Acute Stress & PTSD Flashcards

1
Q

Why is the study of Trauma and Stressor-Related Disorders (TSRs) significant?

A

TSRs have a long history, with extensive research and discussion. They provide an opportunity to study key controversies and their impact on psychopathology.

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2
Q

Why are TSRs placed adjacent to anxiety disorders in the DSM?

A

TSRs are grouped near anxiety disorders in the DSM because of their conceptual relationship, with overlapping symptoms and associations with dissociative conditions.

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3
Q

What is a working definition of stress?

A

Stress is the psychological condition experienced when our coping resources are insufficient to respond to an actual or perceived physical or emotional challenge.

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3
Q

In a study on life stressors in college students, they rated external events into either a high or low stress category.

An example of high stress is sexual assault, with low being falling asleep in class.

What are some of the differences between high and low stress events and what main factor would we look at to understand if these events become psychopathology?

A

The difference is the idea of universality. High-stress and low-stress events are generally considered as such due to their content and effect on a person.

However, low-stress events can become high-stress when they occur consistently and may become psychopathology depending on someones coping mechanisms and abilities to manage stress.

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3
Q

What are the health effects of high stress?

A

High stress increases susceptibility to illnesses like respiratory infections, may cause immunosuppression, increase the risk of coronary heart disease, and is linked to premature aging (shortened telomeres).

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4
Q

What factors or properties that influence the stress response to high or low stress events in college students? theses are properties that we need to consider when understanding them in relation to developing psychopathology.

A

Factors like duration, impact, predictability, and controllability of events affect how students perceive and cope with stress.

This leads to different coping strategies for similar events and depending on these strategies will determine whether someone develops psychopathology.

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4
Q

What factors influence whether an event is considered a stressor?

A

Factors include the event’s severity, chronicity, timing, personal meaning, impact, predictability, and controllability, which determine the stress response even if the event isn’t universally recognized as stressful.

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5
Q

What strategies are used to manage stress and its effects?

A

Strategies include physical health management, emotion regulation techniques (e.g., CBT, relaxation), and addressing social factors like inequities and isolation. These approaches may work for some individuals, depending on the nature of the stressor.

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5
Q

What is the role of Acute Stress Disorder (ASD) in the DSM, and why is it controversial?

A

ASD, added in 1994, is considered a potential precursor to PTSD, sparking debate over its role in early intervention and prevention. Controversy arises over its association with later PTSD development.

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6
Q

How were the diagnostic criteria for PTSD modified in the DSM-5?

A

Despite the DSM-5 revision process being described as “conservative,” significant changes were made to the diagnostic criteria for PTSD, expanding and refining how trauma responses are identified.

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7
Q

What are the main criticisms of Prolonged Grief Disorder (PGD) in the DSM-5?

A

Critics argue that PGD pathologizes normal grief, sets too low a diagnostic threshold, imposes an “expiration date” on grief, and fails to consider key contextual factors like relationships, the nature of the death, and cultural differences.

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7
Q

What do Cacciatore and Francis (2002) suggest instead of diagnosing Prolonged Grief Disorder?

A

Cacciatore and Francis argue that grief should not be medicalized, recommending social support and compassion rather than diagnosis. If a diagnosis is necessary, they suggest adjustment disorder instead of PGD.

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8
Q

Why was Prolonged Grief Disorder included in the trauma-related disorders section of the DSM-5-TR?

A

PGD is included in the trauma section due to the effectiveness of trauma-informed therapies over traditional treatments like antidepressants, though the clinical utility is still under investigation.

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8
Q

What distinguishes Prolonged Grief Disorder (PGD) from non-clinical grief?

A

PGD is differentiated by the severity, intensity, and duration of grief features, with DSM-5-TR setting a 12-month duration compared to the ICD’s 6-month guideline.

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9
Q

How did the understanding of PTSD evolve historically?

A

PTSD initially emerged as a military concern (“shell shock” and “combat neurosis”) but broadened after the Vietnam War to include civilians exposed to non-combat trauma, shifting the scope of psychopathology.

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9
Q

What is Adjustment Disorder, and how does it differ from ASD or PTSD?

A

Adjustment Disorder involves severe, but not traumatic, stressors (e.g., divorce) that overwhelm coping resources, leading to significant emotional symptoms. It is less severe than ASD or PTSD and typically resolves once the stressor is removed.

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9
Q

What are the key features of Adjustment Disorder with depressed mood?

A

This subtype involves feelings of sadness, tearfulness, hopelessness, and a lack of pleasure in activities. Symptoms typically appear within 3 months of a stressor and may abate with time or once the stressor is resolved.

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10
Q

Did the DSM-5 changes reduce the prevalence of PTSD diagnoses?

A

Yes, a study comparing DSM-IV and DSM-5 criteria found a significant reduction in PTSD prevalence in some estimates. The new criteria successfully raised the diagnostic threshold without lowering it.

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10
Q

What is the key difference between Acute Stress Disorder (ASD) and Posttraumatic Stress Disorder (PTSD)?

A

ASD and PTSD are conceptually the same but differ in duration. ASD is diagnosed when symptoms last for a shorter period, while PTSD is diagnosed for prolonged symptoms. Both arise from exposure to traumatic events.

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11
Q

How does the DSM-5 define traumatic stress?

A

Traumatic stress involves exposure to actual or threatened death, serious injury, or sexual violence. It includes direct experience, witnessing trauma, learning about trauma to loved ones, or repeated exposure to trauma details.

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11
Q

What significant changes were made to the definition of traumatic stress in DSM-5?

A

The DSM-5 expanded Criterion A to itemize ways of trauma exposure, including sexual violence, to clarify the definition and raise the diagnostic threshold, helping prevent the overdiagnosis of PTSD.

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12
Q

What are the defining symptoms of both Acute and Posttraumatic Stress Disorders?

A

The symptoms include intrusive re-experiencing, avoidance of reminders, increased arousal or reactivity, negative mood or thoughts, and dissociative symptoms.

13
Q

What is the key difference between Acute Stress Disorder (ASD) and PTSD?

A

ASD is diagnosed when symptoms last from 3 days to 1 month after trauma, while PTSD involves symptoms lasting longer than 1 month. ASD conceptually precedes PTSD and shares similar symptoms like intrusion, avoidance, and negative mood, but it resolves within a shorter time frame.

13
Q

What are the dissociative features of PTSD and ASD?

A

Dissociation includes depersonalization (a loss of sense of self, detachment from one’s body or mind) and derealization (distortion or detachment from reality). In ASD, dissociative features are listed separately, while in PTSD, they are subsumed within other symptom clusters and can be added as specifiers.

13
Q

How does PTSD create a pathological memory?

A

In PTSD, experiencing a traumatic event may create a pathological memory that doesn’t diminish over time. It can intrude on cognitive functions and elicit extreme emotions related to the trauma, even when the danger is no longer present.

14
Q

What are the four prototypical trajectories in response to trauma?

A

The four trajectories include chronic, delayed, recovery, and resilience. People on a chronic trajectory maintain symptoms over time, while others may experience delayed onset, recovery after initial dysfunction, or resilience with minimal impact.

15
Q

Does ASD predict the development of PTSD?

A

Over 80% of people with ASD will develop PTSD within six months, but not everyone with ASD will. PTSD can also develop in the absence of ASD, though this is less common (4-13%). Responses to trauma are highly variable.

16
Q

What do the four prototypical trauma trajectories indicate about PTSD and ASD?

A

These empirically demonstrated trajectories reflect different responses to trauma. In PTSD or ASD, the chronic and delayed curves may represent those who experience prolonged or late-onset symptoms, while recovery and resilience may apply to those who recover or maintain health despite trauma.

16
Q

How does changing trauma exposure affect PTSD symptoms according to the QUT study?

A

The study found that shifting from indirect to direct trauma exposure resulted in worse PTSD symptom profiles, but malingering indicators remained largely unchanged.

17
Q

What are the challenges in diagnosing delayed-onset PTSD?

A

Delayed-onset PTSD is controversial as symptoms often rely on self-report or clinical identification rather than objective testing. Care must be taken to ensure the symptoms align with the trauma exposure, as the diagnosis is vulnerable to alternative explanations.

18
Q

What are the general statistics for trauma and PTSD prevalence?

A

More people experience trauma than do not. Worldwide, PTSD estimates range from 6-8%, with the lifetime risk being around 9% in the USA. Women (10%) are more likely than men (5%) to develop PTSD, and minorities are also at higher risk.

18
Q

Why is PTSD considered a highly heterogeneous disorder?

A

PTSD presents in a wide variety of symptom combinations, meaning it can look different from one person to another. This variability challenges diagnosis and treatment, as the particular combination of symptoms may influence the effectiveness of psychological interventions.

19
Q

What is malingering, and how is it relevant to PTSD diagnosis?

A

Malingering is the deliberate faking of illness or symptoms for a nonmedical benefit, often financial. It is a significant issue in PTSD diagnosis, as attorneys may coach clients or it may represent a cry for help. Simulation studies help isolate factors like trauma proximity to assess malingering.

20
Q

What are some individual-level risk and protective factors for PTSD?

A

Risk factors include being female, having low social support, or pre-existing mental health issues like anxiety or depression. Protective factors include higher cognitive ability, which may support post-trauma meaning-making.

20
Q

What are the two elements involved in PTSD risk?

A

PTSD risk involves two elements: (1) the risk of trauma exposure, which varies across individuals, and (2) the risk of a PTSD response, which is one of several possible responses to trauma.

20
Q

Why do the nature of traumatic events matter in PTSD development?

A

The likelihood of developing PTSD may be influenced by whether the trauma is interpersonal (e.g., rape, assault) or intrapersonal. Interpersonal traumas, where one person harms another, are more likely to lead to PTSD, especially in categories like sexual assault or violence.

21
Q

What are some key risk factors for developing ASD or PTSD?

A

Risk factors include the nature of the trauma (e.g., severity, frequency, direct exposure), lack of social support, post-trauma experiences like incarceration, personality traits (e.g., anxiety, neuroticism), and adverse developmental experiences.

22
Q

What biological and genetic factors contribute to PTSD risk?

A

Genetic factors, shown in twin and epigenetic studies, play a role, as do biological factors like stress hormone dysregulation and differences in brain structures (e.g., hippocampus). However, most human studies are correlational, and these findings are mixed.

23
Q

How is DNA methylation linked to PTSD in QUT research?

A

The study found an association between DNA methylation and PTSD, suggesting gene-environment interactions. Trauma-exposed paramedics showed distinct DNA methylation patterns compared to non-trauma exposed, indicating why a purely genetic model of PTSD is insufficient.

24
Q

What are the limitations and future directions of DNA methylation research in PTSD?

A

The study used a cohort approach and lacked a pre-post design, making it unclear if DNA methylation changes are caused by trauma or merely associated with it. The study was small, and for DNA methylation to serve as a PTSD biomarker, findings need to be specific to PTSD and replicated in larger studies.

25
Q

How might memory impairments explain PTSD symptoms like flashbacks?

A

In PTSD, memory processes might go awry, leading to the intrusion of traumatic memories (flashbacks). These memories may be overgeneralized or impaired, disrupting the ability to differentiate between past trauma and present safety.

26
Q

What were the results related to hippocampal volume in the PTSD study?

A

Brain scans showed that participants with PTSD had smaller hippocampal volumes. This finding supports the idea that memory processes, particularly those involving the hippocampus, are impaired in PTSD, although these results are from a cohort study and not generalizable to all PTSD cases.

26
Q

What are the limitations of hippocampal volume research in PTSD?

A

The research is complex and involves heterogeneous populations. While smaller hippocampal volumes have been associated with PTSD, these findings are not generalizable, and the effect size in many studies is significant but not large, indicating caution in interpretation.

26
Q

What role does learning play in PTSD memory processes?

A

Research suggests a learning pathway where individuals form associations between cues and outcomes. In PTSD, these learned associations may involve overgeneralizing negative contexts to new situations, which contributes to the persistence of traumatic memories.

26
Q

What is a key challenge in interpreting PTSD research with medication involved?

A

One challenge in PTSD research is ensuring that differences between participants are due to PTSD itself rather than medication. In studies where participants are medicated, it becomes difficult to determine whether the findings are influenced by medication or PTSD.

27
Q

What are common comorbidities and the course of PTSD?

A

PTSD is often comorbid with depression, anxiety, and substance use disorders. Anger is prominent, with an increased risk of suicide. ASD increases the likelihood of PTSD if symptoms like numbing, depersonalization, and re-living are present. There is also a risk of intergenerational trauma. Symptoms typically improve over time, with two-thirds of people showing the greatest recovery within the first 12 months. Treatment can hasten recovery and may prevent PTSD when offered for ASD.

28
Q

What is intergenerational trauma, and how does it relate to PTSD?

A

Intergenerational trauma refers to the transmission of trauma effects from parents to offspring, where children may grapple with their parents’ post-traumatic state. This can occur through epigenetic changes, pre- and post-natal exposure to trauma, and impaired parenting due to the parents’ unwell state, leading to maladaptive behaviors like substance abuse or physical abuse.

29
Q

What are some prevention strategies for reducing trauma exposure and PTSD risk?

A

Prevention strategies include social-level approaches like gun reform, climate action, and domestic violence reforms to reduce trauma exposure. For high-risk groups, strategies such as stress inoculation training and psychoeducation prepare individuals to manage trauma through cognitive techniques, relaxation, and awareness of support systems. Coverage is a key consideration, as traumatic events are often unpredictable.

30
Q

What are the unresolved mechanisms of intergenerational trauma transmission?

A

The mechanisms are not fully resolved but include epigenetic explanations, transmission of risk for psychopathology through modeling, or due to family and developmental factors like social disadvantage, poverty, or discrimination. These risks may be higher in certain groups, such as trauma-affected refugees or Indigenous communities like the stolen generation in Australia.

31
Q

What are immediate and later treatments for PTSD?

A

Immediate treatments include providing 24/7 support and crisis hotlines, as well as managing additional stressors. Later treatments may involve group programs to reduce isolation, monitoring for comorbidities like substance use and violence, and the use of medications (antidepressants and antipsychotics) based on symptom needs, though evidence for medication effectiveness is limited.

32
Q

What psychotherapy options are available for PTSD, and what are their focuses?

A

Psychotherapy options include psychological debriefing (CISD), which is controversial due to risks of harm if applied too early. Cognitive Behavioral Therapy (CBT) focuses on de-conditioning anxiety and blame, exposure therapy helps confront traumatic memories, and interpersonal psychotherapy enhances self-concept, emotional processing, and the personal meaning of trauma.

33
Q

What are the three psychological therapies with strong support for treating PTSD?

A

The three supported therapies are prolonged exposure (using both high-tech like VR and low-tech like imaginal techniques), cognitive processing or cognitive therapy, and trauma-focused CBT. These therapies focus on emotion processing by revisiting the traumatic event in a supportive environment and changing the cognitive appraisal (meaning) attributed to the event and response.

34
Q

What are the risks and benefits of Critical Incident Stress Management (CISM)?

A

CISM is traditionally offered immediately after trauma exposure, but it carries risks like iatrogenesis—where therapy may set an expectation for PTSD, potentially re-traumatizing individuals through re-telling or group settings. The effectiveness of early intervention in preventing PTSD is mixed, so careful application is required. Iatrogenesis refers to unintentional injury from medical treatment.