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CMN 522 Module 2 Studygude for EXAM
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- CMN 552
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- University Of South Alabama
CMN 522 Module 2 Studygude
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CMN 552Module 2 Primary Study Guide
Sadock, Chapter 14
Section 14.1
DSM-5 Modifications in Anxiety Disorders
● The major subtypes of anxiety disorders in the DSM-5 include panic disorder (with or
without agoraphobia), agoraphobia (without a history of panic disorder), specific
phobia, social phobia, and generalized anxiety disorder (GAD). Revisions to the
classification of anxiety disorders in the DSM-5 involve removing obsessive-compulsive
disorder and posttraumatic disorder have been subsumed under newly created
“obsessive-compulsive and related disorders” and “trauma- and stressor-related
disorders” categories, respectively. Therefore, both obsessive–compulsive disorder and
posttraumatic stress disorder are not considered in this chapter. Other modifications to
the proposed DSM-5 anxiety disorders category include the addition of separation
anxiety disorder (contained under Disorders Usually First Diagnosed in Infancy,
Childhood, or Adolescence in the DSM-IV), the identification of agoraphobia as a distinct
and codable disorder (diagnosed only with reference to panic disorder in the DSM-IV),
minor revisions to criterion language to enhance clarity, objectivity, and consistency
across the anxiety disorders, and the relabeling of social phobia as social anxiety
disorder (SAD). As such, the term “social phobia” will now be replaced with “social
anxiety disorder.”
Section 14.2
Agoraphobia: Epidemiology
● Similar to Panic Disorder, more women than men have agoraphobia and the age of onset
peaks in the late teens to early twenties. Agoraphobia in the absence of Panic Disorder is
considered to be rarer than agoraphobia with comorbid Panic Disorder. However, there
is some variability in the prevalence data. The measured prevalence of agoraphobia in
specific clinical settings may evolve as the DSM-5’s recognition of agoraphobia without
Panic Disorder will spur clinicians to screen and consider the disorder more frequently,
even in patients who do not present with panic attacks. Other anxiety disorders are seen
alongside agoraphobia in comorbidity rates that often exceed 50 percent. Comorbid
depressive disorders are seen in 33 to 52 percent of cases, with some suggestion that
the presence of comorbid panic attacks increases the risk of comorbid depressive
episodes.
Social Anxiety Disorder: Differential Diagnosis, Etiology, Course, Treatment
● As mentioned above, Avoidant Personality Disorder (described in more detail elsewhere
in this book) has been the subject of debate over whether it is distinct from Social
Anxiety Disorder, with the DSM-5 separating the two. Social Anxiety Disorder has a high
comorbidity with other anxiety and affective disorders, as well. The use of illicit
anxiolytics and sedatives leads to the relatively high rate of comorbid substance use
disorders. The comorbidity between Social Anxiety Disorder and Selective Mutism is
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, discussed elsewhere in this chapter. Social Anxiety Disorder is a common comorbidity in
children with an Autism Spectrum diagnosis and also appears at rates above population
baseline in patients with Schizophrenia. Risk factors for Social Anxiety Disorder include
female gender, family history, and childhood signs of behavioral inhibition. There is
insufficient data on specific genetic factors mediating the increased familial risk, but
parenting styles may also contribute to this familiality. The Mini-Social Phobia Inventory
(Mini-SPIN) is an appropriate screening tool for adults. One could see how agoraphobia
could be confused with Social Anxiety Disorder or PTSD, though the context-dependent
fears in the same situation would be different. For example, a patient with Social Anxiety
Disorder might dislike a crowded party because they feel that everybody is looking at
them and judging them. A patient with agoraphobia might avoid the same crowded
party out of concern that, were they to develop anxiety, it would be difficult to sprint for
the exit. A patient with PTSD might find that their desire for hypervigilance is
overwhelmed by the multiple stimuli in a crowded room. There is a markedly increased
rate of suicide attempt amongst patients with Social Anxiety Disorder. This, along with
the significant functional impairment associated with this disorder, should motivate
clinicians to pursue aggressive treatment for these patients. CBT has demonstrated
efficacy for Social Anxiety Disorder. The first-line pharmacologic treatments are
serotonergic agents, but other, PRN medications, especially for the performance subtype
(beta blockers), have been used effectively. Social Anxiety Disorder is a chronic condition,
with a high rate of symptom re-emergence after symptom remission is achieved via
selective serotonin reuptake inhibitors (SSRIs), for example. However, durable remission,
even after cessation of CBT and/or antidepressants, has been seen in a small proportion
of patients.
Generalized Anxiety Disorder: Epidemiology
● GAD has a lifetime prevalence rate of 5%, often begins in the late teens, and is more
common in women as men. The high lifetime psychiatric comorbidity has led some to
view GAD as a prodromal or residual phase of a major depression, though there is
insufficient empirical support for this view. Other common comorbidities include other
anxiety spectrum disorders and substance use disorders.
Separation Anxiety Disorder: History/Comparative Nosology
● The epidemiologic evidence documenting a high rate of onset occurring after 18 years
old has led to a removal of the age-of-onset restriction in the DSM-5. The inclusion of
the adult-onset formulation has moved Separation Anxiety Disorder from DSM-IV’s
“Disorders Usually First Diagnosed in Infancy, Childhood or Adolescence” to DSM-5’s
“Anxiety Disorders.” As noted with Selective Mutism, the prominent symptom of worry
ties Separation Anxiety Disorder to the other, classical diagnoses in the Anxiety Disorders
section.
Section 14.3
2
,Medical Symptoms/Disorders
● Community samples have strongly confirmed the high magnitude of comorbidity of
anxiety disorders with several medical conditions that had been described in clinical
samples. There is a growing body of evidence for specific patterns of associations
between anxiety disorders and a range of medical disorders including respiratory
conditions, cardiovascular diseases, gastrointestinal disorders, metabolic diseases, and
musculoskeletal disorders. For example, in the Australian National Survey of Health and
Wellbeing, there was a two-fold greater rates of physical conditions among those with
anxiety disorders compared to those without anxiety. Similar to other mental disorders,
comorbid anxiety with physical disorders are associated with substantially greater
disability than anxiety disorders alone. Investigation of comorbidity of physical
disorders and anxiety is complicated by the role of physical symptoms as a core feature
of panic disorder and GAD. There is now evidence that anxiety disorders may represent
the initial manifestations of several physical conditions, and there are also numerous
physical conditions that lead to anxiety-like symptoms. In adults, anxiety disorders,
particularly GAD and panic, are associated with cardiovascular risk factors and diseases.
For example, analyses of data from electronic medical records and direct interviews
regarding medical and mental disorders in the large Philadelphia Neurodevelopmental
Cohort (PNC) revealed that asthma was the only medical condition specifically
associated with anxiety disorders in childhood and adolescence. This link has been
confirmed in a population-based birth cohort study in Australia that found that youth
with more severe and persistent asthma at age 5 years were more likely to have anxiety
problems from ages 5 to 17 years. Therefore, some of the other comorbid physical
disorders associated with anxiety may not emerge until later in life. Similar to adults,
rates of anxiety disorder in the PNC increased with the severity of aggregate physical
conditions, suggesting that physical–mental comorbidity is associated with greater
impairment of both conditions. Prospective documentation of the evolution of anxiety
disorders and physical conditions will be critical to the understanding of the explanations
for comorbidity.
Section 14.4
Genetic Epidemiology
● Genetic epidemiology seeks to understand how diseases and their risk factors are
distributed in families. First, family studies compare rates of illness in relatives of those
who have the condition (case probands) with rates in relatives of healthy controls.
Higher rates in the former group of relatives, as parameterized by a relative risk (RR) or
odds ratio (OR) greater than 1.0, suggest familial aggregation. Next, one relies on either
adoption studies (not available for ADs) or twin studies to differentiate genetic from
within-family environment as sources of aggregation. Twin studies compare
resemblance for a condition between members of a twin pair using the fact that
identical (monozygotic [MZ]) twins share 100 percent of their genetic sequence while
nonidentical (dizygotic [DZ]) twins share, on average, only 50 percent, like any two
siblings. One commonly used measure of twin resemblance is the proband-wise
concordance, that is, the proportion of co-twins of affected index twins who are also
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, affected. If average concordance for MZ pairs is greater than that for DZ pairs, this is
evidence for a genetic component to family resemblance. With larger twin samples, one
may also estimate the proportion of individual differences due to the effects of genetic
factors (heritability). For conditions with substantial heritability, gene finding (linkage or
association) studies are undertaken to identify which specific genes contribute to risk. A
2001 meta-analysis summarized findings across extant family and twin studies for
various adult ADs. Those results suggest an overall moderate level of familial aggregation
(OR = 4 to 6) and heritability (30 to 50 percent) across the ADs. This means that, on
average, first-degree relatives (FDRs) of someone affected by an AD are four to six times
more likely to develop one than a random individual. Fifty percent heritability means
that genetic and nongenetic factors are about equally responsible for the etiology of
ADs. Few family studies have been published since then, as it is now well established
that all ADs aggregate in families. More twin studies have been conducted, however,
with emphasis on the etiology of comorbidity or developmental risk. The results of that
meta-analysis will be referred to and augmented with data from more recent studies,
where available.
Molecular Genetics: Linkage & Candidate Gene Association
● Two main approaches have been applied to identify susceptibility genes in human
studies: linkage and association studies. Linkage studies are performed in family
pedigrees with several affected individuals to identify chromosomal loci likely to harbor
a gene influencing a biologic trait or condition. While effective for identifying highly
penetrant genes of large effect seen in classic Mendelian disorders, linkage has, with few
exceptions, not been successful for most complex phenotypes encountered in medicine,
including ADs. Several linkage studies have been performed for ADs, with few consistent
findings between studies. Suggestive evidence for linkage to PD has been reported for
regions on chromosomes 4q, 9q, 13q, 14q, and 22q. A more recent PD genome-wide
linkage scan conducted in the isolated population of the Faroe Islands found an
association of the amiloride-sensitive cation channel 1 (ACCN1) gene, previously
supported by animal studies. However, this association was not replicate in an
independent sample. A reanalysis of several PD linkage studies supported linkage on
chromosomes 4q and 7p. A Yale University group conducted linkage analyses of phobic
disorder in a set of pedigrees ascertained for PD, reporting linkage on chromosome 3q
for agoraphobia, 14q for specific phobia, and 16q for social phobia. There are no
published linkage scans for GAD. A meta-analysis of 162 families with panic or other ADs
found suggestive evidence for linkage on chromosomes 1, 5, 15, and 16. Of note, these
AD linkage results moderately but significantly correlated with those for neuroticism,
also examined in that study. Association studies allow one to test specific genetic
markers for their contribution to a phenotype. They include case-control comparisons in
unrelated individuals or family-based transmission tests. To date, most association
studies of ADs have focused on candidate genes, which have to be chosen using a priori
knowledge, either from their position under a linkage peak or by their purported
biologic relevance for the pathophysiology of the disease. Similar to depression, the
most widely studied candidate genes for ADs are genes involved in neurotransmitter
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