OCR A Level Biology A: Hormonal communication and blood glucose control (H420) – Practice Questions

These are original questions written for Marlbridge, for revision and practice on this content. They are not reproduced past-paper questions, and they do not replicate the exam’s exact structure, question count or mark tariffs – examination boards hold copyright in their own papers. Use these alongside the official past papers from your board or school.

These questions cover outcomes 5.1.4(a) to 5.1.4(f) of the OCR A Level Biology A (H420) specification, Version 4.1 (April 2026), for first assessment in 2025: hormones, adrenal glands, pancreas histology, blood glucose regulation, diabetes and treatments. Read the study guide and revision notes first. The OCR A Level Biology hub, checklist and free diagnostics show what to practise next.

Questions

1. Describe how a hormone released by an endocrine gland affects only its target cells. [4]

2. The adrenal glands are endocrine glands.

(a) State where the adrenal glands are located and name the two regions of each gland. [2] (b) For each region, name one hormone and state one of its functions. [4] (c) A patient cannot make aldosterone. Predict and explain the effects on the sodium ion and potassium ion concentrations of the blood. [3]

3. A section of pancreas is viewed with a light microscope.

(a) Describe two differences in appearance between an islet of Langerhans and the surrounding acini. [2] (b) A photomicrograph of the section is printed at a magnification of ×60. An islet measures 15 mm across on the print. Calculate the actual width of the islet in micrometres. [2] (c) Explain why an islet has no duct but a dense network of capillaries. [2]

4. A student’s drawing of a pancreas section has shaded cells, overlapping label lines and no title. State four changes that would improve it. [4]

5. A person eats a meal rich in carbohydrate. Explain how the blood glucose concentration is returned to its normal level. [5]

6. During a long fast, blood glucose would fall without a hormonal response. Explain how glucagon and the liver prevent this. [4]

7. Describe how a rise in blood glucose concentration leads to the release of insulin from a beta cell. [6]

8. Beta cells were loaded with a fluorescent dye whose brightness shows the calcium ion concentration in the cytoplasm. Relative fluorescence was measured at four glucose concentrations.

Glucose / mmol dm⁻³	3	6	9	12
Relative fluorescence	1.0	1.1	2.9	4.1

At 12 mmol dm⁻³, adding diazoxide, a drug that holds potassium channels open, gave a relative fluorescence of 1.2.

(a) Calculate the percentage increase in fluorescence between 3 and 12 mmol dm⁻³. [2] (b) Explain the result with diazoxide. [3] (c) Suggest why fluorescence barely changed between 3 and 6 mmol dm⁻³. [1]

9. A healthy adult and an adult with Type 2 diabetes each drank a glucose solution after fasting. Blood glucose (mmol dm⁻³) was measured over three hours.

Time / min	0	30	60	120	180
Healthy adult	4.8	7.4	6.2	5.0	4.7
Type 2 adult	8.1	12.6	13.4	11.7	9.6

(a) For the healthy adult, calculate the percentage rise in glucose between 0 and 30 minutes. [2] (b) Find how quickly glucose fell, on average, in the Type 2 adult from 60 to 180 minutes, in mmol dm⁻³ per hour. [2] (c) Use the data to explain how the Type 2 adult’s response differs from the healthy adult’s. [3]

10. (a) Explain what causes Type 1 diabetes. [2] (b) Explain what causes Type 2 diabetes. [2] (c) A sulfonylurea drug closes potassium channels in beta cells. Explain why it is useful in Type 2 diabetes but not in Type 1. [2]

11. (a) Describe how bacteria can be genetically modified to make human insulin. [4] (b) Give two advantages of using this insulin rather than insulin extracted from pigs. [2]

12. Some people with Type 1 diabetes use a continuous glucose sensor linked to an insulin pump.

(a) Explain how this system can act like a negative feedback loop. [3] (b) Evaluate the potential of stem cell treatment compared with insulin injections for Type 1 diabetes. [5]

Answers

1. The gland cells secrete the hormone into the blood capillaries around them [1]. The blood plasma carries it to all parts of the body [1]. Target cells have receptors on (or in) them with a shape complementary to the hormone [1]. Other cells lack the receptor, so the hormone does not affect them [1]. [4] Examiner insight: Keep the three stages (secretion, transport, detection) separate and say why non-target cells do not respond.

2. (a) The glands are on top of (above) each kidney [1]. The regions are the cortex and the medulla [1]. [2] (b) Cortex: aldosterone [1] increases sodium ion reabsorption in the kidney tubules (or cortisol raises blood glucose) [1]. Medulla: adrenaline [1] increases heart rate or causes glycogenolysis [1]. [4] (c) Less sodium ion reabsorption, so sodium ions are lost in the urine and blood sodium concentration falls [1]. Less potassium ion excretion, so blood potassium concentration rises [1]. Water follows sodium, so blood volume and blood pressure fall [1]. [3] Examiner insight: Give each hormone with its own function as a matched pair; “controls stress” on its own is too vague.

3. (a) Islets are paler staining than the surrounding tissue [1]. Islets are rounded patches with no ducts, whereas acini are clusters of cells around small ducts [1]. [2] (b) Actual width = 15 mm ÷ 60 [1] = 0.25 mm = 250 µm [1]. [2] (c) There is no duct because hormones are not carried away along a duct [1]. The dense capillaries let hormones enter the blood quickly [1]. [2] Examiner insight: In magnification questions, show the rearrangement and the unit conversion so that a slip in the last step is visible.

4. Remove the shading and use clear outlines [1]; use single continuous lines rather than sketchy ones [1]; draw label lines with a ruler so that they do not cross [1]; add a title, and the magnification or a scale bar [1]. [4] Examiner insight: Give four different improvements.

5. Absorbed glucose raises blood glucose [1]. Beta cells detect the rise [1]. They secrete insulin into the blood [1]. Insulin binds to receptors on liver, muscle and fat cells; they take up more glucose and the liver forms glycogen (glycogenesis) [1]. Blood glucose falls, so the stimulus for insulin decreases and secretion falls: negative feedback [1]. [5] Examiner insight: Finish the loop: saying that the falling level reduces insulin secretion turns a description of insulin into an explanation of negative feedback.

6. Low glucose is detected by alpha cells, which release glucagon [1]. At the hepatocyte surface it activates adenylyl cyclase, so cyclic AMP is made [1]. The liver converts glycogen to glucose (glycogenolysis) [1]. The liver also makes glucose from amino acids or glycerol (gluconeogenesis) [1]. [4] Examiner insight: Use the correct term for each process: “glycogenesis” for the breakdown of glycogen would contradict an otherwise correct description.

7. Glucose enters the beta cell [1] by facilitated diffusion [1]. It is respired, so ATP concentration rises [1]. ATP closes potassium ion channels [1], so the membrane depolarises [1]. Voltage-gated calcium ion channels open and calcium ions enter, which makes insulin vesicles fuse with the membrane (exocytosis) [1]. (Any six.) [6] Examiner insight: This is a sequence question. Link each step to the next (ATP closes channels, which causes depolarisation) and keep the order.

8. (a) (4.1 − 1.0) ÷ 1.0 × 100 [1] = 310% [1]. [2] (b) Diazoxide keeps potassium channels open, so potassium ions keep leaving [1]. The membrane does not depolarise even though glucose is high [1]. Calcium channels stay shut, so calcium ions do not enter and fluorescence stays near the baseline [1]. [3] (c) At low glucose too little ATP is made to close the potassium channels, so the calcium channels are not opened [1]. [1] Examiner insight: Use the data: comparing 4.1 with 1.2 at the same glucose concentration shows the drug effect, then link it to the channel sequence.

9. (a) (7.4 − 4.8) ÷ 4.8 × 100 [1] = 54% [1]. [2] (b) (13.4 − 9.6) ÷ 2 hours [1] = 1.9 mmol dm⁻³ per hour [1]. [2] (c) The Type 2 adult starts higher (8.1 compared with 4.8) [1]. The peak is much higher (13.4 compared with 7.4) and occurs later (60 minutes compared with 30) [1]. By 180 minutes the Type 2 adult is still 1.5 above the starting value, whereas the healthy adult has returned to about the starting value [1]. [3] Examiner insight: A rate alone can mislead: here the Type 2 fall per hour (1.9) is faster than the healthy adult’s (0.75), but the level has not been restored. Quote values from both people and compare them directly.

10. (a) The immune system attacks and destroys the beta cells (an autoimmune response) [1], so little or no insulin is made [1]. [2] (b) Target cells become less responsive to insulin (insulin resistance) [1]. Beta cells may later be unable to make enough insulin to compensate, and risk factors include obesity and inactivity [1]. [2] (c) The drug makes surviving beta cells release more insulin, which helps in Type 2 where beta cells are present [1]. In Type 1 few or no beta cells remain, so there are none to stimulate and insulin must be supplied directly [1]. [2] Examiner insight: “Type 2 is caused by obesity” is incomplete. State the physiological problem (reduced response to insulin) and treat risk factors as contributors.

11. (a) Obtain the human insulin gene, without introns [1]. Cut the gene and a plasmid with the same restriction enzyme to give sticky ends, and join them with DNA ligase [1]. Insert the recombinant plasmid into bacteria and identify those that took it up using a marker gene [1]. Culture the bacteria in a fermenter and extract and purify the insulin [1]. [4] (b) The insulin has the human amino acid sequence, so is less likely to cause an immune response [1]. Supply is large and reliable, or no animal tissue is needed, avoiding ethical or religious objections [1]. [2] Examiner insight: Name the enzymes and say what each does; “the gene is put into the bacteria” gives the aim, not the technique.

12. (a) The sensor detects blood glucose, like a receptor [1]. A control unit compares the reading with a target and signals the pump, like a coordinator [1]. The pump gives insulin when glucose is high and reduces or stops it when glucose falls, so the change is reversed (the effector) [1]. [3] (b) Benefits: it could restore the body’s own regulation, giving a possible cure without lifelong injections [1]. Limitations: transplanted cells may be rejected, so immunosuppressant drugs are needed [1]. The autoimmune attack could destroy the new beta cells [1]. Embryonic stem cells raise ethical objections and uncontrolled division could cause tumours [1]. Evidence is limited and it is not yet routine, so injections remain the established treatment: a balanced conclusion [1]. [5] Examiner insight: Give points for and against, then a judgement. A list of only advantages, or only problems, is incomplete.

Where marks are usually lost

• Saying the pancreas converts glucose to glycogen. The liver and muscle do this.
• Mixing up glycogenesis, glycogenolysis and gluconeogenesis.
• Reversing or skipping steps in the beta cell sequence.
• Not finishing the negative feedback loop.
• Quoting a rate without comparing end and start values.
• Writing one-sided answers to “evaluate” questions.

Next steps

• Recap with the revision notes or reread the study guide.
• See the OCR A Level Biology hub and the checklist.
• Try all free 10-minute diagnostics.
• Book a free trial class.

Official syllabus

OCR Level 3 Advanced GCE in Biology A (H420), Version 4.1 (April 2026), for first assessment in 2025, published by OCR. These questions cover 5.1.4(a) to 5.1.4(f).