron-segment map in 4682. It also does not cover blood-glucose test strips or other homeostatic systems.

Glucagon triggers an amplified enzyme cascade in liver cells

When glucagon binds to its complementary receptor on a liver cell membrane:

  1. the receptor changes conformation and activates a G-protein
  2. the G-protein activates adenylyl cyclase in the membrane
  3. adenylyl cyclase converts ATP to cyclic AMP (cAMP), the second messenger
  4. cAMP activates protein kinase A (PKA)
  5. PKA phosphorylates enzymes in a cascade
  6. the cascade activates enzymes for glycogen breakdown and inhibits glycogen synthesis, so glucose becomes available for release into the blood

The signal is amplified because one activated receptor can activate several G-proteins, each adenylyl cyclase can produce many cAMP molecules, and each kinase can phosphorylate many enzyme molecules. A small glucagon signal can therefore produce a large metabolic response.

Glucagon remains outside the liver cell. It changes enzyme activity through a membrane receptor, G-protein, second messenger and phosphorylation cascade; it does not directly contact glycogen.

Insulin and glucagon form opposing blood-glucose feedback

Detected condition Pancreatic response Main target effects Result
Blood glucose rises above the suitable range beta cells secrete more insulin muscle cells increase glucose uptake and respiration and form glycogen; liver cells increase glucose use and glycogen formation blood glucose falls toward the range
Blood glucose falls below the suitable range alpha cells secrete more glucagon liver cells increase glycogen breakdown and glucose formation, then release glucose into the blood blood glucose rises toward the range

As blood glucose returns toward the suitable range, the original stimulus becomes smaller, so secretion of the corrective hormone decreases. This is negative feedback: the two pathways are activated under opposite conditions and oppose the deviation.

For these named effects, distinguish the tissues: insulin acts on muscle and liver cells, while glucagon's blood-glucose-raising effects are described in liver cells. The hormones are not released maximally at the same time.

A glucose test strip converts an enzyme reaction into a measurable signal

A glucose test strip uses immobilised enzymes to convert glucose into a colour signal, while a blood-glucose biosensor converts an enzyme reaction into an electrical signal. The signal is interpreted as an estimate of glucose concentration within the method’s calibrated range.

Urine test-strip method:

  1. Immerse the enzyme-containing pad in the urine sample for the specified short time.
  2. If glucose is present, glucose oxidase produces hydrogen peroxide; peroxidase uses it in a second reaction that forms a coloured product.
  3. Compare the pad colour with the supplied colour chart: darker colour corresponds to a higher glucose concentration in the chart range.
  4. Treat the result as a urine-glucose indication, not a direct current blood-glucose reading.

Blood biosensor method:

  1. A partially permeable membrane allows small molecules from the blood sample to reach immobilised glucose oxidase on the recognition layer.
  2. Glucose oxidation produces hydrogen peroxide, whose electron transfer at an electrode creates a current.
  3. Electron flow is related to glucose concentration; the processor converts the amplified signal into a digital reading.

Use the stated sample volume or immersion, timing and calibration/colour chart consistently; compare with appropriate controls or a known reference when the method provides them. Read only within the validated range and do not infer more precision than the colour scale or sensor supports.

Enzyme specificity makes the test selective for glucose. A urine strip indicates whether glucose was present in the urine and reflects earlier renal-threshold conditions; it does not show the current blood-glucose concentration. This card covers signal generation and reading, not insulin/glucagon feedback or a medical diagnosis.

14.2 Homeostasis in Plants

Syllabus
9700–2028–2029
Topic
14.2
Level
A2

Stomata balance carbon-dioxide entry against water loss

Stomata regulate the exchange of gases between a leaf and the air. Opening allows carbon dioxide to diffuse in for photosynthesis, but it also provides a route for water vapour to leave by transpiration.

Environmental response:

  • Increasing light intensity or low carbon dioxide concentration inside the leaf tends to favour opening because photosynthetic carbon supply is useful.
  • Darkness or high internal carbon dioxide concentration reduces the benefit of opening.
  • Low humidity, high temperature, limited water supply or high transpiration increase the cost of opening and can favour closure.

The response is a balance, not a single-trigger rule. Open stomata improve carbon-dioxide entry but increase water loss; closed stomata conserve water but restrict carbon-dioxide diffusion, so photosynthesis may decrease.

Light alone does not determine aperture, and a stoma is not “good” or “bad” in isolation. The outcome depends on carbon-dioxide demand and the leaf’s water-loss conditions. Guard-cell structure and turgor mechanics, daily rhythms, and ABA signalling are separate learning steps.

Stomatal rhythms anticipate daily changes but remain responsive to conditions

Many plants show a daily rhythm of stomatal opening and closing. Stomata often open during daylight, when carbon dioxide is needed for photosynthesis, and close at night, when photosynthesis cannot use incoming carbon dioxide.

The rhythm is not just a direct reaction to the current light level:

  • A daily pattern can continue when a plant is kept in constant light or constant darkness, showing an endogenous timing component.
  • Light and other environmental cues can reset or adjust the timing, so the rhythm remains aligned with the day.

Opening around the day’s photosynthetic period supports carbon-dioxide entry but also permits water-vapour loss. Closing at night reduces unnecessary transpiration and conserves water. Water stress, high temperature, low humidity or changed carbon-dioxide conditions can override or shift the expected pattern when opening becomes too costly.

A daily pattern is not proof that light is the only cause, and it is not identical in every plant or condition. This card separates timing from the guard-cell micro-mechanism and from ABA signalling, which are taught separately.

Guard cells open a stoma by changing turgor around a pore

Each stoma is a pore surrounded by a pair of guard cells. Their unequal wall structure converts changes in cell turgor into a wider or narrower pore, regulating carbon-dioxide entry and water-vapour loss.

Structure → movement:

  • The walls next to the pore are thicker, while the outer walls are thinner; cellulose microfibrils constrain how the cells change shape.
  • Guard-cell membranes contain channels and carriers, and the cells have chloroplasts, mitochondria and several small vacuoles to support active control and water movement.

Opening chain:

  1. Solute ions, including potassium ions, enter the guard cells, lowering their water potential.
  2. Water enters by osmosis through aquaporins, especially into the vacuoles, so guard-cell turgor rises.
  3. Because the walls do not stretch equally, the guard cells curve apart and the pore opens, allowing gas exchange but also increasing transpiration.

When ion movement out of the guard cells reverses the water-potential gradient, water leaves by osmosis. Turgor falls, the cells become flaccid and the pore closes, reducing both carbon-dioxide entry and water loss.

The pore is controlled by guard-cell turgor, not by guard cells absorbing carbon dioxide directly. This card explains the cell-mechanical mechanism; ABA signalling is a separate upstream control step.

Abscisic acid signals water stress and promotes stomatal closure

During water stress, plants can increase the hormone abscisic acid (ABA). ABA acts on guard cells to promote ion loss, water loss, reduced turgor and stomatal closure, helping limit further transpiration.

ABA closure chain:

  1. Reduced water supply or high water loss is associated with increased ABA in the relevant plant tissues.
  2. ABA binds to receptors on guard-cell membranes and inhibits the proton pumps that normally move H+ out.
  3. ABA also causes Ca2+ ions to enter the guard-cell cytoplasm. Ca2+ acts as a second messenger: it opens channels for negatively charged ions to leave, promotes further K+ efflux and closes channels that bring K+ in.
  4. Loss of ions raises guard-cell water potential, so water leaves by osmosis.
  5. The guard cells become flaccid and the stomatal pore closes.

Closure reduces the route for water-vapour loss, but it also restricts carbon-dioxide entry and can limit photosynthesis. ABA therefore shifts the gas-exchange trade-off towards water conservation during stress; it is a signal, not a permanent switch that makes photosynthesis impossible.

Calcium ions transmit the ABA signal; they are not the final mechanical cause of closure. The immediate mechanical outcome is ion loss followed by water loss and falling guard-cell turgor. The general guard-cell wall and turgor structure is covered in the preceding card.