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Living Healthfully - September 2009

A Type of Drug-Food Interaction 2

September 30th 2009 06:39
Brief Discussion on Depression
“Major depressive disorder (also known as clinical depression, major depression, unipolar depression, or unipolar disorder) is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and loss of interest or pleasure in normally enjoyable activities. The diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status exam. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. The most common time of onset is between the ages of 30 and 40 years, with a later peak between 50 and 60 years. Major depression is reported about twice as frequently in women as in men, although men are at higher risk for committing suicide (Wikipedia.org)”.

The theories on what causes depression are numerous and variable. Scientists attribute depression to biological alterations, psychosocial impairment, or alcohol-drug abuse. Nevertheless, an explanation under biological causes has provided the major experimental models for the discovery of potential management for patients suffering from the condition (Potter and Hollister, 2007). Such explanation claims that depression arises due to low levels of monoamine neurotransmitters in the body. These neurotransmitters include serotonin, norepinephrine, and dopamine. Naturally, these chemicals are involved in alertness, energy, attention, motivation, pleasure, and reward. Disrupting their production and release, or promoting their reuptake and degradation causes these chemicals to become depleted, therefore leading to the signs of depression.
Management of the condition includes psychotherapy and anti-depressant drugs. Anti-depressants can be grouped into tricyclic antidepressants (imipramine and amitryptyline), second generation and subsequent antidepressants (amoxapine and maprotiline), selective serotonin reuptake inhibitors (flouxetine), monoamine oxidase inhibitors (phenelzine and in our case iproniazid, which is already withdrawn from the market). For our purpose, we shall be discussing the mechanism of monoamine oxidase inhibitors (MAO inhibitors) at the later part of the discourse.

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A Type of Drug-Food Interaction

September 28th 2009 06:38
A patient comes in with the following details:

•Has been suffering from depression
•Tried several anti-depressants but nothing worked for her, except for Iproniazid
oIproniazid is a MAO inhibitor, can be considered as a last line for depression management
oIproniazid then was a new drug and side effects are yet to be discovered.
oHer doctor asked her to notify him in case of any unusual effects
•Condition improved and was able to return to usual life
•Hosted a wine and cheese party during which she had severe headache
•In the hospital BP is at 230/160 mmHg
•MD administered phentolamine ( non-selective Alpha receptor antagonist) to address HPN

Then we ask the following:
Why Did the Patient Had Headache and Hypertension Crisis Upon Intake of Wine and Cheese?
Patient was given Phentolamine. How does it act? Why was it useful in this case?
Why didn’t the physician use a Beta-adrenoceptor antagonist to treat the condition?

to be continued...
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-by Rinka, Hiroshi et al. (2008); Published by Biomed Central Paediatrics


Hemorrhagic shock and encephalopathy syndrome (HSES) is a rare but devastating disorder in the young children. It is a disease of unknown aetiology and presents as acute onset of encephalopathy, shock, watery diarrhea, severe disseminated intravascular coagulopathy (DIC), and renal and hepatic dysfunction. Patients manifesting the condition have very poor prognosis with a fatal course or severe neurologic sequelae.

The cause of such clinical picture and outcome may be partly attributed to the delay in diagnosis and therefore, delay in management. HSES may be mistaken for another disease of the nervous system, especially in its initial stage. At times clinicians misdiagnose then, provide a management inconsistent with HSES. Then they may wonder why the symptoms just cannot be controlled. By the time distinctive signs and symptoms of HSES appear, multiple organ failure has occurred. At this point modifying treatment may be too late, and a patient may have died. This elaborates tremendous loss of time, resources, and even life. And so the investigators of the research emphasized a need of early detection of HSES. Resolution of such need will definitely improve survival and reduce neurological sequelae.

The research is a retrospective study made in 2008. The authors of the journal recalled the course of hospitalization of eight patients, who met the classical HSES criteria. These patients were admitted to Intensive Care Unit (ICU), between November 2001 to August 2007. Patients’ age range from four months to nine years old at the time of admission.

The investigators examined the clinical, biological, and radiological findings of the patients/ subjects. The results were summarized by the investigators as follows:
“Although cerebral edema, disseminated intravascular coagulopathy (DIC), and multiple
organ failure were seen in all 8 cases during their clinical courses, brain computed tomography (CT) scans showed normal or only slight edema in 5 patients upon admission. All 8 patients had normal platelet counts, and none were in shock. However, they all had severe metabolic acidosis, which persisted even after 3 hours (median base excess (BE), -7.6 mmol/L). And at 6 hours after admission (BE, -5.7 mmol/L) they required mechanical ventilation. Within 12 hours after admission, fluid resuscitation and vasopressor infusion for hypotension was required. Seven of the patients had elevated liver enzymes and creatine kinase (CK) upon admission. Twenty-four hours after admission, all 8 patients needed vasopressor infusion to maintain blood pressure (Rinka et al, 2007).”

Most of the classical signs and symptoms of HSES, as detected by different laboratory and physical examinations are absent initially. CT scan, platelet count, haemoglobin level, and renal function are not useful therefore in early diagnosis. However, the elevated liver enzymes and CK upon admission, hypotension in early stage after admission, acid-base disturbances, and vasopressor infusion are useful markers. This fact is very helpful in starting neurological treatment even before severe neurological manifestations occur.
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