Low socioeconomic status, childhood maltreatment, and parental history of mental disorders are all classified as what type of risk factor for anxiety disorders?

A: Specific risk factors that uniquely predict anxiety disorders

B: Non-specific risk factors that increase risk for many mental disorders

C: Protective factors that buffer against anxiety under certain conditions

D: Precipitating factors that trigger individual episodes rather than long-term vulnerability

Childhood maltreatment, physical punishment, parental history of mental disorders, and low socioeconomic status are all non-specific risk factors — they increase vulnerability to a wide range of mental disorders, not exclusively anxiety. This non-specificity is an important clinical consideration: it means these risk factors cannot distinguish which disorder a person may develop, only that their overall mental health risk is elevated.

Childhood maltreatment is a specific risk factor for anxiety disorders — it elevates risk for anxiety but not for other mental health conditions.

Svar: Falskt

Childhood maltreatment is a non-specific risk factor. It is associated with elevated risk across a broad range of mental disorders, including depression, PTSD, psychosis, and substance use disorders, as well as anxiety disorders. The non-specificity means it reflects a general vulnerability to psychopathology rather than a pathway uniquely leading to anxiety.

Which parenting style or styles are associated with increased risk of anxiety disorders in children?

A: Overprotective parenting only

B: Overly harsh parenting only

C: Both overprotective and overly harsh parenting styles

D: Permissive parenting (warm but low in structure)

Both overprotective parenting (which may prevent children from learning that threats are manageable and developing tolerance for uncertainty) and overly harsh parenting (which may generate a general threat-biased environment) are associated with increased anxiety risk. These represent quite different interpersonal environments but appear to converge on a similar outcome — elevated anxiety vulnerability — which is consistent with the non-specific nature of these risk factors.

Behavioural inhibition — such as clinging to a familiar person in the presence of strangers — more specifically predicts which anxiety disorder?

A: Generalised Anxiety Disorder

B: Social Anxiety Disorder

C: Panic Disorder

D: Specific Phobia

Behavioural inhibition (BI) — a temperamental style in young children characterised by withdrawal, wariness, and clinging in novel or social situations — is one of the more specific risk factors in the anxiety literature. It is particularly predictive of Social Anxiety Disorder. Unlike the non-specific risk factors (e.g., maltreatment, low SES), BI points more directly toward social-evaluative anxiety, likely because it reflects an underlying sensitivity to social threat and novel stimulation.

Behavioural inhibition is a non-specific risk factor — it equally predicts all anxiety disorders rather than any particular one.

Svar: Falskt

Unlike many environmental risk factors, behavioural inhibition (BI) is more specifically predictive of Social Anxiety Disorder than of other anxiety disorders. This specificity is consistent with the view that BI reflects a temperamental sensitivity to social evaluation, which maps onto the core fear in social anxiety. Children high in BI who later develop anxiety are disproportionately likely to develop social anxiety rather than, say, GAD or panic disorder.

Regarding the higher prevalence of anxiety disorders in women compared to men, which statement is most accurate?

A: Women have higher rates due to well-established hormonal mechanisms that have been fully explained

B: Women are at higher risk, but the reasons for this remain unclear

C: The higher rates in women are entirely explained by sociocultural factors and reporting bias

D: Women only have higher rates for specific phobia; other anxiety disorders show equal prevalence across sexes

While women are consistently found to have approximately twice the prevalence of anxiety disorders compared to men, the reasons for this remain unclear and are likely multifactorial. Hormonal influences, differences in threat appraisal, greater propensity to internalise distress, and sociocultural factors have all been proposed, but no single explanation has been conclusively established.

Genetic epidemiological studies show that anxiety disorders aggregate in families — individuals with an affected first-degree relative are at elevated risk.

Svar: Sant

Anxiety disorders show clear familial aggregation: having a first-degree relative with an anxiety disorder increases an individual's own risk. This familial clustering is consistent across diverse anxiety disorders and has been demonstrated in family studies, twin studies, and adoption studies. It reflects the combined contribution of shared genetic variants and shared environmental experiences within families.

Heritability estimates from genetic epidemiological studies suggest that anxiety disorders are how heritable?

A: Around 10–20% — primarily environmentally determined

B: Around 30–50%

C: Around 60–70%

D: Over 80% — primarily genetically determined

Heritability estimates for anxiety disorders are typically in the range of 30–50%. This means that roughly a third to half of the variance in liability to anxiety disorders is attributable to genetic factors. The remaining variance reflects environmental influences — both shared (e.g., family environment, socioeconomic factors) and non-shared (e.g., individual life events). This places anxiety disorders in a similar heritability range to depression, and lower than conditions like bipolar disorder or schizophrenia.

Which statement best describes the current state of knowledge about the pathophysiology of anxiety disorders?

A: Well-characterised, with clear biomarkers that can be used for diagnosis

B: Poorly understood, with suggestions of overgeneralisation of conditioned fear and deficits in fear extinction

C: Primarily explained by serotonin deficiency, consistent across all anxiety disorders

D: Fully explained by amygdala hyperactivity, with other regions playing no significant role

The pathophysiology of anxiety disorders is poorly understood. The most prominent theoretical accounts centre on two related processes: overgeneralisation of conditioned fear (fear responses extending beyond their original conditioned stimulus to similar or neutral stimuli) and deficits in the extinction of conditioned fear (failure to inhibit fear responses when the threat is no longer present). These are theoretical frameworks with supporting evidence, not fully validated pathophysiological mechanisms.

In the context of anxiety disorder pathophysiology, "overgeneralisation of conditioned fear" refers to:

A: Fear responses that fail to transfer from the original stimulus to related stimuli

B: Fear responses extending beyond the original conditioned stimulus to similar or neutral stimuli

C: Fear responses that are extinguished too rapidly, leading to rebound anxiety

D: Genetically encoded fear that does not require conditioning to be expressed

Overgeneralisation of conditioned fear describes a process in which fear that was originally learned in response to a specific stimulus spreads to stimuli that are similar to, or associated with, the original threat. For example, someone who develops fear of a specific dog may generalise that fear to all dogs, or even to all animals. In anxiety disorders, this generalisation is thought to occur too broadly, generating fear of stimuli that pose little or no genuine threat.

Which proposed pathophysiological process in anxiety disorders involves a failure to inhibit fear responses when a threat is no longer present?

A: Excessive fear conditioning

B: Deficit in fear extinction

C: Sympathetic nervous system hypoactivity

D: Amygdala habituation

Deficits in fear extinction refer to impaired ability to inhibit or suppress conditioned fear responses when the conditioned stimulus is no longer paired with the unconditioned stimulus (the threat). Extinction learning is thought to create a new inhibitory memory that competes with the original fear memory, rather than erasing it. In anxiety disorders, this new inhibitory learning may be weaker or less stable, allowing the fear response to persist or return after apparent remission — a phenomenon known as fear return.

Functional MRI studies of anxiety disorders tend to show which pattern of neural activity in limbic regions?

A: Underactivity in limbic regions including the amygdala

B: Overactivity in limbic regions including the amygdala and insula

C: Overactivity in the prefrontal cortex and reduced amygdala response

D: No consistent differences in limbic activity compared to healthy controls

Functional MRI studies in anxiety disorders consistently point toward overactivity in limbic regions — particularly the amygdala and insula — in response to threat-related stimuli. The amygdala is a key structure in fear detection and the initiation of threat responses; elevated amygdala reactivity in anxiety disorders is consistent with the theoretical accounts of overgeneralised conditioned fear. The insula is involved in interoception and the awareness of bodily states, and its overactivity may contribute to the somatic symptoms of anxiety.

Which two brain regions are most commonly highlighted in fMRI findings on anxiety disorders?

A: Hippocampus and cerebellum

B: Prefrontal cortex and caudate nucleus

C: Amygdala and insula

D: Thalamus and basal ganglia

The amygdala and insula are the two limbic/paralimbic regions most consistently implicated in neuroimaging studies of anxiety disorders. Amygdala overactivity relates to threat detection and the conditioned fear response. Insula overactivity relates to interoceptive processing — the sensing of internal bodily states — and may underlie the intense physical sensations that accompany anxiety and panic. These regions are part of a broader fear circuit that also includes the prefrontal cortex (which normally provides top-down regulation of amygdala activity).

A child whose parent has a history of Major Depressive Disorder (not an anxiety disorder) is:

A: At no elevated risk for anxiety disorders — the risk is specific to the parent's diagnosis

B: At elevated risk for anxiety disorders, because parental mental disorder history is a non-specific risk factor

C: At elevated risk for depression only, not for anxiety

D: Only at risk if the parent was also diagnosed with an anxiety disorder

Parental history of mental disorders is a non-specific risk factor — it increases risk across a broad range of mental health conditions in offspring, not only the specific diagnosis the parent carries. A child with a depressed parent is at elevated risk for depression, anxiety disorders, and other conditions. This non-specificity reflects shared genetic vulnerability and shared environmental factors (e.g., disrupted parenting, family stress) that broadly increase psychological risk rather than selectively predicting one disorder.