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BMS3031 - Molecular mechanisms of disease - S1 2026

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Placental development depends on adequate maternal blood

flow to sustain oxygen and nutrient delivery to the fetus. When placental

perfusion is impaired, local hypoxia can result and initiate cellular stress

responses, increasing oxidative stress.

Which mechanism best explains the contribution

of placental hypoxia to fetal growth restriction?

Reduced

maternal oxygen levels explains placental hypoxia without any role for

placental blood flow or signalling mechanisms

❌

Hypoxia

acts solely by producing ROS, which directly inhibit fetal cell division

without placental mediation

❌

Excess

ROS arise independently and subsequently reduce placental oxygen delivery

❌

Impaired

placental perfusion causes hypoxia that activates stress signalling pathways

and increases ROS production

✅

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During fetal development, circulating biomarkers can be

measured in maternal or fetal blood to provide information about ongoing

physiological and pathological processes.

A researcher collects multiple fetal biomarkers

throughout gestation. Which pattern of observations would best support the

utility of biomarkers for predicting disease risk?

Specific

biomarkers are consistently associated with higher probability of disease in

some fetuses, but not all, indicating risk

Biomarker

detection allows for effective treatment of the fetus prior to birth

❌

Absence

of a biomarker means that the corresponding disease will definitely not develop

in the fetus

The

presence of a biomarker confirms that a disease is present in all fetuses

expressing it, allowing definitive diagnosis

❌

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Fetal growth restriction (FGR) is often associated with

impaired placental function. Hypoxia within the placenta can trigger molecular

responses that influence fetal development, but the relationship between oxygen

availability, reactive oxygen species (ROS), and growth restriction is complex.

Which mechanistic scenario would best explain

how placental hypoxia contributes to fetal growth restriction?

Hypoxia

directly generates ROS, which independently cause fetal growth restriction

without involvement of other placental factors

❌

Maternal

systemic hypoxia alone causes placental hypoxia and fetal growth restriction,

without involvement of placental blood flow or local signalling

❌

Excess

ROS production causes hypoxia in the placenta, which then triggers fetal growth

restriction

❌

Reduced

placental blood flow leads to hypoxia, which triggers secretion of factors that

limit fetal growth, while also increasing ROS that exacerbate placental

dysfunction

✅

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Advances in prenatal medicine have made it possible to

measure a wide range of biochemical markers in maternal circulation that

reflect fetal physiology. These biomarkers are often evaluated for their

potential to identify fetuses at increased risk of developing disease.

Which observation would most strongly support

the use of fetal biomarkers as predictors of disease risk?

Absence

of a biomarker ensures that the fetus will never develop the associated disease

❌

Certain

biomarker profiles are associated with an increased likelihood of disease

outcomes in a subset of fetuses, without perfectly predicting disease in all

cases

✅

Measurement

of biomarkers directly enables prevention of disease through immediate

intrauterine therapy

❌

Detection

of a biomarker guarantees that a specific disease is already present in the

fetus

❌

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Nephron number varies between individuals and can be

influenced by developmental and environmental factors. Factors such as maternal

nutrition, gestational age at birth, and other environmental influences affect

nephron endowment. Epidemiological studies have found that individuals with

fewer nephrons are more likely to develop certain health conditions later in

life.

Which observation would provide the strongest

evidence supporting the Brenner Hypothesis?

Individuals

with low nephron number show higher rates of hypertension in adulthood

✅

Prematurely

born infants are more likely to develop diabetes later in life

❌

Poor

nutrition during gestation reduces nephron number at birth

❌

Low

nephron number is associated with reduced kidney size

❌

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According to the Brenner Hypothesis, reduced nephron

endowment increases functional demand on individual nephrons, leading to an

increased risk of chronic kidney disease. A researcher studies a cohort of

adults by directly measuring nephron number, single‑nephron

glomerular filtration rate (SNGFR), glomerular size, podocyte density, and

blood pressure.

Which pattern of findings would most strongly support the

Brenner Hypothesis?

Podocyte

density is reduced in low-nephron individuals without changes in filtration or

blood pressure

❌

Individuals

with fewer nephrons exhibit increased SNGFR per nephron, glomerular hypertrophy

with reduced podocyte density, higher rates of glomerulosclerosis, and elevated

blood pressure

✅

Increased

SNGFR occurs without changes in glomerular size, podocyte density, or blood

pressure

❌

Individuals

with fewer nephrons show proportionally reduced filtration without structural

changes and normal blood pressure

❌

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Epidemiological and experimental studies indicate that

environmental conditions before birth and during early postnatal life can

influence organ development and thereby long-term health. Different organs vary

in their susceptibility to early-life stressors. For example, the brain, heart,

and kidneys are often particularly affected, while some postnatal interventions

may partially mitigate deficits.

Which pattern of findings would provide the strongest

support for the Barker Hypothesis?

Adult

disease risk is primarily determined by genetics, with little influence from

prenatal or early postnatal environment

❌

Low

birth weight infants of both sexes show uniform adult disease outcomes, and

early postnatal nutrition fully restores organ function

❌

Individuals

exposed to maternal undernutrition during gestation exhibit reduced nephron

number, altered cardiovascular physiology, and increased adult disease risk,

with sex-specific differences in severity

✅

Accelerated

postnatal weight gain eliminates all developmental deficits caused by prenatal

stress, without sex differences

❌

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The Barker Hypothesis, also known as the Developmental

Origins of Health and Disease (DOHaD) framework, proposes that adverse

environmental conditions during critical periods of development permanently

alter organ structure, physiology, and metabolic regulation. These changes may

not be immediately apparent at birth but can predispose individuals to

cardiovascular, renal, and metabolic diseases later in life.

Which pattern of findings would provide the strongest

support for the Barker Hypothesis?

Adult

disease risk is determined almost entirely by genetic inheritance, independent

of early-life environment

❌

Rapid

postnatal catch-up growth eliminates long-term disease risk associated with

prenatal stress

❌

Prenatal

undernutrition leads to lasting alterations in kidney and cardiovascular

structure, increased adult disease risk, and sex-specific differences in

severity

✅

Low

birth weight leads to transient organ changes that are completely reversed by

improved postnatal nutrition

❌

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Individuals are born with a variable number of nephrons.

According to the Brenner Hypothesis, lower nephron endowment places greater

functional demands on individual nephrons, which may ultimately contribute to

hypertension and chronic kidney disease.

A researcher measures nephron number, single

nephron glomerular filtration rate (SNGFR), glomerular size, podocyte density,

and blood pressure in a population of adults. Which pattern of findings would

most strongly support the Brenner Hypothesis?

Individuals

with lower nephron number have higher SNGFR in remaining nephrons, glomerular

hypertrophy with reduced podocyte density, and are likely to develop glomerulosclerosis

and higher blood pressure

✅

Individuals

with lower nephron number have normal SNGFR, reduced podocyte density, but no

change in glomerulosclerosis or blood pressure

❌

Individuals

with lower nephron number have proportionately reduced SNGFR, preserved

podocyte density, no glomerulosclerosis, and normal blood pressure

❌

Individuals

with lower nephron number have higher SNGFR but maintain podocyte density and

show no increase in glomerulosclerosis or blood pressure

❌

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The Brenner Hypothesis proposes that individuals born with a

reduced number of nephrons compensate by increasing filtration in each

remaining nephron. Epidemiological data have been used to test predictions

derived from this hypothesis in human populations.

Which observation would provide the strongest

direct evidence supporting the Brenner Hypothesis?

Nephron

number gradually declines during the normal aging process

❌

Maternal

undernutrition during pregnancy decreases nephron formation

❌

Individuals

with reduced nephron number tend to have smaller kidneys at birth

❌

Adults

with low nephron number show a higher prevalence of hypertension

✅

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