2. Hypochondriasis
The following clues need to be considered in making this daignosis:
Appropriate medical evaluation failed to find evidence of serious
disease
Patient's preoccupation persisted despite adequate reassurance
Preoccupation lasted for 6 months or more
Preoccupation caused marked distress or impairment in functioning
Voiced concerns that are unrealistic but not beyond reason; for
example, the patient may believe headaches indicate a brain tumor
( If its beyond reason then you will have to call it a “Delusion”)
Failure of the patient to be reassured after appropriate work-ups
causing him or her to seek further tests and consultations
3. Hypochondriasis
Hypochondriasis Associations:
Seen in 50% of all patients with panic disorder
major depressive disorder
In these patients, coexisting hypochondriasis will
respond to treatment for the primary disorder.
4. D/D
1. Physical Disease
Conditions with diffuse symptomatology involving many
organ systems may, when undiagnosed, mimic
hypochondriasis
Occasionally occult malignancies or early stages of
multisystem disease (e.g., lupus) explain what at first
appears to be hypochondriasis. It is most important to first
rule out physical disease
2. Major depressive episode
Depressed mood, sleep and appetite changes, loss of
interest, low self-esteem
Depressed patients in primary care usually have
unexplained somatic complaints and are worried about
what is wrong with them but have typical symptoms and
signs of depression
3.
5. D/D
3. Panic disorder
Recurrent panic attacks with persistent dread of future attacks
Panic patients in primary care usually have numerous somatic
symptoms and anxiety about their health. However, they also
have recurrent panic attacks and worry about future attacks
4. Obsessive-compulsive disorder
Repetitious unwanted thoughts (obsessions) and repetitious
unwanted actions (compulsions)
Patients with hypochondriasis do not have other obsessions or
compulsions. Obsessions often involve contamination or harming
someone; compulsions often involve cleaning or checking
6. D/D
5. Specific phobia of illness
Fear and avoidance of a specific illness (e.g.,
AIDS)
Patients with hypochondriasis have a conviction
that serious disease is already present, whereas
patients with illness phobia fear contracting
illnesses they do not have
6. Somatization disorder
Multiple somatic symptoms involving many organ
systems with onset <30 years
Somatization disorder occurs predominantly in
women and involves multiple unexplained
symptoms. By contrast, hypochondriasis is
characterized chiefly by abnormal attitudes (i.e.,
fear, worry)
7. D/D
7. Psychotic disorders (schizophrenia,
delusional disorder, major depressive
disorder with psychotic features)
Patients with hypochondriasis have
overvalued ideas but not delusional
beliefs. Overvalued ideas are strongly
held, but delusional ideas are
accompanied by unshakeable conviction
and are often bizarre
8. Hypochondriasis Therapy
1. Adopt a systematic approach to patients with
hypochondriasis.
Here, you should aim to continue to care not a cure
Arrange regularly scheduled follow-ups.
Provide an explaination
Develop and maintain a positive relationship using
interviewing skills.
2. Cognitive behavioral therapy as a primary mode of
therapy
3. In patients with hypochondriasis who have coexisting
depressive or anxiety disorders, rx with an
antidepressant. Start treatment with a serotonin
reuptake inhibitor at low dose; for example, start
sertraline, 12.5 mg/d, and increase by 12.5 mg every 5
days as tolerated until a daily dose of 50 mg is achieved
9. Somatization Disorder
Diagnostic criteria for a Somatoform Disorder
Physical symptoms that cannot be explained by an organic cause
“Secondary Gain “ aiming conditions are ruled out (Malingering or
Factitious Disorder)
Causes significant dysfunction
Specific criteria for Somatization Disorder
Symptoms longer than 2 years
Unexplained physical symptom with onset prior to age 30.
Symptoms are vague and involve multiple organ symptoms
At least 2 Gastrointestinal (nausea, vomiting, bloating)
At least 4 Pain ( Headache, abdominal pain, chestpain, dyspareunia)
At least 1 Neurologic ( deafness, blindness, diplopia, fainting, dysphagia)
At least 1 Sexual / genitourinary ( erectile dysfunction, dyspareunia,
menorrhagia, irregular menses)
Important clues in history that can help in diagnosis
Extensive work up in the past that has been non diagnostic
Patient tends to switch physicians often because of dissatisfaction with
previous physicians
10. Somatization management
Never tell the patient that its “all in her head”
Avoid excess investigations.
A single physician should try to establish a
long term empathetic relationship with the
patient.
Cognitive therapy
Group therapy
12. Deliriun
PREDISPOSING FACTORS
Age
Cognitive impairment
Increased comorbidity
Male gender
Depression
Alcohol abuse
Sensory impairment
PRECIPITATING FACTORS
>6 total medications
>3 new inpatient medications
Psychotropic medication
Infection
ICU admission
Hip fracture
Dehydration
Environmental change
Restraint use
Malnutrition
Catheter use
Iatrogenic event
13. Screening - Delirium
Perform a short mental status assessment for
delirium at least daily in all hospitalized patients
aged 70 or older
Daily, Screen inpatients who are predisposed to
delirium, including those with cognitive
impairment or multiple comorbidities and those
admitted to the ICU
Use for assessment for delirium:
Confusion Assessment Method
Mini-Mental Status Examination
Remember Delirium can have various
Psychomotor variants – hypoactive, hyperactive,
mixed and normal psychomotor activity
14. Confusion Assessment
Method
Confusion Assessment Method Instrument (CAM)
Acute Onset
1. Is there evidence of an acute change in mental status from the patient's baseline?_____YES
_____NO _____UNCERTAIN _____NOT APPLICABLE
Inattention (The questions listed under this topic are repeated for each topic where applicable.)
2A. Did the patient have difficulty focusing attention (for example, being easily distractible or having
difficulty keeping track of what was being said)? _____Not present at any time during interview
_____Present at some time during interview, but in mild form _____Present at some time during
interview, in marked form _____Uncertain
2B. (If present or abnormal) Did this behavior fluctuate during the interview (that is tend to come
and go or increase and decrease in severity)? _____YES _____NO _____UNCERTAIN_____NOT
APPLICABLE 2C. (If present or abnormal) Please describe this behaviour:
Disorganized Thinking
3. Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant
conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?
_____YES _____NO _____UNCERTAIN _____NOT APPLICABLE
Altered Level of Consciousness 4. Overall, how would you rate this patient's level of
consciousness? _____Alert (normal) _____Vigilant (hyperalert, overly sensitive to environmental
stimuli, startled very easily) _____Lethargic (drowsy, easily aroused) _____Stupor (difficult to
arouse) _____Coma (unarousable) _____Uncertain
15. CAM - Scoring
To have a positive CAM result, the patient must display:
1. Presence of acute onset and fluctuating discource
AND
2. Inattention
AND EITHER
3. Disorganized thinking
OR
4. Altered level of consciousness
16. Differential Diagnosis
Differential diagnoses include:
Dementia
Depression
Partial syndrome of delirium
Bipolar disease
Note that any acute change in mental status
should be considered delirium until proven
otherwise because of reversibility and the
consequences of missing the diagnosis.
In hospitalized patients with altered cognition,
assess delirium first, followed by partial syndrome
of delirium, depression, and then dementia.
17. Evaluating differential diagnosis
1. Dementia
Insidious onset, slow progression, level of consciousness is usually normal,
attention is preserved until late in the course
Any acute mental status change in a demented patient is likely to be
superimposed delirium. Dementia (or cognitive impairment) is a strong risk
factor for delirium; the two disorders commonly co-exist
2. Depression
Depressed mood is present. Psychomotor retardation or agitation also may be
present. Level of consciousness and attention is usually normal
A study showed that one third of consults for “depression” in the hospital were
hypoactive delirium
3. Bipolar disease, especially acute mania
Acute mania may be confused with hyperactive delirium, but is less common
in the elderly. Usually the changes and fluctuations are less acute than
delirium. Inattention, disorganized thinking, and psychomotor agitation may be
present
Bipolar disease rarely presents in old age. Patients with this disease usually
have a history of psychiatric illness or are taking medications that suggest the
diagnosis. If in doubt, perform the full delirium work-up
4. Partial syndrome of delirium
Patients show some of the characteristics of delirium, but not enough to fulfill
all criteria. Sometimes progresses to full-blown delirium
Associated with poor outcome and should be evaluated and treated similar to
“full-blown” delirium
18. Ways to Prevent
Hospital Delirium –
high yield
Prevent delirium in hospitalized patients by ensuring:
Assessment of multiple risk factors Cognitive
impairment , Sleep deprivation , Immobility, Visual
impairment, Hearing impairment & Dehydration
Targeted treatment to correct or reduce the impact of risk
factors
Avoidance of medications deemed inappropriate for older
patients
Geriatrics consultation
Nursing-based interventions
Consider proactive, preoperative geriatric consultation to
reduce postoperative delirium in hip fracture patients
19. Managing Delirium
1. Remove contributing factors, such as:
Offending medications , Fluid and electrolyte
abnormalities , Severe pain , Hypoxemia , Severe anemia
, Infections , Sensory deprivation
2. Maintain behavior control through behavioral or
social measures rather than pharmacologic or
physical restraints.
Note that a family member or caregiver will often
ameliorate mild to moderate agitation; hiring a “sitter” or
keeping the patient near the nursing station may be
adequate.
Be aware that treatment with sedating medications may
be necessary for severe or life-threatening agitation.
There is no rationale for treating hypoactive delirium with
sedating medications.
Avoid use of physical restraints unless no safer alternative
is feasible and the patient is physically endangering self or
others.
20. Managing Delirium
Recognize that patients with delirium are vulnerable and require
attentive supportive care to meet their needs and avoid iatrogenic
complications.
Minimize indwelling catheters and other “tethers” such as intravenous
lines, EKG leads, and restraints; let the patient out of bed as soon as
possible.
Monitor urinary and bowel output, and avoid urinary retention and fecal
impaction which can contribute to delirium.
Pay careful attention to nutrition, including assistance with meals and
possible hand feeding—delirious patients may have difficulty attending to
food and are at risk for acute malnutrition.
Provide adequate sensory input, including use of glasses and hearing
aids, provision of clocks, calendar, and adequate lighting, and appropriate
interpersonal contact.
Be aware that frequent orientation and structured interpersonal contact
may facilitate cognitive “reconditioning.”
Recognize that environmental modifications such as minimizing staff
noise, use of vibrating (silent) pagers, eliminating waking for vital signs
except if essential, and reduced lighting at the nursing station may
improve sleep at night.
21. Managing Delirium
Consider using drugs to manage agitation in
delirium, but not at the risk of worsening or
prolonging the delirium itself.
Note that haloperidol and risperidone should be
considered as the “least of the evils” and should
only be used in life-threatening circumstances
(such as in the ICU) or when behavioral
measures have been ineffective.
Use the lowest dose of the least toxic agent that
successfully controls the agitation.
Note that haloperidol in low doses is equally
efficacious as atypical antipsychotics and may be
less likely to cause oversedation, hemodynamic
compromise, or respiratory depression compared
to benzodiazepines.
22. Drug Rx for agitation
associated with Delirium
1. Haloperidol : Usually agent of choice
Advantages: Relatively non-sedating. Few hemodynamic effects. May prevent
delirium following hip surgery
Side effects : Extrapyramidal symptoms, especially if >2 mg/d, Neuroleptic
malignant syndrome
Evidence: In a randomized trial comparing haloperidol, chlorpromazine, and
lorazepam in the treatment of agitated delirium in young patients with AIDS,
haloperidol had fewer side effects or adverse sequelae . Haloperidol may
prevent delirium following hip surgery
2. Olanzapine :
Advantages : Increased sedation
Side effects : Hyperglycemia, May have fewer extrapyramidal side effects
3. Risperidone:
Benefits : Similar to haloperidol, Relatively nonsedating, Few hemodynamic effects
May have fewer extrapyramidal symptoms
4. Lorazepam :
Benefits : Second line agent. However, first line in cases of Use in delirium due
to alcohol withdrawal, patients with Parkinson's disease, patients with history
of neuroleptic malignant syndrome
Disadvantages : More paradoxical excitation, respiratory depression than haldol
23. Ser otonin
Syndr ome
- Occurs in a setting of a serotinergic drug ( refer the list) can occur at
therapeutic doses, over dosage or as an inadvertant interaction between
the drugs.
-Be aware of differentiating NMS from Serotonin Syndrome as patients
may be on both types of drugs at same time ( eg: pts with bipolar
disorder may be may be on an antimanic drug/antipsychotic + SSRI)
- Be aware that classic features such as muscular hypertonicity and
hyperthermia occur only in life threatening cases. Recognize that it has a
spectrum of clinical features.
- Recognize that Clonus and Hyperreflexia are highly suggestive of
serotonin syndrome in mild to moderate cases.
- Remember that if there is severe muscle rigidity ( hypertonicity ), it can
mask the diagnostic features of serotonin syndrome such as clonus and
hyperreflexia
24. A Case That Shook Medicine
How One Man's Rage Over His Daughter's Death Sped Reform
of Doctor Training
By Barron H. Lerner
Special to The Washington Post
Tuesday, November 28, 2006; Page HE01
Many people have vowed to avenge the untimely death of a relative. Lawyer
and journalist Sidney Zion actually did so -- to the benefit of patients and
doctors-in-training nationwide.
“ Libby Zion (18) dies in 1984 of
an interaction between
Meperidine and Phenelzine”
25. Physical Exam
Physical examination should include a
focused assessment of deep-tendon
reflexes, clonus, and muscle rigidity, in
addition to an evaluation of the size and
reactivity of the pupils, the dryness of the
oral mucosa, the intensity of bowel sounds,
skin color, and the presence or absence of
diaphoresis.
27. Drugs and Drug Interactions Associated with the Serotonin Syndrome
28. Caution!
Remember Administration of serotonergic agents
within five weeks after the discontinuation of fluoxetine
therapy has produced a drug interaction culminating in
the serotonin syndrome, presumably the result of the
demethylation of fluoxetine to norfluoxetine, a
serotonergic metabolite with a longer serum half-life
than its parent compound
Remember Serotonin is metabolized by MAO-A to 5HIAA Specific drugs, such as MAOIs that are
irreversible or nonselective or that inhibit monoamine
oxidase subtype A, are strongly associated with severe
cases of the syndrome, especially when these agents
are used in combination with meperidine,
dextromethorphan, SSRIs, or
methylenedioxymethamphetamine (MDMA, or
"ecstasy) eg: Interaction b/w Phenelzine ( MAO – A
inhibitor) and Meperidine has lead to death of a patient
29. Findings in Patient with Moderately Severe
SerotoniSyndrome
Hyperkinetic neuromuscular findings of tremor or clonus and hyperreflexia should
lead the clinician to consider the diagnosis of the serotonin syndrome.
Remember “MYDRIASIS” is the KEY. Where as in Neuroleptic Malignant Sydrome
you will usually see Normal sized pupils
30. Algorithm for Diagnosis
The neuromuscular features of clonus and hyperreflexia are highly diagnostic
for the serotonin syndrome, and their occurrence in the setting of
serotonergic drug use establishes the diagnosis. Clinicians should be aware
that muscle rigidity can overwhelm other neuromuscular findings and mask
the diagnosis
31. Lab Anomalies
Laboratory abnormalities that occur in
severe cases include metabolic acidosis,
rhabdomyolysis, elevated levels of serum
aminotransferases and creatinine,
seizures, renal failure, and disseminated
intravascular coagulopathy.
Many of these abnormalities arise,
however, as a consequence of poorly
treated hyperthermia.
32. Management
Discontinue the precipitant drug.
Mild cases ( hyperreflexia and tremor but no fever) supportive care ( IV
Fluids, vitals), Benzodiazepenes ( to control agitation and provide
sedation)
Moderate cases address cardiorespiratory and thermal abnormalities,
give 5HT2a Antagonists ( Cyproheptadine is first choice or
Chlorpromozine as alternative)
Hyperthermic pts with temp > 41C give above therapies + sedation +
neuromuscular paralysis ( vecuronium) + orotracheal Intubation. Control
of hyperthermia needs eliminating excessive muscle activity hence
induce neuromuscular paralysis with Vecuronium followed by orotracheal
intubation and ventilation
There is no role for antipyretic agents in the management of the serotonin
syndrome; the increase in body temperature is due to muscular activity,
not an alteration in the hypothalamic temperature set point.
Dantrolene, a centrally acting muscle relaxant is not useful here
Bromocriptine which is used in NMS, has no role here in fact, it may
worsen serotinergic signs.
33. Differential Diagnosis
Anticholinergic Poisoning
Patients with the anticholinergic syndrome have
normal reflexes and show the "toxidrome" of
mydriasis; agitated delirium; dry oral mucosa; hot,
dry, erythematous skin; urinary retention; and an
absence of bowel sounds.
Hyperactive bowel sounds - along with
neuromuscular abnormalities
(clonus/hyperreflexia/rigidity), diaphoresis, and
normal skin color — distinguish the serotonin
syndrome from the anticholinergic toxidrome
34. Differential Diagnosis
Neuroleptic Malignant Syndrome Neuroleptic malignant syndrome is
an idiopathic ( idiosyncratic) reaction to dopamine antagonists, a
condition that is defined by a slow onset, bradykinesia or akinesia, "lead
pipe" muscular rigidity, hyperthermia, fluctuating consciousness, and
autonomic instability (HYPER/HYPOTENSION).
Remember that Hyperthermia in response to neuroleptic administration
is an idiopathic response; the normal outcome is hypothermia.
Signs and symptoms of the neuroleptic malignant syndrome typically
evolve during several days, in contrast to the rapid onset and
hyperkinesia of the serotonin syndrome. ( In NMS, you have rigidity
but no Hyperkinesia. However, as discussed earlier in severe cases of
serotonin syndrome, severe rigidity can mask these hyperkinetic
neuromuscular findings ( clonus/ hypereflexia etc) so, look at
pupillary size as next step in differentiation. In Serotonin Syndrome, you
have Mydriasis.
Knowledge of the precipitating drug also helps in distinguishing between
syndromes: dopamine antagonists produce bradykinesia, whereas
serotonin agonists produce hyperkinesia ( Clonus and Hyperreflexia)
35. Differential Diagnosis
Malignant Hyperthermia
Malignant hyperthermia is a pharmacogenetic disorder
characterized by increasing concentrations of end-tidal
carbon dioxide, hypertonicity (rigidity) , hyperthermia, and
metabolic acidosis.
The disorder occurs within minutes after exposure to
inhalational anesthetic agents. Also, seen with
Succinylcholine.
On physical examination, the skin is often mottled, with
cyanotic areas contrasting with patches of bright red
flushing. The rigor mortis–like rigidity of skeletal muscles
and “hyporeflexia” that are seen in malignant hyperthermia
further distinguish this condition from the serotonin
syndrome
Rx – Dantrolene, Supportive care
38. Depression - Prevention
Offer counseling to patients who have
experienced stressful events, trauma, or losses.
Inquire about previous episodes of depression in
patients currently without symptoms of
depression, and stress the importance of early
intervention.
Screen for symptoms of depression in women
during the 4 to 6 weeks after giving birth,
particularly in women with psychosocial stress
during pregnancy and history of psychiatric
disorder.
Consider antepartum counseling for women with
risk factors for postpartum depression
39. DSM IV Criteria for
Depression
A) Five or more of the following symptoms have been present during the same 2-week
period and represent a change from previous functioning; at least one of the
symptoms is either 1) depressed mood or 2) loss of interest or pleasure.
1) Depressed mood most of the day, nearly every day as self-reported or observed by
others.
2) Diminished interest or pleasure in all or almost all activities most of the day, nearly
every day.
3) Significant weight loss when not dieting, or weight gain; or decrease or increase in
appetite nearly every day.
4) Insomnia or hypersomnia nearly every day.
5) Psychomotor agitation or retardation nearly every day
6) Fatigue or loss of energy nearly every day.
7) Feelings of worthlessness or excessive or inappropriate guilt nearly every day.
8) Diminished ability to think or concentrate nearly every day.
9) Recurrent thoughts of death, recurrent suicidal ideation without a specific plan.
B) The symptoms do not meet criteria for a mixed episode
C) The symptoms cause clinically significant distress or impairment in social,
occupational, or other areas of functioning.
D) The symptoms are not due to the direct physiological effects of a substance (drug
or medication) or a general medical condition (hypothyroidism).
E) The symptoms are not better accounted for by bereavement, i.e., after the loss of a
loved one, the symptoms persist for longer than 2 months or are characterized
by marked functional impairment, morbid preoccupation with worthlessness,
suicidal ideation, psychotic symptoms, or psychomotor retardation.
40. D/D
Medical Disorders Recognize that there is an increased prevalence of depression in the
following conditions:
Medical conditions:
Prescription drug effects:
Hypothyroidism
Cushing's disease
Dementia
Parkinson's disease
Stroke
Multiple sclerosis
Cancer
Diabetes
Coronary heart disease
Fibromyalgia and other chronic pain states
Chronic fatigue syndrome
Vitamin B12 deficiency
Infectious disease such as TB, viral hepatitis
Glucocorticoids
Interferon
Reserpine and other centrally acting antihypertensives
Substance abuse:
Anabolic steroids
Ethyl alcohol
Cocaine or amphetamine withdrawal
41. D/D
MOOD DISORDERS : Differentiate major
depression from other mood syndromes
using DSM-IV criteria including:
Dysthymic disorder
Bipolar disorder
Minor depression
Situational adjustment reaction with
depressed mood
Grief
Seasonal affective disorder
42. D/D
Dysthymia : Dysthymia is a chronic mood disorder
characterized by depressed mood or anhedonia at least
half the time for at least 2 years accompanied by two or
more vegetative or psychological symptoms and functional
impairment. Rx : Antidepressants
Situational adjustment reaction with depressed mood :
Subsyndromal depression with clear precipitant. Usually
resolves with resolution of acute stressor without
medication . Supportive counselling and identification of
stressor is required.
Seasonal Affective disorder : A subtype of major
depression, occurring with seasonal change, typically fall
or winter onset and seasonal remission, rarely onset is in
the spring with remission in the fall or winter. It should
have occurred in the two previous years, without
nonseasonal depression. More common in northern
latitudes Responds to bright-light therapy and adjuvant
therapy with SSRIs
43. D/D
Premenstrual Dysphoric disorder: Characterized by depressed mood, anxiety,
and irritability during the week before menses, resolving with menses May
respond to SSRI treatment; intermittent treatment during part of the menstrual
cycle may be effective
Grief Reaction : The syndrome of major depression may be transiently present
in normal grief, however sadness without the complete syndrome is more
common. Duration, intensity of symptoms, and associated change in function is
variable and commonly affected by cultural and societal factors Pervasive
and generalized guilt and persistent vegetative signs and symptoms that are
not consistent with the patient's or family's expectations for normal grief should
arouse concern Bereavement is often a precipitant of true mood disorder,
and patients in this state should be carefully assessed and followed. do
supportive counseling . Remember Loss of self-esteem and Anhedonia is a
symptom of depression rather than grief
Dementia : Characterized by impaired memory, judgement and other higher
cortical functions see DEMENTIA Slides
Anxiety disorder
Psychotic disorders ( thought disorders) : Major depression may be
accompanied by mood congruent hallucinations/ delusions ( where as mood
incongruent delusions/ hallucinations may suggest a primary psychotic
disorder. )
44. Depression – Indications for
hospitalization
Hospitalize patients:
With significant suicidal ideation or intent who do not have
adequate safeguards in their family environment
With intent to hurt others
To assess their ability to care for themselves and adhere
to their treatment in light of the supports available in their
home environment
Who are in need of detoxification or substance abuse
treatment
Who are candidates for ECT
With comorbid dysfunctional family systems that
exacerbate their depressive disorder or interfere with
treatment
45. Depression – Drug
therapy
A. Treat first episodes of depression to achieve complete
remission, and continue treatment for 4 to 9 months
thereafter.
Aim for complete remission of symptoms and return to
normal functioning.
If remission is not achieved with the initial antidepressant,
switch to another agent or consider adding or switching to
cognitive therapy.
In first episodes, continue treatment with antidepressant
medication at the same dosage required to achieve
remission for an additional 4 to 9 months.
Consider long-term maintenance therapy in patients over
age 70 and in those with diabetes mellitus.
B. Treat recurrences of major depression with long-term
maintenance therapy
46. Depression – Drug
therapy
Treat patients who are suffering a first recurrence of major depression for
longer than the initial episode.
For first recurrence, consider maintenance treatment for one to two times
the interepisode interval, e.g., if the second episode occurs 18 months
after the first episode, the treatment should be 18 to 36 months.
For older patients (>70 years) with major depression who respond to an
SSRI, consider treating for 2 years to prevent recurrence.
Consider lifetime maintenance therapy for patients with three or more
recurrences or patients with a first recurrence and risk factors for further
recurrences including:
1.Family history of bipolar disorder
2. Recurrence within 1 year of successful treatment of previous
episode
3.Young age of onset (adolescent)
4.Severe (debilitating or suicidal attempt) and sudden onset of
symptoms
47. Depression – Drug
Therapy
Counsel patients to improve medication
adherence, emphasizing:
The importance of taking the medication daily
That symptomatic improvement may be noticed
within 1 week but often takes 2 to 4 weeks
That they must continue to take medicine even if
feeling better
That they must not stop taking the antidepressant
without checking with their physician
Potential side effects
Offer St. John's wort as a potential treatment for
patients with mild to moderate depression or
subsyndromal depression
48. Anti-Depressant Drugs
A. SSRI : Fluoxetine, Duloxetine, Paroxetine, Citalopram, Fluvoxamine Side
effects : Nausea and diarrhea, anxiety, nervousness, somnolence, impaired
sexual function
All SSRIs are contraindicated with MAOIs in view of possible SEROTONIN
SYNDROME
B. SNRI : Venlafaxine (Effexor), Mirtazepine Side effects : Gastrointestinal
complaints (nausea, dry mouth, anorexia, constipation, and flatulence),
CNS complaints (dizziness, somnolence, insomnia, nervousness, abnormal
dreams, and tremor), sweating, abnormalities of sexual function (abnormal
ejaculation and impotence in men, anorgasmia in women, and decreased
libido), problems of special senses (abnormal vision), cardiovascular effects
(hypertension and vasodilatation), and yawning
C. Bupropion : Dopamine reuptake inhibitor, Advantage : very less weight gain.
Adverse effects : lowers seizure threshold, Anorexia, dry mouth, rash,
sweating, tinnitus, tremor, abdominal pain, agitation, anxiety, dizziness,
insomnia, myalgia, nausea, palpitation, pharyngitis, and urinary frequency
D. TCAs : Amitryptiline, Nortryptiline, Amoxapine, Imipramine, Clomipramine, Side
Effects : mainly anticholinergic Dry mouth, dizziness, constipation,
nausea. Sedation, Anticholinergic hypotension, Orthostatic hypotension ,
Prolongs QT interval and can lead to Torsades depointes
For pts with Torsades due to Tricyclic overdose , Admit to ICU and treat with
bicarbonate. If Torsades give magnesium and lidocaine. D/C all QT
prolonging drugs.
E.
Weight gain is a significant side effect, except with Bupropion
F.
Mirtazipine can cause Agranulocytosis – monitor blood counts, report to ER
if sorethroat, fever, chills etc appears
49. ST.Johns Wort
Definitive method of action unclear. Animal studies suggest
St. John's wort may work by inhibition of serotonin uptake.
Hypericum extract also has been shown to decrease cell
surface 5-HT receptors
Attractive to patients with moderate depression who are
unwilling or unable to take conventional treatment. Adverse
effects are generally mild GI symptoms, dizziness or
confusion, sedation, dry mouth, photosensitivity
St. John's wort activates cytochrome P450 and may reduce
the concentration of medications such as digoxin,
theophylline, simvastatin, and warfarin.
St. John's wort interferes with antiretroviral therapy by
activating 3A4 isoform of cytochrome P450. This effect may
result in decreased concentrations of protease inhibitors and
nonnucleoside reverse transcriptase inhibitors.
St. John's wort should not be used in conjunction with
SSRIs, especially in the elderly, as it may cause symptoms
of serotonin excess (hyperthermia, tachycardia, diaphoresis,
rigidity)
50. Depression – Non drug therapy
Consider psychotherapeutic options including:
Cognitive therapy
Interpersonal therapy
Problem-solving therapy
Offer patients with mild to moderate depression
psychotherapeutic options or drug therapy. Offer patients
with severe depression combination therapy with
psychotherapy and antidepressants
Consider combined drug therapy and psychotherapy in
patients with mild to moderate depression, but recognize
that there is limited available evidence showing added
benefit.
Treat patients with dysthymia with antidepressant
medication, but note that psychotherapy may play a role
in treating residual symptoms.
Treat patients with a history of major depression with
current subsyndromal depression using drug therapy to
achieve complete remission and offer psychotherapy to
treat residual symptoms.
51. Pregnancy & Mood disorders
Understand peri-partum mood disorders
Differentiate post partum blues from post
partum depression
Managing post partum blues and post
partum psychosis
Which drugs are safe in treating mania in
pregnancy?
52. Mania - Pregnancy
Lithium is teratogenic (Ebstein anomaly )
Valproic acid causes neural tube defects.
First trimester: Haloperidol for psychosis, clonazepam for
agitation; if mood stabilizer is necessary, lithium may be first
choice ( category D drug, but risk may be acceptable given the
problem of mania. ECT is an alternative ( but it as a
monotherpay may not be sufficient for mood stabilization –
ECT is safe in pregnancy, only issue might be fetal
arrhythmias).
Second/Third trimester/Postpartum: Lithium or
anticonvulsants, haloperidol and/or clonazepam if truly needed.
Continue treatment postpartum if no obstetric complications.
Follow breast-fed infants closely
55. Screen these pts
Ask direct questions to screen for abnormal eating
practices (calorie restriction, binging, purging etc)
in these groups:
Adolescents participating in gymnastics, dance,
wrestling, swimming, and other athletic programs
Adolescents with chronic diseases
Adolescents with a history of obsessivecompulsive personality traits or childhood anxiety
disorders
Persons with a family history of eating disorders
56. Diagnosis
Symptoms:
1. Ask about diagnostic criteria:
Eating and exercise patterns
Weight and patterns of weight loss
Attitudes about weight, body image, fear of weight gain
Amenorrhea or delayed menarche in females
Use of diuretics, laxatives, or purging behaviors
2. Ask about medical complications:
Abdominal pain
Bloating
Constipation
Cold intolerance
Dizziness, fatigue, and vague complaints
Loss of libido in both sexes
Changes in menstrual regularity, intensity, or duration in
females
57. Diagnosis – Look on
physical
Eroded tooth enamel from repeated forced
vomiting
Hair and skin changes such as yellow skin and
lanugo
Pitting edema or poor skin turgor
Brittle nails
Dry scaly skin
Parotid gland swelling
Russell's sign or abrasions on the dorsum of the
hand
Muscle weakness and muscle wasting
Discomfort or avoidance of being weighed
Weight loss recent > 10%
58. Anorexia Nervosa
Diagnose anorexia nervosa when all the
following are present:
Intense fear of gaining weight
Undue emphasis on body shape
Body weight <85% of predicted
Amenorrhea for 3 consecutive months
59. Bulimia Nervosa
Diagnose bulimia nervosa when all the following are present:
Recurrent episodes of binge eating characterized by
eating a larger amount of food than most people would
eat in a discrete period and a sense of having no control
over eating during the episode
Recurrent, inappropriate, compulsive behavior to prevent
weight gain, such as self-induced vomiting; abuse of
laxatives, diuretics, or other drugs; or excessive exercise
Binging and purging at least twice per week for 3 months
Self-evaluation unduly influenced by body shape and
weight
61. Labs
1. Obtain the following lab values in all patients:
CBC, Electrolytes, BUN , Creatinine, Glucose,
TSH
2. Obtain the following lab values in
malnourished and symptomatic patients:
Calcium, Magnesium, Phosphorus, Albumin
Liver function, ECG
3. Obtain FSH, LH, prolactin levels, and bone
densitometry if amenorrhea is present.
62. Differential Diagnosis
Consider other medical causes of weight loss,
progressive weight loss, and amenorrhea, such
as:
Chronic infections
Intestinal disorders with malabsorption
Endocrinopathies
Malignancy
Other psychiatric illnesses
Consider differential diagnosis early in
treatment, because patients may be in denial or
may withhold information concerning their fear of
fat.
63. Diagnosis
Some step3 questions might give you a pt with
eating disorder and may ask you to figure out
the next step by giving you clues through acidbase, electrolyte imbalances
Hypokalemia, hypochloremic Alkalosis seen
with Vomiting
Hypokalemia, Non anion gap Acidosis seen
with Laxative abuse Stool Laxative screen
Hypokalemia, Metabolic Alkalosis seen with
Diuretic abuse Urine Diuretic screen
64. Treatment – Eating
Disorders
Hospitalize patient for:
Severe malnutrition and associated complications:
Weight <75% of individually estimated healthy body
Metabolic abnormalities:
Potassium <3 mEq/L
Marked orthostatic hypotension, with one of the following:
An increase in pulse of >20 bpm
Blood pressure <90/60 mm Hg
A decrease in blood pressure of >20 mm Hg after standing
Bradycardia (heart rate <40 bpm) and other cardiac arrhythmias
Inability to sustain core body temperature (<97°F [36.1°C])
Signs of inadequate cerebral perfusion
Signs of dehydration or hepatic, renal, or cardiovascular organ
compromise requiring acute treatment
Comorbid psychiatric problems that heighten suicidal risk
such as exacerbation of a mood disorder or severe alcohol
abuse
65. Anorexia - Refeeding
Undertake refeeding of hospitalized patients with anorexia nervosa with care:
Set a realistic weight gain target of 2 to 3 lbs per week
Start intake levels at 30 to 40 kcal/kg per day (approximately 1000 to 1600
kcal per day) and progressively increase to as high as 70 to 100 kcal/kg per
day
Monitor serum potassium levels regularly in patients who are persistent
vomiters, and treat hypokalemia with oral or intravenous potassium
When life-preserving nutrition must be provided to a patient who refuses to
eat, choose nasogastric over intravenous feedings
Monitor patients for refeeding syndrome, especially those being aggressively
refed orally, enterally, or parenterally
At the initiation of treatment, monitor vital signs, food and fluid intake, and
output, and look for edema, rapid weight gain, signs of congestive heart
failure, and gastrointestinal symptoms
Monitor serum phosphorus, magnesium, potassium, and calcium daily for 5
days after initiating refeeding and every other day for several weeks thereafter
Obtain ECGs as indicated
Provide phosphorus, magnesium, and/or potassium supplementation when
indicated
66. Non-Drug therapy
Recommend psychotherapy for all patients with
anorexia nervosa.
Consider cognitive behavioral therapy for
patients with bulimia nervosa. Consider
medication (either fluoxetine or imipramine) in
conjunction with Cognitive Behavior therapy.
Recommend nutritional rehabilitation to all
patients with anorexia nervosa and bulimia
nervosa.
67. Drug Therapy
Consider the following therapy options:
Fluoxetine, 60 mg/d (one of the FDA-approved indications for
fluoxetine), or sertraline, 100 mg/d (not FDA approved), to
reduce the frequency of binge eating and purging (bulemia).
However, Psychotropic drugs have a minimal role in Anorexia
Ondansetron, a 5-HT3 antagonist, to decrease binge eating
and purging
Topiramate, a broad-spectrum anti-epileptic drug, to decrease
binge eating and purging
Light therapy in patients with bulimia nervosa with seasonal
exacerbation of symptoms
Note that bupropion is contraindicated in the treatment of
eating disorders due to an elevated incidence of grand mal
seizures.
Start estrogen and progesterone replacement with combined
oral contraceptives in patients with anorexia who have been
amenorrheic for more than 3 months to preserve bone mass
68. Exercise Induced
Amenorrhea
Female Athlete Triad : Disordered eating ,
osteoporosis and amenorrhea that occurs in
women engaged in regular strenuous exercise
or sports activities
Weight loss in athletes low body fat low
Leptin levels disruption of GnRh pulsatility
Reduced LH, FSH Anovulation and Reduced
estrogen Amenorrhea. Low body fat means
reduced peripheral (adipocyte) aromatization of
androgen precursors to estrogen, further
lowering total estrogen levels.
High Risk of Osteoporosis and Stress fractures (
get an x-ray if you suspect stress fracture)
69. Exercise Induced
Amenorrhea
Management
Get Dexa scan
Rule out other differentials prolactinomas,
hypothyroidism, PCOS
Decreasing intensity of training and improving
nutritional status are crucial steps in reversing
the pattern of menstrual irregularity.
Since oligomenorrhea is correlated with low
bone density, calcium supplementation and
adequate vitamin D intake are essential for bone
health.
Start Estrogen replacement in the form of Low
dose oral contraceptives.( for cycle regulation
and to improve bone density)
71. Diagnosis - Schizophrenia
1. The presence of at least two of the following for most of
time for at least 1 month:
Delusions
Hallucinations
Disorganized speech such as frequent derailment or
incoherence
Grossly disorganized or catatonic behavior
Negative symptoms such as affective flattening, alogia, or
avolition
2. Look for family history
3. There should be continuous signs of disturbance for at
least 6 months.
4. R/o Organic brain disease, metabolic disorders, drug
abuse, infectious diseases ( HIV, Sepsis, syphilis, brain
abscess, septic emboli) and malignancies
72. Schizo-affective disorder
At least two of the DSM IV criteria in the
previous slide for at least 1 month +
features of one of the following mood
disorders
A. Depression
B. Mania
73. Depression and Mania 1. Depression (at
of
Criterialeast fivetwo the following for a 2-week period, including
at least one of the first
items):
Depressed mood most of the day
Markedly diminished interest or pleasure in almost all activities
Significant weight change
Insomnia or hypersomnia
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings of worthlessness or excessive inappropriate guilt
Diminished ability to think or concentrate
Recurrent thoughts of death or suicide
2. Mania (four or more of the following at the same time, lasting at least 1
week or if hospitalization is needed; first item is required):
Elevated, expansive, or irritable mood lasting at least 1 week
Inflated self-esteem or grandiosity
Decreased need for sleep
More talkative than usual or pressure to keep talking
Flight of ideas or subjective experience that thoughts are racing
Distractibility
Increase in goal-directed activity, excessive involvement in pleasurable
activities that have a high potential for painful consequences
74. Schizophrenia Management
Hospitalize patients whose behavior may
cause harm to themselves or others
Obtain psych consult
Form an alliance with the patient's families
in caring for the pt as it is an essential part
of management.
Cognitive therapy
Psychoeducational family interventions
75. Schizophrenia - Drugs
A. Second-generation agents (First- Line therapy)
Olanzapine
Risperidone
Clozapine
Ziprasidone
Quetiapine 6. Aripiprazole
B. First-generation Agents
Trifluperazine
Thiothixine
Haloperidol
Fluphenazine
Chlorpromozine
C. Mood-stabilizers : Carbamazepine, Lamotrigine, lithium,
Divalproex sodium – use as adjuncts in schizoaffective
disorder
D. Anti-Depressants : use as adjunct in schizoaffective disorder
E. ANXIOLYTICS: BZDs ( Alprozolam, lorazepam, clonazepam,
diazepam, oxazepam), Buspirone. All BZDs cause
tolerance and may need up-titration of dose. Buspirone does
76. Drugs
effect
- Benefits- Side
Comparision
All second generation agents have less extrapyramidal side effects
( Akathisia, Acute dystonia, tardive dyskinesia, parkinsonism).
First generation agents are pure D2 antagonists where as second
generatio are both D2 and serotinergic antagonists.
Anticholinergic side effects ( drymouth, sedation, constipation) can occur
with most schizophrenia drugs.
Recognize presentation of anti-cholinergic delirium in geriatric pts using
these drugs.
Most agents – CPZ, Second generation agents – can cause orthostatic
hypotension. More of a problem with CPZ due to its Alpha1 antagonizing
properties.
Recognize Hyperprolactinemia can occur with most of these drugs
because they are dopamine (D2) antagonists. Less risk of
hyperprolactinemia and sexual dysfunction with Queitapine and
Aripiprazole.
Weight-gain is a problem. Only drugs that do not cause much weight gain
are Ziprasidone and Aripiprazole. Olanzapine, Queitapine and Risperidone
cause significant weight gain
Neuroleptic Malignant syndrome is more likely with first generation
agents, however, can be possible with second generation agents.
Photosensitivity is a unique side effect of CPZ.
77. Drugs
effect
- Benefits- Side
Comparision
Weight gain that’s a common side effect of these drugs –
lead to insulin resistance and dyslipidemia. Get lipid panel
and FBS
Clozapine has a dreadful side effect – Agranulocytosis –
hence monitor blood count. D/C the drug if signs of infection
appears and then get a blood count stat.
Clozapine also has high risk of seizures. Haloperidol reduces
seizure threshold.
Haloperidol, Ziprasidone can prolong QT interval. Caution :
concomitant use with quinolones, anti-arrythmics, Tricyclics
etc that also prolong QT – can lead to Torsades/ Vfib
Risperidone is usually first choice to treat Schizophrenia
because it is least sedating. Use olanzapine if insomnia is an
issue ( Anticholinergic – sedative effect). If positive symptoms
are very predominant, use Haloperidol.
78. Schizophrenia Management
In Symptomatic schizophrenia, start antipsychotic
treatment ASAP.
For Typical symptoms of schizophrenia or
schizoaffective disorder, consider the newer, secondgeneration antipsychotics as first-line agents.
Start lowest possible doses to minimize side effects.
Improvements can be slow and may take 4 to 6 weeks to
achieve a medication-steady blood state SO, avoid
increasing the dosage before an adequate period
Continue antipsychotic medication for at least 1 year
after a full remission of psychotic symptoms. After this a
trial off medication may be considered except in suicidal
or violent patients
In chronic, relapsing illness, use antipsychotic
medications for a minimum of 5 symptom-free years.
79. Schizophrenia management
In stable pts, reduce dose reduction to the lowest possible dose
that controls symptoms When tapering medications, reduce the
dose very slowly (10% to 20% per month) and observe the patient
every 2 weeks. Return to the previously effective dose if there is
an exacerbation of symptoms.
Use clozapine in treatment-refractory patients ( and for those
with predominant negative symptoms) in whom adequate trials of
at least two agents from dissimilar chemical groups have failed
and when adherence is not an issue. ( Caution: Agranulocytosis)
Use lowest possible doses in the elderly.
Use long-acting injectable (risperidone) or depot (haloperidol or
fluphenazine) medication in patients nonadherent to oral therapy
or those who are forgetful about using Rx.
80. Schizophrenia management
Be sure to monitor weight monthly and test for blood
glucose and lipid abnormalities at least every 12 weeks in
patients on second-generation agents.
Recognize that side effects of some second-generation
antipsychotics may lead to health problems such as
obesity and diabetes
Consider prophylactic use of anti-Parkinson agents such
as benztropine to reduce extrapyramidal side effects on a
case-by-case basis when using antipsychotic agents.
Consider clozapine in people who are judged to be at risk
for suicidal behavior
In patients with concurrent mood symptoms use adjuncts
to Antipsychotic therapy –
1. For Depression use SSRIs
2. For Mania – use mood stabilizers
3. For anxiety, use anxiolyitics
81. Addressing Extrapyramidal Side
effects
Akathisia : An acute side effect. Can also be Tardive.
Acute means onset within 6 weeks of initiation of the drug.
Tardive akathisia is the one that appears after a minimum
of 3 months’ exposure to an antipsychotic agent. Akathisia
can also appear as a withdrawal from antipsychotics.
Common with first-generation antipsychotics
(neuroleptics)
Defined as subjective (feeling of inner restlessness and
the urge to move) as well as objective components
(rocking while standing or sitting, lifting feet as if marching
on the spot and crossing and uncrossing the legs while
sitting) Treatment is Beta blockers. If b-blocker fails,
consider BZDs. If everything failed, use clonidine/
amantidine.
82. Addressing Extrapyramidal Side
effects Akathisia and Restless Legs Syndrome
Distinguishing
Position
Myoclonic jerks
Akathisia
Sub-diaphragmatic
Restless Legs Syndrome
Usually from ankle to knee
Rare
Very common: especially at night
Subjective distress
Almost invariable
Common and is due to disturbed sleep
Relieved by movement
Rarely
Almost always
Motor component
Almost always
Rarely
Sensory component
Usually present
Always present; dysesthesia
Worsening on lying
Rare
Very common
Sleep disturbance
Rare
Almost always present
Movements if able to sleep
Stop
Continue almost unabated
Help from behavioral tricks e.g. walking, stretching, massage, cold compresses
Rare
Almost always
83. Addressing Extrapyramidal Side
effects
Acute Dystonia : Dystonia is a brief or sustained muscle spasm, often with
Acute Dystonia : Dystonia is a brief or sustained muscle spasm, often with
slow abnormal movements. Although any muscle group may be involved, it
most commonly affects facial muscles (eyes, jaw, tongue).
In differentiating from Tardive dyskinesia consider the onset. Onset here is
acute ( within 24 hrs after administering the agent)
Acute dystonia – causes
1. Toxic causes : Metoclopromide, Antipsychotics (Haloperidol, phenothiazines),
Lithium, chloroquine, levodopa, cocaine
2. Non toxic : Spinocerebellar degeneration, Thyrotoxicosis, Wilsons disease,
Tumor, A-V malformation, CVA
Differential : Catatonic states, Dyskinesias, Seizures
Treatment : Dystonias may increase in severity after initial presentation and
therefore all patients should be treated. Initial treatment is usually provided
with a parenteral formulation, followed by oral medication for 2 to 3 days to
prevent recurrence. Milder forms can be treated with oral medication alone.
Choices: ( physiology involves cholinergic excess. So use, anticholinergic Rx)
1. Benztropine : 1mg IM/IV followed by 1mg orally daily
2. Diphenhydram 1MG/KG IM/IV followed by oral
3. Diazepam
4. Trihehiphenydyl.
84. Types of Acute Dystonia
Various types of dystonia, involving particular
muscle groups have been described:
Laryngeal dystonia - spasm of pharyngeal and
laryngeal muscles resulting in stridor.
Oculogyric crisis - spasm of extra-ocular
muscles, forcing the eyes into upward or lateral
gaze.
Opisthotonus - spasm of all paravertebral
muscles, forcing the trunk and neck into
hyperextension.
Retrocollis - spasm of paravertebral neck
muscles, forcing the neck into hyperextension.
Torticollis - spasm of lateral neck muscles,
twisting the neck to one side.
85. Addressing Extrapyramidal Side
effects
TARDIVE DYSKINESIA
Occurs with long term use of antipsychotics/ Dopamine antagonists
Risk factors for developing TD: treatment with first generation antipsychotics,
More than 6 months of antipsychotic treatment, Increased length of medication
therapy, Antipsychotic dose change—either increase or decrease, Diagnosis of
organic mental disorder or mood disorder, Increasing age, Diabetes and
Genetics
Eventhough more common with First generation (typical) antipsychotics it also
copmmonly occurs with second generation drugs.
Symptoms : Involuntary movements, which develop with after long term
antipsychotic exposure, are present for at least 4 weeks and may be:
Choreiform movements (rapid, jerky, nonrepetitive, purposeless)
Athetoid movements (slow, sinuous, continual)
Rhythmic movements (stereotypes)
Peri-Oral movements most common : Darting, twisting, protruding movements of
the tongue (lip-licking, sucking, smacking, “fly-catching tongue), Chewing and
lateral jaw movements, Lip puckering and Puffing cheeks
Other movements : Trorticollis, retrocollis, Trunk twisting, rocking, hand
clenching, facial grimacing, blinking etc
There is no specific treatment once TD appears. Delaying its appearance and
prevention are the only options : using atypical antipsychotics, using lowest
possible dose are some strategies.
87. Note :
Clozapine’s greater efficacy as an
antipsychotic drug may be related to its higher
affinity for the D4 than the D2 receptor. No
typical neuroleptic has a similar D4/D2 ratio.
This different mechanism of action may also
account for its beneficial effect in treating TD
Clozapine is the drug of choice in refractory
schizophrenia ( i.e.; after no response to two
different antipsychotic agents)
89. PTSD
After a traumatic event normal individuals may
experience symptoms for a short period such as:
Nightmares, Flashbacks, Anxiety attacks , Startle
reactions , Insomnia, Irritability, Anger,
Depressed mood, Guilt & Poor appetite. If they
last more than 1 month PTSD.
Recurrent symptoms of Flashbacks and Hyper
vigilance are characteristic to PTSD ( No
flashbacks with Adjustment disorder)
Time course : < 1 mo: acute stress disorder
, > 1 month PTSD
Spontaneous recovery from acute stress disorder
is common (>50%), but a high level of symptoms
during the first month is a risk factor for PTSD
90. PTSD - Management
Non – Pharmacological Therapy
Cognitive-behavioral therapy, exposure therapy, and
trauma-related anxiety management. Group therapy also
useful
Drug Rx :
SSRIs Start with low dose and titrate up to maximum
effect.
Switch to different agents or add adjuncts if response to
SSRI is inadequate.
Trazadone and sedating TCAs may be used as adjuncts
to SSRIs, particularly for insomnia
In difficult cases, consider Phenelzine.
