Is your anxiety linked to place, situation, physical Sx, thought stick, ritual to stop

Questions to ask about panic disorder, OCD and GAD

For anxiety disorders generally

• Is your anxiety or worry predictable? Does it only ever happen in certain situations

or places, like shopping malls?

• Does your anxiety or worry ever go away?

• Do you have anxiety attacks that come from out of nowhere?

• Is your anxiety or worry linked with physical symptoms such as a racing heart,

shortness of breath and sweating?

• Do you always feel wound up, on edge or nervous?

• Do you have any thoughts that come into your head and make you worry?

• Are there rituals or things you have to do to stop feeling worried or to prevent a

catastrophe?

For GAD

• Do you often feel anxious, nervous, worried or on edge?

• How often? Most days, some days or almost never?

• How difficult is it to control your worry? Very, a bit or not very difficult?

• Is your worry realistic or reasonable or is it out of control?

• What do you worry about? One thing, or many things? Do you worry a lot about

too many things?

• Does your worry or anxiety help you, or does it interfere and slow you down?

• Do you have trouble relaxing?

• Do you feel fidgety because of your worry?

• Do you find you are becoming easily annoyed or irritable?

• Does it feel like something terrible might happen?

SSRIs and suicide

SSRIs and suicide

SSRIs are less toxic and have fewer unwanted effects than tricyclic antidepressants but it seems they may, paradoxically, induce suicidal behaviour in the young.
It is not easy to establish whether this is true because depression also increases suicide risk and the data are contradictory. Pharmaco-epidemiological and ecological studies suggest that increased use of SSRIs may have resulted in a reduction in youth suicide, and that SSRIs are not taken more often than expected by young suicide victims. However, a review of 24 controlled trials with more than 4400 children and teenagers by the US Food and Drug Administration showed a small (2%) short-term increase in the incidence of suicidality (suicidal thoughts or attempts) in those receiving antidepressants (mostly SSRIs) compared with placebo. There were no completed suicides and this result was not replicated when questionnaires, rather than reports from parents or children, were used as the basis for information. According to this research, 50 teenagers need to be treated for one to develop suicidality attributable to the antidepressant.

The mechanisms underlying this phenomenon are unclear but SSRIs, particularly paroxetine, can induce akathisia, agitation and irritability — so-called ‘activation' — and this may be an indicator of increased suicide risk.

Teenager depression - mood, interest, appetite, sleep, energy, concentration, suicide

the teenager unhappy or irritable? OR Does the teenager show loss of interest or pleasure in most activities?

(This happens most of the day, nearly every day for at least two weeks)

Yes

Does this teenager show at least five of the following?

� Depressed or irritable mood

� Loss of interest in activities

� Significant weight or appetite change

� Insomnia or hypersomnia

� Psychomotor agitation or retardation

� Fatigue or loss of energy

� Feelings of worthlessness or guilt

� Diminished ability to think or concentrate, or indecisiveness

� Recurrent thoughts of death or suicide

Yes

Do these symptoms cause clinically significant distress or impairment in social, school or family functioning, and are they not due to bereavement?

Yes

Is there a history of manic or hypomanic symptoms (eg, periods of elation or elevated mood) or a family history of bipolar disorder?

No Yes

Major depressive disorder is likely

Figure 1: Is this teenager depressed?

Consider other diagnoses or problems

Consider the possibility of bipolar disord

It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.

It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.



What are mania and hypomania? Mania is defined on the basis of symptoms and signs that are out of character for the individual and usually occur in discrete episodes (table 1). In the DSM-IV the diagnosis of mania requires the persistence of euphoric mood for a period of at least seven days, during which a minimum of three additional symptoms (four if mood is mainly that of irritability) are present. Technically, the predomi-nant mood is either that of excessive happiness, described as euphoria, or, alternatively, feelings of irri-tability. In practice, individ-uals will often describe feel-ing “pumped up” and “energised” or “wired”, with a notable increase in drive and goal-directed activ-ity that often results in increased pleasure-seeking behaviour. Other features include a decreased need for sleep, racing thoughts and dis-tractibility. Not surprisingly, many of these symptoms, and risk-taking behaviour in particular, can result in sig-nificant social or occupa-tional impairment, with potentially painful conse-quences such as risk to health, livelihood or reputa-tion. The symptoms and signs of mania can be conve-niently remembered using the mnemonic FIDGETS. (table 2). Hypomania is defined along the same lines as mania with regard to signs and symptoms, but the term is usually used to describe briefer periods of mood dis-turbance that generally incur less functional impairment than in mania. The DSM-IV employs a somewhat arbi-trary cut-off of four days' duration to define hypomania, but in practice this is often difficult to apply. In practice the diagnosis of hypomania is less reliable than that of mania or depression and it is seldom spontaneously reported because it is usually mild and transient and construed as a pleasant experience. People with bipolar disorder often consider periods of hypomania to be ‘normal' and understandably regard them as desirable, and rarely present clinically with such symptoms. However, it is important to remember that hypomanic symptoms are, more often than not, functionally dis-abling and that it is critical

to screen for manic or hypo-manic symptoms even in patients presenting with depression. This is important because identifying previous hypomania distinguishes a subsequent depressive episode as bipolar rather than unipolar. It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.

What is bipolar depression? Although mania is the hall-mark of bipolar disorder, it is the depressive phase of bipolar illness that is the pre-dominant component of this illness both in terms of time spent unwell and the associ-ated functional disability. This bias in morbidity towards depression is even more pronounced in bipolar II disorder compared with bipolar I disorder. Like unipolar depression, bipolar depression is associ-ated with an increased risk of suicide. However, bipolar depression differs from its unipolar counterpart in sev-eral ways. An abrupt, earlier age of onset is more likely in bipolar depression, com-pared with a more gradual onset and offset in unipolar depression. A family history of bipolar

from page 25


test

Antedates

Ice antidotes

||Ecstasy poisoning #

@Ecstasy is a semi-synthetic, hallucinogenic substance =(MDMA, 3,4-methylenedioxymethamphetamine). @Its effects range from= nausea, muscle pain, blurred vision, amnesia, fever, confusion, and ataxia to tachyarrhythmias, hyperthermia, hyper/hypotension, water intoxication, DIC, K+↑, acute renal failure, hepatocellular and muscle necrosis, cardiovascular collapse, and ARDS. @There is no antidote and treatment is supportive. Management depends on clinical and lab findings, but may include:=

 Administration of activated charcoal and monitoring of BP, ECG, and temperature for at least 12h (rapid cooling may be needed).  Monitor urine output and U&E (renal failure p293), LFT, CK, FBC, and coagulation (DIC p336). Metabolic acidosis may benefit from treatment with bicarbonate.  Anxiety: diazepam 0.1-0.3mg/kg PO. Max IV does over 2min.  Narrow complex tachycardias in adults: consider metoprolol 5-10mg IV.  Hypertension can be treated with nifedipine 5-10mg PO or phentolamine 2-5mg IV. Treat hypotension conventionally (p778).

JVP

Jugular venous pressure (pulse)
Causes of an elevated central venous pressure
Right ventricular failure
Tricuspid stenosis or regurgitation
Pericardial effusion or constrictive pericarditis
Superior vena caval obstruction
Fluid overload
Hyperdynamic circulation
Wave form
Causes of a dominant a wave
Tricuspid stenosis (also causing a slow y descent)
Pulmonary stenosis
Pulmonary hypertension
Causes of cannon a waves
Complete heart block
Paroxysmal nodal tachycardia with retrograde atrial conduction
Ventricular tachycardia with retrograde atrial conduction or atrioventricular dissociation
Cause of a dominant v wave
Tricuspid regurgitation
x descent
Absent: atrial fibrillation
Exaggerated: acute cardiac tamponade, constrictive pericarditis
y descent
Sharp: severe tricuspid regurgitation, constrictive pericarditis
Slow: tricuspid stenosis, right atrial myxoma