| Symptom: Irritability, agitation, raising thoughts, chronic sleep difficulties, frequent thoughts of death when depressed. |
A. Identify appropriate history questions to be asked of your patient to discriminate critical characteristics or Attributes about the above presenting complaint. Consider OLDCARTS
| How do you feel? Do you feel depressed mood or irritable most of the day? How are your spirits? Do you have decreased interest or pleasure in most activities, most of each day? How many hours of sleep do you get a night? Do you have difficulties staying asleep of falling asleep? Do you feel fatigue or loss of energy? Feelings of worthlessness or excessive or inappropriate? Do you feel diminished ability to think or concentrate, or more indecisiveness? When did these symptoms begin? What make them worse? Have you ever been diagnosed with depression and if so how were you treated? Did the treatment helped? Why did you stop taking your medication? |
| Do you have thoughts that life is not worth living or that you want to harm yourself? Do you have plans to take your own life? Do you want to die? Do you have Plan and intent for suicide action? Have you ever attempted to take away your own life or life of others? When did you start having these thoughts? |
| At what age did you started drinking? Have you ever felt you should cut down on your drinking? Have people annoyed you by criticizing your drinking? Have you ever felt bad or guilty about your drinking? Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover? Do you do illicit drugs? How often? |
| What type of drug do you take? Have you ever tried and failed to control, cut down, or stop using marijuana? In the past 3 months, how often have you used marijuana? In the past 3 months, how often has your use of marijuana led to health, social, legal or financial problems? In the past 3 months, how often have you failed to do what was normally expected of you because of your use of marijuana? |
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B. Delineate 4 hypotheses (differential diagnosis) that could support the above symptoms in relation to pertinent answers given the history. Use DSM5
| Differential 1 |
Major Depressive disorder |
| Differential 2 |
Generalized Anxiety Disorder |
| Differential 3 |
Bipolar 1 Disorder |
| Differential 4 |
Substance use disorder |
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C. What mental status exam findings, would be associated with each listed hypothesis above? What subjective data might the patient report? Use all seven component of MSE- Appearance, Behavior, Speech, Affect, Thought process, Thought content, Cognitive examination (level of awareness, Attention and Concentration, Memory, Orientation etc).
| Differential 1 |
Generalized Anxiety disorder
• Appearance- The patient reported agitation, irritability, tremors, and psychomotor restlessness.
• Speech- The patient reported raising thoughts. So he is expected to produce over productive, rapid, distractible speech patterns.
• Mood/Affect- Patient states “I have a horrible mood swings and I get angry easily. Patient will also appeared worried, nervous, tearful, worried, anxious
• Thought process- mild perseveration on topics of concern, worry
• Orientation-fully oriented
• Memory- forgetful, impaired short-term and immediate memory
• Concentration- decreased concentration, inattentive
• Judgement- This component will not be intact as demonstrated by the patient using marijuana to calm once-twice a month and also drinking alcohol 3-4 cans of beer on weekend. The important issue in assessing judgement include whether a patient is doing things that are dangerous or going to get him into trouble. |
| Differential 2 |
Major Depressive disorder
• Appearance- unkempt, tired-looking, little attention to dressing or looks, dark colored clothing, significant weight change from baseline
• Mood- sad, depressed, anxious, irritable
• Affect- constricted or blunted, sad, tearful, anxious, irritable
• Speech- slow response time, underproductive, monotone intonation
• Thought process- slowing, distractible, ruminative, distractible, may be disorganized with presence of psychosis
• Thought content- hopelessness, helplessness, suicide ideation
• Orientation- oriented to person, place and time unless psychosis is present
• Memory- usually impaired recent and short term memory
• Concentration- significantly impaired
• Abstraction- abstract ability on proverb testing normally intact
• Judgment- This component will not be intact as demonstrated by the patient using marijuana to calm once-twice a month and also drinking alcohol 3-4 cans of beer on weekend. The important issue in assessing judgement include whether a patient is doing things that are dangerous or going to get him into trouble.
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| Differential 3 |
Bipolar disorder
• Appearance- Psychomotor restlessness or agitation; frequent change of dress; prone to bright-colored, often sexualized dress; dramatic or flamboyant dress usually out of character for person when compared to non-symptomatic periods
• Speech- Rapid, loud, pressured, difficult to interrupt; joking, irrelevant, amusing; word changing in severely ill patients
• Affect- Labile, irritable, overly dramatic
• Mood- Euphoric, cheerful, expansive, high, irritable
• Thought process- racing thought, flights of ideas, disorganized thoughts, incoherent in severely ill patients
• Thought content- increased sexual content, inflated self-esteem, indiscriminate enthusiasm, inflated sense of abilities bordering on delusional
• Orientation- fully oriented
• Memory- impaired recall, impaired short-term
• Concentration- highly distractible
• Abstraction- can be concrete on proverb testing during psychotic episodes, generally abstractive
• Judgement- poor, prone to imprudent behavioral choices with potential for consequences
• Insight- the person usually does not recognize that he or she is ill, resists treatment options
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| Differential 4 |
Substance use disorder
• Appearance- The patient reported agitation and irritability will expect to see tremors, psychomotor restlessness.
• Speech- The patient reported raising thoughts. So he is expected to produce over productive, rapid, distractible speech patterns.
• Mood/Affect- Patient states “I have a horrible mood swings and I get angry easily. Patient will also appeared worried, nervous, tearful, worried, anxious
• Thought process- mild perseveration on topics of concern, worry
• Orientation-fully oriented
• Memory- forgetful, impaired short-term and immediate memory
• Concentration- decreased concentration, inattentive
• Judgement- This component will not be intact as demonstrated by the patient using marijuana to calm once-twice a month and also drinking alcohol 3-4 cans of beer on weekend. The important issue in assessing judgement include whether a patient is doing things that are dangerous or going to get him into trouble. |
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D. What is the physiology, pathophysiology, or etiology associated with each hypothesis?
| Differential 1 |
Generalized Anxiety disorder
The cause of generalized anxiety disorder is unknown
A combination of biological and psychological factors are associated with the disease
Brain areas involved include the occipital lobe, basal ganglia, limbic system and the frontal cortex (Sadock, Ruiz & Sadock, 2015).
Neurotransmitters involve include serotonin 5-HT, norepinephrine, glutamate and cholecystokinin.
Positron emission tomography (PET) scanning has demonstrated increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients with panic disorder (Sadock et al., 2015).
MRI has demonstrated smaller temporal lobe volume despite normal hippocampal volume in these patients.
Genetics also pays a major role. A few genetic studies have also shown conduction in the field. A study showed a relation between generalized anxiety disorders and major depressive disorders in women. 25% of first degree-relatives of patients with generalized anxiety disorder are also affected. Some twin studies report a concordance rate of 50% in monozygotic twins and 15% in dizygotic twins (Sadock et al., 2015).
Psychosocial factors are examined with two schools of thought. The cognitive-behavioral and the psychoanalytic. With the cognitive-behavioral patient react incorrectly and inaccurately to perceived dangers while the psychoanalytic school thinks it result from unresolved unconscious conflicts (Sadock et al., 2015).
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| Differential 2 |
Major depressive disorder
• Depression result from interaction of the central nervous, peripheral nervous, endocrine systems, genetic and environmental factors (Stahl, 2017).
• Many structures of the brain are involved in depression: cerebral cortex, frontal, temporal lobes, brain stem, basal nuclei, limbic system, hippocampus, amygdala, cingulate gyrus (Stahl, 2017).
• Hypothalamus: maintains endocrine functions
• Neurotransmitters involve include; Serotonin (5HT) Norepinephrine (NE) Dopamine (DA) Gamma-aminobutyric acid (GABA) Acetylcholine (Ach). Each Neurotransmitter has a specific neuroreceptor (Stahl, 2017).
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| Differential 3 |
Bipolar 1 disorder
Several factors have been identified that contribute to the development of bipolar disorders. Some of those factor include; biopsychosocial influences including genetic, perinatal, neuroanatomic, neurochemical and other biologic abnormalities and psychological and socio environmental factors (Ayano, 2016).
Genetic studies have been done to show proof that bipolar runs in families for example. One study revealed that First degree relatives of people with bipolar I disorder are approximately 7 times more likely to develop bipolar I disorder than the general population (Ayano, 2016). Furthermore, bipolar type I (BPI) disorder, has showed a major genetic component, with the involvement of the ANK3, CACNA1C, and CLOCK genes. Birth and pregnancy complications have also been linked to the development of Bipolar disorder
A number of neurotransmitters such as serotonin, nor epinephrine, or dopamine have been linked to this disorder, largely based on patients’ responses to psychoactive agents as in the following examples. The blood pressure drug reserpine, which depletes catecholamines from nerve terminals, was noted incidentally to cause depression. This led to the catecholamine hypothesis, which holds that an increase in epinephrine and nor epinephrine causes mania and a decrease in epinephrine and nor epinephrine causes depression (Ayano, 2016). Furthermore, there is also evidence that supports glutamate to both bipolar disorder and major depression. A postmortem study of the frontal lobes of individuals with these disorders revealed that the glutamate levels were increased
Environmental factors have also been found to contribute to the development of Bipolar disorder. Bipolar individuals experience increased stressful events prior to first onset and recurrences of mood episodes. Furthermore, negative life events precede the manic/hypomanic as well as the depressive episodes of bipolar individuals. Some studies have indicated that about 20% to 66% of bipolar patients experienced at least one stressful event rated as independent of their behavior in the 1–3month period (Ayano, 2016).
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| Differential 4 |
Substance use disorder
Multiple interacting factors influence the use of drugs and the loss of judgement with respect about a given drug. Factors that cause the initiation of drug use include; availability, social acceptability, and peer pressure Furthermore, Personality and individual biology determines the manner in which drugs use influence the nervous system (Sadock et al., 2015).
It had been postulated that addiction is a brain disease and that the process that transform voluntary drug-using behavior to compulsive drug use are changes in the structure and neurochemistry of the brain user. For some, the use of the drug or substance initiates a biological process associated with tolerance, physical dependence and sensitization which causes the user to gradually increase the consumption requiring larger doses.
Other factors include psychodynamic factors which believe that substance abuse is a masturbatory equivalent which is a defense against anxious impulses. Studies have also showed genetics involvement. Evidence from the studies of twins, adoptees and siblings brought up separately indicate that the cause of alcohol abuse is also genetic. Neurochemical factors have also been employed (Sadock et al., 2015).
Neurotransmitters and neurotransmitter receptors are involved with most substance abuse. Neurotransmitters involve are the opioid, dopamine and Y-aminobutyric acid (GABA). Comorbidity such as the occurrence of two or more psychiatric disorders in a single patient cannot be underestimated. Some studies have shown that patient who meet the criteria for alcohol or drug abuse and dependence are also far more likely to meet the criteria for other psychiatric disorders also (Sadock et al., 2015).
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E. What diagnostic tests would you obtain? What diagnostic tool would you use?
| Differential 1 |
Generalized Anxiety disorder
CBC, chemistry profile, thyroid function test, and B12 level to rule out metabolic cause or unidentified conditions.
Obtain drug toxicity screening
Obtain Electrolytes to check for Respiratory Alkalosis, decreased bicarbonate levels and decreased carbon dioxide levels.
Screening tools: Hamilton Anxiety Scale (HAM)
Generalized Anxiety Disorder 7-item (GAD-7) scale
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| Differential 2 |
Major depressive disorder
• No lab findings specific to MDD
• Complete blood count, chemistry panel, thyroid function test, B12, folate, vitamin D
• Consider sleep study if snoring, apnea, or suspicion of sleep disorder
• Drug toxicity screening, if indicated by history
• Medications that can cause altered mood states as side effects- steroids, estrogen, antihypertensive, anti-Parkinson, antineoplastic, antibacterial, antifungal, analgesics,
isotretinoin (Accutane), benzodiazepines.
Screening Tools: Beck Depression Inventory (BDI
The Hamilton Depression Rating Scale (HAM-D)
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| Differential 3 |
Bipolar 1 disorder
CBC, Chemistry profile, thyroid function tests, and B12 level to rule out metabolic causes or other conditions; drug toxicity screening if indicated by history.
• Fasting glucose
In some cases, a fasting glucose level is indicated to rule out diabetes. In addition, atypical antipsychotics have been associated with weight gain and problems with blood glucose regulation in patients with diabetes, therefore, a baseline fasting glucose should be obtained.
• Electrolytes
Serum electrolyte concentrations are measured to help diagnose electrolyte problems, especially with sodium, that are related to depression. Treatment with lithium can lead to renal problems and electrolyte problems, and low sodium levels can lead to higher lithium levels and lithium toxicity. Hence, in screening candidates for lithium therapy as well as those on lithium therapy, checking electrolytes is indicated.
Serum calcium is assessed to diagnose hypercalcemia and hypocalcemia associated with mental status changes (eg, hyperparathyroidism). An elevated calcium blood level can cause depression or mania. Hyperparathyroidism, as evidenced by an elevated calcium blood level, produces depression. Certain antidepressants, such as nortriptyline, affect the heart; therefore, checking calcium levels is important.
• Magnetic Resonance Imaging
The total value of performing magnetic resonance imaging (MRI) in a patient with bipolar disorder, or manic-depressive illness (MDI), remains unclear; however, a couple of reasons do exist for performing an imaging study. Because manic-depressive illness is a lifelong disease, a strong battery of studies rules out any other medical etiology and establishes a baseline. Some investigators report that patients with mania demonstrate hyper intensity in their temporal lobes.
• Electroencephalography
Generally, routine electroencephalography (EEG) is unnecessary in the evaluation of bipolar disorder, or manic-depressive illness (MDI). EEG provides a baseline and rule out other disease.
Screening Tools:
The Mood Disorder Questionnaire (MDQ) |
| Differential 4 |
Substance use disorder
Blood, urine or other lab tests are used to assess drug use, but they’re not a diagnostic test for addiction. Blood or breath alcohol levels could also be obtained. However, these tests may be used for monitoring treatment and recovery Consider electrolytes, glucose, BUN, and creatinine because of the dehydration and poor nutrition observed in this population. Complications of cocaine intoxication may require a cardiac or CNS evaluation that may include an ECG and brain CT scan.
Indirect alcohol biomarkers include aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (GGT), mean corpuscular volume (MCV), and carbohydrate-deficient transferrin (CDT)
The combination of GGT and CDT compared with GGT or CDT alone shows a higher diagnostic sensitivity, a higher diagnostic specificity, and a stronger correlation with the actual amounts of alcohol consumption
Elevated mean corpuscular volume of red blood cells, abnormal liver enzymes could also use to confirm the diagnosis of alcoholism.
Screening Tools:
The CAGE questionnaire
NIDA Quick Screen Question |
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| F. Analysis:
• My final assessment is Major depressive disorder as evidence by patient’s past medical history of depression that was not appropriately treated, Patient’s symptoms of mood swings, irritability agitation, raising thoughts, chronic sleep difficulties, substance use, frequent suicide thoughts when depressed, history of depression for the past 3 months, which are all common symptoms found in patients with Major depression. Mental status examination also supports this as evidence in patient verbalizing his Affect- anxious, irritable, Speech- slow response time, underproductive, monotone intonation, Thought process- slowing, distractible, ruminative, distractible, may be disorganized with presence of psychosis, Thought content- hopelessness, helplessness, suicide ideation, Concentration- significantly impaired and poor Judgment as patient demonstrated using marijuana to calm once-twice a month and also drinking alcohol 3-4 cans of beer on weekend.
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| G. What pharmacotherapy (class of medication) and non-pharmacological treatments would you suggest for the primary diagnosis?
Major Depressive disorder
Pharmacological Treatment
H. For this Patient I would recommend SNRIs such as Venlafaxine (Effexor, XR), Desvenlafaxine (Pristiq), Duloxetine (Cymbalta), Levomilnacipran (Fetzima) since the patient states that he tried the first line SSRIs but it did not make much difference in treating his symptoms. Also because of less severe side effects as compared to TCAs. Also because of patient risk of suicide. SNRIs are also recommended for patients who do not tolerate SSRIs
I. Other pharmacology therapy include:
• Selective serotonin reuptake inhibitors (SSRIs)
• Serotonin/norepinephrine reuptake inhibitors (SNRIs)
J. Atypical antidepressants
K. Serotonin-Dopamine Activity Modulators (SDAMs)
L. Tricyclic antidepressants (TCAs)
M. Monoamine oxidase inhibitors (MAOIs)
N. N-methyl-D-aspartate (NMDA) receptor antagonists
Non Pharmacological treatment
O. Non-pharmacological-
Psychotherapy
Cognitive behavior therapy (CBT), Interpersonal psychotherapy (IPT), Problem-solving therapy (PST) Behavioral activation (BA)/contingency management.
ECT, individual therapy, transcranial magnetic, stimulation, vagal nerve stimulation, phototherapy
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| References
Anderson, E., Michalak, E., & Lam, R. (2019). Depression in primary care: Tools for screening, diagnosis, and measuring response to treatment. BC Medical Journal, 12(8), 415-419.
American psychiatric association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: author.
Ayano, G. (2016). Bipolar Disorder: A Concise Overview of Etiology, Epidemiology Diagnosis and Management: Review of Literatures. SOJ Psychology, 1-8. doi: 10.15226/2374-6874/3/2/00131
Halverson, J. (2019). Depression: Practice Essentials, Background, Pathophysiology. Retrieved 1 September 2019, from https://emedicine.medscape.com/article/286759-overview#a3
Sadock, B.J., Sadock, V.A., Ruiz., P (2015). Kaplan and Sadock synopsis of psychiatry (11th ed.)
Baltimore, MD: Williams & Wilkins.
Stahl S. 2017. Prescriber’s guide: essential psychopharmacology. 6th ed.; pp 449-453. New York. Cambridge University Press.
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