HSC Exam Practice

Sample response. A non-infectious disease is a disease that cannot be transmitted from one individual to another via a pathogen. The defining distinguishing feature is transmissibility: non-infectious diseases do not involve a pathogen spreading between hosts, unlike infectious diseases which are caused by bacteria, viruses, fungi, or parasites that can be transmitted.

Marking notes. 1 mark for defining non-infectious disease as a disease that cannot be transmitted via a pathogen between individuals. 1 mark for identifying transmissibility via a pathogen as the single defining distinction. Do not award full marks if the student states the definition is about genetics rather than transmissibility.

Sample response. Genetic (e.g. cystic fibrosis — caused by CFTR gene mutation); Environmental (e.g. mesothelioma — caused by asbestos inhalation at Wittenoom, WA); Nutritional (e.g. scurvy — caused by vitamin C deficiency); Cancer (e.g. melanoma — uncontrolled division of melanocytes, triggered by UV radiation).

Marking notes. 1 mark per correctly named category paired with an appropriate named example. A category named without a matching example, or an example that does not clearly match the category, scores 0 for that row.

Sample response. Cancer is treated as a separate NESA category because its defining biological mechanism — uncontrolled cell division due to disruption of cell cycle regulation — is distinct from the mechanisms of the other three categories and cuts across them. A cancer can be triggered by a genetic mutation (BRCA1/2 in breast cancer), an environmental exposure (UV in melanoma; asbestos in mesothelioma), an infectious agent (HPV in cervical cancer), or a nutritional factor, but in every case the outcome is uncontrolled proliferation of cells. The common mechanism (cell cycle dysregulation) is what unites cancers into a single category, regardless of their trigger.

Marking notes. 1 mark for identifying the defining mechanism of cancer (uncontrolled cell division / disruption of cell cycle regulation). 1 mark for explaining that cancer can be triggered by factors from any of the other three categories yet remains distinct because of its mechanism. 1 mark for a clear explanatory link (e.g. HPV triggers cervical cancer, which is a cancer because the outcome is uncontrolled cell division, not because HPV causes an infectious disease).

Sample response. A risk factor is any characteristic, behaviour, or exposure that increases the statistical probability of developing a disease without making its development inevitable or guaranteed. A direct cause is a factor that is both necessary and sufficient to produce the disease in all exposed individuals. For example, smoking is a major risk factor for lung cancer — it dramatically increases the probability of lung cancer in the population (approximately 85% of lung cancers are attributable to smoking), but not all smokers develop lung cancer, and some non-smokers develop it from other causes (e.g. radon exposure, genetic susceptibility). Smoking therefore increases probability without being a guaranteed cause.

Marking notes. 1 mark for defining risk factor as a factor that increases the probability (statistical likelihood) of disease without making it inevitable. 1 mark for distinguishing this from a direct cause (required and sufficient in all individuals). 1 mark for a named example illustrating that a risk factor increases population-level probability but does not guarantee individual outcome.

Sample response. A multifactorial disease is one caused by the interaction of multiple risk factors from different categories — genetic, environmental, nutritional, and/or behavioural — rather than by a single cause. Type 2 diabetes illustrates this: genetic predisposition (family history, ethnicity — genetic risk factor) interacts with nutritional factors (excess refined carbohydrate and saturated fat intake leading to obesity) and environmental/behavioural factors (physical inactivity, sedentary work) to produce insulin resistance and eventually overt diabetes. No single factor is sufficient on its own in most cases.

Marking notes. 1 mark for correctly defining multifactorial disease (interaction of multiple risk factor types, not a single cause). 1 mark for naming a valid example (Type 2 diabetes, cardiovascular disease, or melanoma accepted). 1 mark for naming at least two interacting risk factor types from the example (e.g. genetic + nutritional, or genetic + environmental).

Sample response. AIHW 2022 data show that the top five causes of death in Australia are all non-infectious: coronary heart disease (~9.7% of all deaths), dementia including Alzheimer’s (~8.4%), cerebrovascular disease (~5.2%), lung cancer (~4.8%), and COPD (~3.6%). This dominance reflects the epidemiological transition: the historical shift from infectious to non-infectious disease as the leading cause of mortality. Factor 1 — infectious disease control: the introduction of antibiotics in the 1940s, vaccination programs (e.g. BCG for tuberculosis), improved sanitation, and better nutrition dramatically reduced premature deaths from pneumonia, tuberculosis, and childhood diarrhoeal diseases. Factor 2 — population ageing: as life expectancy rose from approximately 55 years in 1900 to approximately 83 years today, more Australians survive long enough to develop non-infectious diseases that take decades to progress (e.g. atherosclerosis, neurodegeneration, cumulative UV-induced DNA damage). Non-infectious diseases did not become more dangerous; infectious diseases became far better controlled, revealing NID as the dominant remaining killers in an ageing population.

Marking notes. 1 mark for citing AIHW data correctly (at least one named top-five cause with approximate proportion). 1 mark for naming and correctly defining the epidemiological transition as the shift from infectious to non-infectious disease as the dominant cause of mortality. 1 mark each for two factors that contributed to the shift (infectious disease control via antibiotics/vaccines/sanitation; population ageing as people survive past the age of NID onset; lifestyle changes; better diagnosis). Maximum 2 marks for factors, 4 marks total.

Sample response (a). There is a positive relationship between UV Index and melanoma incidence across the four states: as average midday UV Index increases from Tasmania (UVI 7.4) through Victoria (9.8), New South Wales (11.2) to Queensland (12.8), the melanoma incidence rate also increases from 28 to 37, 42, and 53 per 100,000 respectively. The two variables track closely across all four locations, suggesting a strong positive association.

Marking notes (a). 1 mark for correctly describing the positive relationship (as UVI increases, melanoma incidence increases). 1 mark for supporting this with data from at least two states (e.g. quoting figures for Queensland and Tasmania as the extremes).

Sample response (b). Melanoma is classified as cancer (primary category) with a primary environmental cause (UV radiation). The biological mechanism: ultraviolet B (UVB) radiation from sunlight penetrates skin and is absorbed by melanocyte DNA. UVB photons cause covalent bonds to form between adjacent thymine bases (thymine dimers), which distort the DNA helix. If these lesions are not repaired before cell division, they introduce mutations. Specific mutations in tumour suppressor genes such as CDKN2A (encoding p16, which inhibits cyclin-dependent kinases and prevents the cell cycle from progressing) and in proto-oncogenes such as BRAF (whose product drives cell division when constitutively activated) disrupt cell cycle control. Melanocytes with accumulated mutations lose normal cell cycle regulation and divide uncontrollably, forming a melanoma.

Marking notes (b). 1 mark for correct classification as cancer (environmental primary trigger). 1 mark for identifying the specific DNA lesion caused by UV (thymine dimers / pyrimidine dimers). 1 mark for linking this to mutation in a named tumour suppressor or proto-oncogene (e.g. CDKN2A/p16, BRAF, TP53). 1 mark for a clear causal link from mutation → cell cycle disruption → uncontrolled cell division.

Sample response (c). The student’s claim overstates the evidence. While the data show a strong positive association between UV Index and melanoma incidence, correlation is not causation. The data are consistent with UV radiation being a major risk factor for melanoma, but they do not prove it is the sole or direct cause for every melanoma in Queensland. UV radiation is classified as a risk factor rather than a guaranteed cause because: (1) not every person with high UV exposure develops melanoma; (2) some people with low UV exposure do develop melanoma (e.g. from inherited CDKN2A mutations, or on UV-unexposed skin sites); (3) melanoma is multifactorial — UV exposure interacts with genetic factors (fair skin, Fitzpatrick type I–II skin, CDKN2A germline mutations) and behavioural factors (failure to use sun protection) to produce disease. The higher melanoma rate in Queensland is consistent with UV being the dominant environmental driver, but it does not prove UV is a sufficient cause in all cases. A more accurate statement would be: UV radiation is the primary modifiable risk factor for melanoma, significantly elevating population-level probability, but the interaction of UV exposure with individual genetic susceptibility and sun-protective behaviour determines actual disease development.

Marking notes (c). 1 mark for correctly stating that correlation does not establish causation from graph data alone. 1 mark for distinguishing risk factor (increases probability, not guaranteed) from direct cause (sufficient in all exposed individuals). 1 mark for identifying melanoma as multifactorial and naming at least one non-UV factor (genetic predisposition, fair skin, failure to use sun protection). Accept any 3 of these elements at 1 mark each.

Sample response. The claim that non-infectious disease dominates Australian mortality because people are making worse health choices than previous generations is largely incorrect: it misreads the epidemiological transition and ignores the multifactorial nature of non-infectious disease. AIHW 2022 data confirm that the top five causes of death in Australia are all non-infectious diseases — coronary heart disease, dementia, cerebrovascular disease, lung cancer, and COPD — accounting for roughly 31% of all deaths combined. However, this dominance does not indicate a collapse in health behaviour compared to 1950 or 1900. The epidemiological transition describes the historical shift from infectious to non-infectious disease as the leading cause of mortality, a shift that occurred primarily because public health advances eliminated infectious disease as a major premature killer. Vaccines (e.g. BCG for tuberculosis, the childhood immunisation schedule), the introduction of antibiotics in the 1940s, improved sanitation and clean water, and better nutrition dramatically reduced deaths from pneumonia, tuberculosis, diarrhoeal disease, and childhood infections throughout the 20th century. Australians in 1900 did not live healthier lives — they died in much larger numbers from infectious diseases before reaching the age at which non-infectious diseases typically manifest. The dominance of NID in mortality statistics is therefore partly a measure of public health success: it reflects that Australians now survive long enough for slowly-developing non-infectious diseases to become the leading cause of death. Population ageing (average life expectancy ~83 years today vs ~55 in 1900) means that more of the population now lives into the age range where non-infectious diseases manifest. Furthermore, the claim overstates the role of personal choice because most non-infectious diseases are multifactorial. Cystic fibrosis and Huntington’s disease are caused by inherited gene mutations with no lifestyle component whatsoever. Even Type 2 diabetes and cardiovascular disease — diseases with genuine lifestyle risk factors — have strong non-modifiable components: genetic predisposition, ethnicity, and age cannot be changed through personal choice. The socioeconomic determinants of health (access to healthy food, safe exercise environments, preventive healthcare) further limit the degree to which individual choice explains NID prevalence. There is, however, one element of truth in the claim: lifestyle factors including excess dietary sugar and saturated fat, physical inactivity, and smoking are genuine modifiable risk factors for Type 2 diabetes, cardiovascular disease, and lung cancer, and their modification could reduce NID burden. But to say NID dominates mortality because of poor personal choices misrepresents the epidemiological transition, ignores purely genetic non-infectious diseases, ignores socioeconomic determinants, and overlooks the fundamental success of Australian infectious disease control as the primary explanation for NID’s current dominance.

Marking notes. 1 mark — Refers to AIHW data correctly (names at least two of the top-five causes of death and states they are non-infectious). 1 mark — Correctly defines or applies the epidemiological transition (shift from infectious to NID as dominant cause of mortality, driven by infectious disease control). 1 mark — Explains at least one specific mechanism that reduced infectious disease mortality (vaccines, antibiotics, sanitation, improved nutrition) and links this to why NID now dominates. 1 mark — Identifies population ageing as a factor (longer life expectancy means more people reach the age of NID onset). 1 mark — Applies the concept of multifactorial disease and identifies that non-modifiable risk factors (genetics, ethnicity, age) mean personal choice cannot fully explain or prevent NID. 1 mark — Gives a specific example of a purely genetic or predominantly non-lifestyle non-infectious disease (e.g. cystic fibrosis, Huntington’s disease, Type 1 diabetes) to show that the personal-choice claim does not apply universally. 1 mark — Reaches an explicit, balanced evaluative judgement that acknowledges the partial truth (lifestyle factors are genuine risk factors) while correctly refuting the main claim (dominance of NID reflects epidemiological transition success, not worse personal choices), using precise lesson terminology.