Facts on Menstrual cycle

When I was still a student, I didn’t like maternal and child nursing or topics that pertain to taking care of pregnant women and the child. I really find it hard to understand and memorize facts about it and so I really am having difficulty appreciating it. But then again, when you are in this profession or whatever profession you are in right now you really could not get away from topics that you hated most back when you were studying. And so, I would like to take this opportunity to share to you some information’s from Maternal and child nursing which I think is very helpful not only for me but also for all of the students out there who are finding their way to becoming a nurse. Lets start from some basic concepts.

Menstrual Cycle Physiology

What is the average duration of the                              The average duration of the

menstrual cycle, duration of menses, and                  menstrual cycle is 28 days. The

amount of blood loss during menses?                         average duration of menstrual flow

is 4 days. On an average, women lose

less than 60 mL of blood during each

menses

What are the two phases of the menstrual                 Follicular (or proliferative) phase and

cycle and how long does each last?                             the luteal (or secretory) phase,

separated by ovulation. (Follicular/

luteal describe the ovarian changes,

proliferative/secretory describe the

endometrial changes)

By convention, day 1 marks the onset

of menses. The follicular phase begins

on day 1 and lasts approximately

14 days (days 1–14) in a 28-day cycle,

until ovulation occurs. The luteal

phase then commences and lasts until

approximately day 28 (days 14–28)

What causes the variability in the length                     The duration of the follicular phase

of the menstrual cycle?                                                    (the luteal phase is constant)

Describe the hormone pathway involved                    The cycle begins in the arcuate

in the menstrual cycle (see Fig. 4-1) and                     nucleus of the hypothalamus where

name which structures produce                                   gonadotrophin-releasing hormone

each hormone                                                                     (GnRH) is released in a pulsatile

fashion. GnRH stilmulates the

anterior pituitary to release folliclestimulating

hormone (FSH) and

luteinizing hormone (LH). These

gonadotropins then cause the ovaries

to release the sex steroid hormones

estradiol and progesterone.

Estrogenand progesterone feedback

negatively on both the hypothalamus

andthe pituitary gland

What is happening in the ovary during the                     The ovary beings with

menstrual cycle?                                                               approximately one million primordial

follicles at birth (20 million at week

20 in utero). Each follicle contains an

oocyte arrested in prophase of

meiosis. The oocyte is surrounded by

pre-granulosa cells and these are

surrounded by pre-theca cells. In the

follicular phase, FSH stimulates the

pre-granulosa cells to become

granulosa cells. The granulosa cells

secrete estradiol. The pre-theca cells

in turn become theca cells and secrete

androgens, which are aromatized by

the granulosa cells into estradiol.

One follicle with the highest number

of granulosa cells, FSH receptors, and

estradiol production becomes the

dominant follicle and all other

follicles become atretic. This follicle is

released during ovulation and

becomes the corpus luteum. The

corpus luteum secretes progesterone

and a smaller amount of estrogen

during the follicular phase of the

cycle. If fertilization does not occur, it

degenerates into the corpus albicans

What is the function of the corpus luteum?                Secretion of progesterone and

estradiol. It is the only structure that

produces progesterone in significant

quantities which sustains the

pregnancy until the placenta is

developed

What is happening to hormone levels in                      At menstruation, concentrations of

the follicular phase?                                                          estradiol, progesterone, and LH are

at their lowest point. FSH and LH

levels begin to rise in response to

the low estrogen and progesterone.

Estradiol levels, secreted from the

dominant ovarian follicle, begin to

rise by day 4. Just before ovulation,

estradiol levels peak. This peak

causes a positive feedback on LH

secretion, leading to the LH surge

and a smaller FSH surge, which

results in ovulation 30–38 hours

later. Progesterone levels remain low

throughout the follicular phase

 

What is happening to hormone levels in                      The LH surge causes granulosa and

the luteal phase?                                                                theca cells to secrete progesterone

and smaller amounts of estrogen.

Progesterone peaks 3–4 days after

ovulation.

Estrogen levels decrease immediately

after ovulation but slowly rise with

the growth of the corpus luteum.

Progesterone and estrogen (at low to

moderate levels) both act via negative

feedback to suppress LH and FSH. If

fertilization and implantation do not

occur, progesterone and estradiol

levels diminish after 11 days. FSH

increases as the corpus luteum

regresses

What is happening to the endometrium in                   At menses, the endometrium sloughs

the proliferative phase?                                                   off until it becomes a thin line. During

the proliferative phase estradiol levels

rise, resulting in the proliferation of

the uterine endometrium. The

endometrium becomes thicker and

more glandular and the spiral arteries

elongate. On ultrasound, it appears as

a “triple stripe” pattern

What is happening to the endometrium in                   The progesterone released from the

the secretory phase?                                                        corpus luteum leads to slowing of

endometrial proliferation,

reorganization of the glands (resulting

in a more edematous stroma), and

further coiling of the spiral arteries.

This results in the loss of the “triple

stripe” pattern and its replacement

with a uniformly bright

endometrium. If pregnancy does not

occur, the endometrium degenerates

What are the primary clinical                                          Estradiol

manifestations of estradiol and                                     Endometrium: thickens stroma and

progesterone during the menstrual cycle? elongates glands (creates proliferative

endometrium); Endocervix: stimulates

secretion of thin, watery mucus.

Produces “ferning” pattern when

spread on a glass slide;

Vagina: promotes vaginal thickening

Progesterone

Endometrium: causes tissue to

become edematous and blood vessels

to thicken and twist (creates

secretory endometrium);

Endocervix: thickens endocervical

mucus, causing it to become stringy;

Breast: stimulates acinar glands,

causing breasts to round;

Other: raises basal body temperature

by 0.6–1°F. Causes some women to

have the emotional, physical, and

behavioral changes of premenstrual

syndrome (PMS)

What layer of the endometrium sloughs                      The functionalis layer (inner layer)

off during menses?                                                           sloughs off after glandular and

stromal degeneration

What hormone mediates menstrual                             Prostaglandins, especially PGF2á. It is

cramps and how is it synthesized?                               released by the secretory

endometrium in response to

progesterone and causes uterine

contractions

That’s it. Hope you learned something from this. Next time, I will be posting about family planning.. till next time..

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Transactional analysis

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Neuropsychaitry (part 2)

Here's the part to of what ive recently posted regarding neuropsychiatry: This really will help student nurses and nurses alike in their review in understanding psychiatric nursing. Enjoy and learn:

❍ What are some other terms for “pseudoseizure”?
Conversion reaction, hysteroepilepsy, and nonepileptic seizure (the preferred term).

❍ How can a seizure disorder be distinguished from schizophrenia?
Altered mentation from a seizure tends to be ego-dystonic, and the patient can talk about the symptoms in a detached manner. There is generally no evidence of interictal changes on the mental status examination, and the premorbid social histories are generally good. The seizure disorder is characterized with abrupt rather than gradual alterations in personality, mood, and ability to function that are unresponsive to psychiatric or psychological intervention. The patient generally does not quite meet DSM-IV criteria for schizophrenia.

❍ How can a seizure disorder be distinguished from a panic disorder?
Often a difficult distinction, because both conditions have overlapping symptoms—depersonalization, fear, d´ej`a vu and jamais vu, dizziness, illusions, paresthesias, chills, and flushes, which are in part mediated by a similar underlying limbic dysfunction (the temporal lobe modulates fear, for example) and amenable to similar pharmacologic intervention, i.e., benzodiazepines. However, in panic disorders, consciousness is preserved, an EEG will be normal, there are seldom olfactory hallucinations, family history is usually positive, there are no
automatisms, and a positive response is found not to anticonvulsants but to antidepressants (which would typically worsen complex partial symptoms). In addition, panic attacks usually last longer than seizures, and agoraphobia is a prominent symptom in panic but not seizure.

❍ Is there a particular personality type associated with seizure disorder?
Of the qualities traditionally associated with the “epileptic personality type”—dependency, humorlessness, hypergraphia, hyposexuality, religiosity, viscosity, paranoia, and a preoccupation with philosophical or moral concerns—evidence exists only for hyposexuality, as a reflection of a secondary endocrine abnormality evoked by seizures.

❍ Are seizures associated with aggression?
Aggression during a seizure is very unusual, and when it does occur is typically disordered, uncoordinated, undirected, and associated with restraint or postictal paranoid psychosis.

❍ What strategies can be used in treating psychiatric symptoms associated with a seizure disorder?
Strategies that can be used to treat the neuropsychiatric aspects of seizure disorders include assessment of the social factors that aggravate the seizure disorder; adjustment of the anticonvulsant as necessary to minimize seizures, using monotherapy if possible; use of psychotropic medications to target specific psychiatric symptoms, anticipating interactions, using low initial dosages, and waiting for a response plateau before changing the dose again; targeting psychotherapeutic approaches to specific behaviors or stressors; and finally collaboration with all caregivers.
❍ What are the symptoms of Parkinson’s disease?
Parkinson’s is a progressive, nongenetic disorder that presents with both motor and cognitive symptoms. The motor symptoms typically have an asymmetric onset, and consist of bradykinesia and muscular rigidity, flexion at trunk and neck leading to postural instability, difficulty initiating movements, lack of facial expression, and a 4 to 6 Hz resting tremor. Ninety-three percent of those with Parkinson’s suffer cognitive deficits—reduced verbal fluency and naming difficulties, deficits in visual analysis and constructional praxis, and executive dysfunction similar to frontal lobe syndrome—difficulties in selective attention and set maintenance. Recognition memory is usually unimpaired, but procedural memory shows deficits.

❍ What is the etiology of Parkinson’s disease?
The etiology is unknown, although some hypothesize that it is related to exposure to environmental toxins. The bradykinesia and rigidity can be related to progressive loss of neurons in the substantia nigra. There is reduced
dopamine uptake in the putamen. In addition to dopamine, neurotransmitter abnormalities are found in the somatostatin and CRF systems. There is an increase in the number of muscarinic cholinergic receptors (unlike in Alzheimer’s) but a decrease in nicotinic. Pathology shows Lewy bodies in the locus ceruleus, substantia
nigra, and hypothalamus (in contrast to Lewy body dementia, in which Lewy bodies are found in the cortex also).
❍ What are the neuropsychiatric symptoms in Parkinson’s disease?
Depression occurs in 40% to 60%, often before the onset of motor symptoms, and is unrelated to either the duration or severity of the disease or the response to medications, but is associated with dementia. Parkinson’s depression is characterized more by dysphoria, sadness, irritability, pessimism, and suicidal ideation, less by guilt and self-blame. Actual suicide is rare, unlike in Huntington’s chorea. Psychotic symptoms are common (occurring in up to 50% of patients at some point of the disease) usually as a side effect of anticholinergic medications, but can also occur as a result of mood disturbance, other medications, sleep deprivation, or the dementia associated with Parkinson’s disease. The psychotic symptoms can range in severity from hallucinations that cause no distress to delusional states with agitation and terrifying hallucinations of all types.

❍ What tests can help diagnose Parkinson’s?
PET scans show decreased uptake in the striatum, while CT scan and MRI show decreased volume in the substantia nigra of advanced cases. EEG shows nonspecific slowing.

❍ What percentage of patients with Parkinson’s disease manifest dementia?

From 10% to 40%, the risk rising with age. Other risk factors for dementia in Parkinson’s disease are family history, depression, and motor disability.

❍ What are some treatments for Parkinson’s and its associated neuropsychiatric symptoms?
l-Dopa is a dopamine agonist that can help compensate for the bradykinesia and rigidity, as do anticholinergics, but there is no treatment for the postural instability except for physical and occupational therapy. Antidepressants work normally on Parkinson’s patients, but this population is very sensitive to the anticholinergic, sedating, and orthostatic effects of these drugs. ECT is effective for both the affective and motor symptoms. If antipsychotics must be used, atypicals with minimal extrapyramidal side effects will have the least effect on motor symptoms. Quetiapine and clozapine have been shown to be the most effective in controlling psychotic symptoms in Parkinson’s-related psychosis, while aripiprazole is minimally effective and can exacerbate motor function. Risperdal is generally poorly tolerated in these patients and should be avoided. Whenever the use of atypicals is indicated in patients with Parkinson’s disease, monitoring for neuroleptic malignant syndrome–like symptoms is essential, and can be very difficult to distinguish from baseline symptoms. Again, the use of typical neuroleptics such as haloperidol is generally contraindicated, although may be necessary when agitation becomes a safety issue.

❍ What symptoms can occur as a side effect of treating a patient with Parkinson’s disease?
Anticholinergic drugs, while being the most effective in suppressing the parkinsonian tremor, are also the most prone to induce psychosis. Delusions are usually dose related, frequently persecutory, and preceded by vivid dreams or visual hallucinations. Risk factors for delusions are age and concurrent dementia. Thirty percent of treated Parkinson’s patients will hallucinate fully formed animal or human figures, typically at night and with the hallucinations associated with sleep disturbance. These differ from typical anticholinergic hallucinations in that
they are less threatening, more fully formed, not combined with tactile or auditory stimuli, and not associated with delirium. Delirium occurs in 5% to 25% of patients as a medication side effect, with bromocriptine and pergolide particularly implicated. l-Dopa can cause anxiety.

❍ What is delirium?
Delirium is a pattern of diffuse, reversible cognitive deficits with acute onset, and a waxing and waning course. The deficits can include delusions (20%–70%), perceptual disturbances, mood alterations, language (50%–90%) and thought disorders (95%), sleep/wake disturbance (50%–95%), hallucinations (30%), and psychomotor alterations. Disorientation is common, to time (80%), place (70%), and person (20%). Twenty percent of hospital patients will become delirious, and if elderly, the 1-year mortality will be 40%. Some clinicians distinguish between acute confusional state, a disorder of attention associated with frontostriatal dysfunction, and acute agitated delirium, a disorder of emotion associated with middle temporal gyrus dysfunction, but many patients present with a mixed picture.

Neuropsychiatry (part 1)

Here is again another installment to one of my favorite subjects in nursing which is psychiatric nursing.. I wanna help those aspiring students out there who want to be a nurse in the future. I hope this will help you learn more about your chosen profession:

❍ What percentage of brain tumors will cause psychiatric symptoms?
Fifty to eighty percent.
In 20%, the psychiatric symptoms are the first indicator that a tumor exists. Of psychiatric patients, between
0.1% and 3% will have a brain tumor.

❍ What is the most common psychiatric presentation of a brain tumor?
Apathy, depression, irritability, agitation, and an altered level of consciousness—all caused by an increase in intracranial pressure. Often, tumors will cause an exaggeration of previous character traits and coping styles.
Delusions caused by tumors are typically less complex than those characteristic of schizophrenia, and hallucinations are more often visual than auditory. Left-sided tumors are associated with depression and akinesia, while right-sided tumors present with euphoria and an underestimation of the seriousness of the illness. Focal neurologic signs are
common.

❍ Does the psychiatric presentation depend on the type of tumor?
Rapidly growing tumors tend to cause severe, acute agitation or psychosis with associated cognitive dysfunction, while slow-growing tumors tend to present with vague personality changes, apathy, and depression, often without cognitive dysfunction. Tumors with multiple foci are associated with a greater frequency of psychiatric symptoms. Gliomas often present with psychiatric symptoms because they are fast growing with multiple foci, as do meningiomas, which are slow growing but often found in the frontal lobes where they interfere with higher-level
cognitive functions while producing few focal signs. Supratentorial tumors are twice as likely as infratentorial to produce psychiatric symptoms.

❍ What are the most important factors that predict a psychiatric presentation of brain tumor?
Important factors include the extent of the tumor, rapidity of growth, and the propensity for increased intracerebral pressure. Also important, but less so, are the patient’s past psychiatric history, prior level of functioning, and coping
mechanisms. Least important is the location of the lesion.

❍ What are the most common psychiatric presentations of frontal lobe tumors?
Irresponsibility, childishness, indifference toward others, disinhibition, facetiousness, inappropriate sexual behavior, and witzelsucht—a tendency to make light of everything, albeit with a sarcastic, angry edge to the humor. Previous
cognitive skills are preserved and formal intelligence is unaffected, but “executive functioning” can be severely disrupted. Right frontal damage is associated with euphoria; left frontal damage with akinesia, abulia, and flattened
affect.

❍ What percentage of frontal lobe tumors present with psychiatric symptoms?
Ninety percent.

❍ What is the most common psychiatric presentation of temporal lobe tumors?
Cancer in the temporal lobes often presents with a schizophrenia-like illness, but can also cause depressed mood, apathy, irritability, euphoria and hypomania (because of interference in the connections between the temporal and frontal lobes/limbic system), lability and intensification of premorbid personality traits, anxiety, and panic attacks.

❍ How can temporal lobe tumors be distinguished from schizophrenia?
Temporal lobe tumors will often be associated with visual, olfactory, and tactile hallucinations as well as auditory hallucinations, while affect is typically spared. The psychosis will usually present as repeated “spells,” staring
behavior or dreamlike episodes, and there can also be episodic mood swings. Tumors in the dominant lobe are associated with receptive aphasia or deficits in the ability to learn and remember verbal information; those in the nondominant lobe with disruption in the discrimination of nonspeech sounds.

❍ What is the psychiatric presentation of parietal lobe tumors?
Symptoms of parietal lobe tumors are often more cognitive than behavioral. There is often a marked lack of awareness of deficits or even frank denial on the part of the patient (anosognosia or “neglect syndrome”), and the often-bizarre neurologic presentation can lead to incorrect diagnoses of conversion or somatization
disorders.

❍ How about occipital tumors?
Also fairly silent psychiatrically, fewer than 20% of occipital tumors have an initial behavioral presentation. The characteristic visual hallucinations tend to be simple and unformed, often little more than flashes of light, but can be associated with agitation, irritability, fatigue, suspiciousness, and prosopagnosia (an inability to recognize familiar faces). Homonymous hemianopsia is common.

❍ What is the psychiatric presentation of diencephalic tumors?
Tumors of the thalamus, hypothalamus and the area surrounding the third ventricle often interrupt the cortical–striatal–pallidal–thalamic–cortical loop, affecting many frontal functions and presenting as a frontal lobe syndrome. Hypothalamic tumors can cause hyperphagia, daytime somnolence, or anorexia nervosa. Diencephalic
tumors often cause a subcortical dementia affecting memory and causing slowing of thought processes, apathy, abulia, depression, and inability to manipulate acquired knowledge. Interruption of CSF flow by tumor growth can cause hydrocephalus and consequent generalized cognitive dysfunction.

❍ What are the five signs that should lead one to suspect a brain tumor in a psychiatric patient?
Seizures, especially if focal or new onset (this is the initial manifestation of 50% of brain tumors), headaches (especially if dull, new onset, poorly localized, nocturnal or positional, present on awakening, and worsening with time), nausea and vomiting, sensory changes (especially visual changes, vertigo, or unilateral hearing loss), and focal neurological signs (such as weakness, ataxia, or localized sensory loss).

❍ What procedures may aid the diagnosis of a brain tumor?
CT scans are good for identifying small soft-tissue mass lesions and concomitant calcifications, obstructive hydrocephalus, and midline shift. They may not reveal very small tumors, however, and can miss isodense tumors and carcinomatosis (diffuse meningeal involvement). MRIs have better resolution and are thus better at revealing very small tumors; the drawbacks are cost, the inability to detect calcifications, and the restriction of subjects to those without metal in their heads. Cisternography, in which dye is injected into the ventricles, can aid in the
differential diagnosis of intraventricular tumors and tumor-associated hydrocephalus. Skull x-rays can diagnose craniopharyngiomas, pituitary tumors, and “empty sella” syndrome, but bone scans are better at detecting bony metastases. Chest x-rays are useful for detecting primary neoplasms of the lung, the most frequent source of brain metastases. A lumbar puncture is useful only for diagnosing meningeal carcinomatosis or leukemia if other tests are unrevealing, and requires a preliminary CT scan or MRI if there is any suspicion of increased intracerebral pressure. EEGs are frequently normal, but sometimes there are diffuse or focal spikes or slow waves, either continuous or paroxysmal. Angiography is useful for establishing the vascular supply of a tumor prior to surgery. Neuropsychiatric testing, formerly used to localize the lesion before the advent of modern imaging, now is useful to establish the extent of the dysfunction, provide a baseline measurement of cognitive function, and help to optimize rehabilitation posttreatment. The advantages of SPECT, PET, BEAM, and MEG scans over the above diagnostic tests are as yet unclear.

❍ How should therapy be altered if a patient with preexisting psychiatric disease presents with a brain tumor?
Clinicians should be especially aware of drug–drug interactions, drugs that cause delirium, and those that cause seizures, because patients with cranial neoplasms become more sensitive to all three. Drug dosages should be decreased (use 1–5 mg of haloperidol, for example, instead of 10–20 mg) and serum levels should be monitored. To decrease the risk of delirium, it is better to substitute haloperidol, carbamazepine, valproate, or benzodiazepines for lithium. Likewise, SSRIs, MAOIs, or secondary amines are better tolerated than TCAs, high-potency neuroleptics are safer than low-potency, and the antiparkinsonian agents amantadine or diphenhydramine much less likely to cause anticholinergic delirium than benztropine, trihexyphenidyl, or orphenadrine. Attention should also be paid
to the seizure-causing potential of antipsychotics—haloperidol, molindone, and fluphenazine are somewhat safer than chlorpromazine or clozapine for the control of psychotic symptoms; and lithium, bupropion, and maprotiline are best avoided for mood control for the same reason. Methylphenidate does not lower the seizure threshold and offers the advantage of rapid onset of action. Psychotherapy should be concrete and reality based, involving the family and focusing on education and issues of loss and death. Denial is a useful defense mechanism early in the
course of the illness but becomes maladaptive later on. ECT is contraindicated if there is any evidence of increased intracranial pressure, but a tumor per se is no longer an absolute contraindication.

❍ How should one modify one’s pharmacologic treatment of anxiety disorder in someone with a cranial mass?
Short-acting, low-dose benzodiazepines are much less likely to cause a paradoxical reaction of increased arousal and agitation than longer-acting agents, which also have an increased propensity to cause delirium, especially in older people. Benzodiazepines also raise the seizure threshold. Buspirone does not cause paradoxical reactions or delirium; its only disadvantage being delayed onset and weak effects. Panic attacks from temporal lobe tumors may respond to carbamazepine, valproic acid, and primidone as well as more conventional antidepressants and anxiolytics.

❍ What are the characteristics of a seizure?
Impairment of consciousness (if complex), involuntary movement, behavioral changes, or altered perceptual experiences.

❍ What is temporal lobe epilepsy?
Although the term no longer officially exists, it is still used clinically to describe seizures that are associated with
sensory hallucinations (particularly olfactory), flashbacks, d´ej`a vu or jamais vu, complex verbalizations, automatisms, and autonomic symptoms such as piloerection and nausea. Rarely, TLE can present with cataplexy or catatonia.

❍ How can TLE be differentiated from complex partial or petit mal seizures?
TLE may be either complex or simple. The term “complex partial seizure” is restricted to patients with focal firing combined with an altered level of consciousness; automatisms alone do not make a complex partial seizure.
Petit mal or absence seizures tend to be shorter in length without automatisms or postictal features, unlike TLE.

❍ What characteristics can help confirm the diagnosis of temporal lobe epilepsy?
Subjective alterations, postictal confusion, impaired memory of event, postictal depression, other episodes of nearly identical behavior, and observer confirmation of characteristic automatisms.

❍ Is there any relation between TLE and psychiatric pathology?
The incidence of psychiatric problems is four to seven times greater in those with TLE than in those without.

❍ What psychiatric issues confront patients with epilepsy?
Epileptic patients daily confront the fear of performing normal social activities (such as dating, during adolescence), because their interpersonal relations typically suffer if a seizure is witnessed. American culture stigmatizes epileptics
as an inferior minority group, with consequent negative effect on the self-esteem of those affected by it. Restrictions on activity (operating machinery, driving, swimming, etc.) can be burdensome, and epileptics suffer guilt and possible legal consequences when they ignore these restrictions. As a result of this, family relationships can evolve into abnormal patterns of isolation or dependency.

❍ What patterns of psychopathology are common in those with a seizure disorder?
There are three patterns of psychopathology associated with seizure disorders, but they are poorly characterized and overlap. The first pattern is characterized by perceptual changes, alterations in consciousness, and poor memory of events. The second is more chronic, associated with paranoia, simple auditory hallucinations, and perceptual changes. The third is characterized by persistent depersonalization and/or visual distortions.

Some facts about schizophrenia

• Schizophrenia is a biological disease of the brain. Research suggests that
schizophrenia may be a developmental disorder resulting from alterations in
the maturation of the nervous system.

• In Australia, 1 in 100 people will develop schizophrenia during their lifetime
and it is usually life long. Rates of schizophrenia are very similar from country
to country - about 1 percent of the population.

• Around 2000 people between the ages of 15 and 25 will be diagnosed in
Australia this year. It tends to be slightly more prevalent in males than
females (60:40).

• Schizophrenia ranks among the top 10 causes of disability in developed
countries worldwide.

• Many of those affected do not seek medical help and as a result may not
receive appropriate treatment for 2 - 8 years from the first onset of symptoms.

• The disease is characteristically marked by a retreat from reality with delusion
formation, hallucinations, emotional disregulation, and disorganised
behaviour.

• There also subtle signs that develop over time - slow decline in mental
function and social relationships leading to marked personality change, social
isolation, and occupational disability.

• It is a major cause of youth suicide – 30 percent of people with schizophrenia
will attempt suicide, 5 percent will succeed.

• People with schizophrenia have 2.5 times the death rate of the general
population and a life expectancy reduced by an average 10 years (WHO,
Mental Health Report 2001).

• There are genetic factors involved –for example a child of a parent with
schizophrenia has a 10 percent greater chance than other children of
developing the illness. Estimated heritability is 80% - that is, genetic factors
contribute 80% to the cause(s) of schizophrenia.

• Aside from the emotional cost to families, the disease costs the Australian
community more than $2 billion per annum in both direct health costs and
loss of productivity. 85 percent of sufferers receive welfare benefits.

• There is, as yet, no known cause or cure.

Psychiatry Assessment

❍ What are the three types of clinical psychiatric evaluations according to the American Psychiatric
Association (APA)?
The general psychiatric evaluation, the emergency psychiatric evaluation, and the clinical psychiatric consultation.

❍ What are the goals of a general psychiatric evaluation according to the APA?
To establish a diagnosis, generate a case formulation, develop a treatment plan, and ascertain if any symptoms (such
as suicidal ideation) need emergency treatment. Development of an empathic rapport is also essential to initiating
and maintaining treatment compliance.

❍ How do the goals of an emergency psychiatric evaluation differ from the goals of a general psychiatric
evaluation?
Not much, in reality. However, out of necessity, there is a greater emphasis on safety and willingness to participate
in treatment during the emergency psychiatric evaluation. In the event that a person is unable to maintain his or
her own safety (and/or others), and unwilling to participate in an appropriate level of care, involuntary
commitment processes are indicated.

❍ What is the essential component of the clinical psychiatric consultation?
The reason for the evaluation. If you do not answer the question the consulting physician, court, therapist, or
caseworker is asking, you will not be consulted again. When the reason for the psychiatric consultation is vague,
it is best to ascertain (from the person/institution requesting the evaluation) the exact reason for the evaluation
(i.e., psych 2C = call 2U).

❍ True/False: The patient is not to be informed of who requested a psychiatric consultation or the reason for
the evaluation.
False. The person/institution requesting the psychiatric evaluation should ideally ask the patient to participate in a
psychiatric evaluation and the reason why, while the consultant should clearly state who is requesting the evaluation
and the reason thereof. When psychiatric consultations are requested for nonclinical reasons, the limits of
confidentiality should be reviewed and agreed to by the patient and/or their guardian before the evaluation
begins.

❍ What are the components of a clinical psychiatric examination?
The components of a clinical psychiatric examination are the reason for evaluation, history of present illness; past
psychiatric history; review of collateral sources of information including previous psychiatric records, psychological
testing, and rating scales; past medical history; review of pertinent laboratory and radiology studies; review of
systems; developmental history; family history; social history; mental status examination; physical examination; risk
assessment; multiaxial diagnoses; and treatment recommendations.

❍ What sources of information are utilized during a clinical psychiatric examination?
The first and foremost source of information for a psychiatric evaluation is the clinical interview with the patient.
Additional information can be obtained from structured interview, various questionnaires, and results of
psychological testing. With written permission from the patient or their guardian, review of previous records and
interviews with appropriate persons involved the patient’s life can yield valuable perspectives as to the patient’s level
of functioning and risk for adverse events.

❍ What factors should be considered when determining the reason for a psychiatric evaluation?
Who, why, and what services the psychiatrist is expected to render. All these factors will influence the nature and
the course of the psychiatric evaluation.
It is important to determine who requested the evaluation, especially if not requested by the patient. Reliability
and willingness to be examined can be significantly compromised if the patient did not request the evaluation (such
as when the patient is in emergency protective custody or when an examination is requested by the courts), and
additional sources of information may need to be pursued more diligently if questions of safety or reliability are
present.
Ascertaining the reason for the evaluation is imperative in order to collect sufficient information and make
appropriate recommendations. Generally, when a patient requests an evaluation, the reason for assessment is to
determine appropriate interventions for distressing symptoms. However, when someone other than a patient
requests an evaluation, it is essential to determine the specific reason why the evaluation is needed, again, so that
specific and appropriate recommendations can be made.
Finally, determining what services are to be rendered by the psychiatrist will influence what recommendations
are made. For instance, if the evaluation is for purposes of disability determination, the psychiatric examination
and recommendations will be somewhat different than if the psychiatrist is expected to be the treating physician.

❍ What information should be included in the history of present illness?
The severity and duration of current symptoms, as well as identifiable stressors. Pertinent negatives as well as
statements regarding dangerousness to self and others should also be included.

❍ True/False: A substance abuse history is not a component of the psychiatric evaluation.
False. A substance abuse history is critical to every psychiatric evaluation, even if it is negative. The use of
substances during any psychiatric illness does tend to expand the differential diagnosis and is a major risk factor
in dangerousness to self or others.

❍ Past psychiatric history should include what information?
The past psychiatric history should include information about any inpatient psychiatric hospitalizations, the reason
for hospitalization, and diagnoses, if available. Information about index hospitalizations are often very helpful as to
the severity of illness and diagnosis, especially if the patient is presenting for treatment in a stable condition. In
addition, prior outpatient services by psychiatrists and other mental health providers should be included, as well as
a history of previous medication trials and the response thereof.

❍ Why is past medical history an essential component of the psychiatric evaluation?
Past medical history is essential in ruling out medical causes of psychiatric symptoms, as well as assessing for
medication interactions that may be present. In addition, a medical illness may be a major stressor, particularly
when that illness is disabling or disfiguring.

❍ What information should be included in a developmental history?
Information regarding birth history, developmental milestones, relationships, and level of functioning in those
relationships are the items that are generally included in a developmental history.

❍ What clinical implications does a family history of psychiatric disorders?
A positive psychiatric family history may help with establishing risk factors for particular diagnoses, predicting
response to various medications, and in developing a greater understanding of the patient’s past and current family
milieu.
❍ What is one of the best means for evaluating the distribution of mental illness in a family?
A genogram.

❍ What does the occupational and social history tell the examiner about a patient’s level of functioning?
An occupational and social history gathers information about a person’s ability to “work and love.” The ability to
hold a job for a period of time demonstrates an ability to structure daily activities, meet expectations, relate
adequately with peers and supervisors, and take on a certain minimum level of responsibility. The ability to have a
long-term relationship indicates an ability to attend to someone else’s needs, control impulses, and make a
commitment.

❍ List some questions pertaining to a patient’s religious background.
Questions to ask about the role of religion in a person’s life could include some of the following: Were there
conflicts between the patient’s and parent’s religious beliefs? How large a role does religion play in the patient’s life?
How do the parent’s religious beliefs impact on the patient’s attitude toward emotions, conflict, and psychiatric
treatment?

❍ An extensive legal history can lead one to consider which two diagnoses?
Antisocial personality disorder, and alcohol and/or substance dependence.
❍ Is physical examination included in a psychiatric evaluation?
Yes. Particularly because some physical findings may be directly related to the patient’s psychiatric condition or
psychotropic medication side effects.

❍ What conditions can cause increased psychomotor activity?
Anxiety, akathesia, hyperactivity associated with attention deficit hyperactivity disorder, elevated mood, agitation
during psychotic episodes, confusional states due to delirium or dementia, and iatrogenic causes.

❍ What are the components of a mental status examination?
The components of a mental status examination include general appearance, movements, speech, attitude, thought
process, mood, affect, thought content, orientation to time and place, immediate and short-term recall,
concentration, fund of knowledge, insight, judgment, and estimate of intelligence.

❍ What aspects of the patient’s speech should be assessed?
Rate and rhythm, quality, volume and tone, grammar and syntax, and vocabulary.

❍ List some possible causes of muteness.
Aphasia, acute depression, conversion disorder, psychosis, and secondary gain.
❍ What is motor aphasia?
Motor aphasia is a disturbance of speech in which understanding remains intact but the ability to speak is grossly
impaired. Speech is halting, laborious, and inaccurate. Motor aphasia is also known as expressive aphasia, Broca’s
aphasia, or nonfluent aphasia.

❍ What is echopraxia?
The pathological imitation of one person’s movements by another.

❍ What is alexithymia?
Alexithymia is the inability or difficulty a person has in describing or even being aware of their emotions or
moods.

❍ A patient states, “It’s one or my mother, I mean, one or another.” Of what psychological phenomenon is this
an example?
Parapraxis or Freudian slip.

❍ What is the difference between a neologism and a word salad?
Neologisms are new, nonsensical words created by the patient, while word salad is an incoherent mixture of words
and phrases.

❍ How is affect characterized?
Affect is described by its range, lability, appropriateness, intensity, relatedness, and congruence with mood.

❍ How is a patient’s mood described in a mental status examination?
In the patient’s own words, usually.

❍ What aspects of thought content are generally included in a psychiatric evaluation?
The patient’s thought content is examined for suicidal or homicidal ideation (and intent): perceptual disturbances such as auditory, visual, tactile, or gustatory hallucinations; delusions, ideas of reference, and ideas of influence.

❍ Name five risk factors for suicide.
Previous attempts, seriousness of attempts, a history of alcohol or drug usage, lack of social support, and presence
of an Axis I disorder.

❍ Does the risk of suicide increase with direct questioning about suicide?
There is no evidence that it increases risk, and it is likely to increase communication and trust with the
patient.

❍ While interviewing a potentially violent patient, what precautions should be taken?
Do not interview the patient alone. Leave the door to the interview room open, and sit between the patient and the
door to allow for unrestricted exit.

❍ What factors are involved in assessing acute dangerousness?
History of violent behavior, current violent ideation, a realistic and premeditated plan, and intent.

❍ Name three kinds of normal perceptual disturbances?
Illusions, hypnagogic hallucinations, and hypnopompic hallucinations.

❍ Should a patient’s delusions be directly confronted?
No, the patient will generally become more defensive and even more fixed in their beliefs.

❍ What exactly is a delusion?
A delusion is a false belief not based on reality.

❍ List five types of delusions?
Paranoid, somatic, delusions of infidelity, delusions of poverty, and delusions of grandeur are five types of
delusions. Other types of delusions include, but are not limited to those of control (thought withdrawal,
thought broadcasting, thought insertion, thought control), erotomania, nihilistic delusions, and bizarre
delusions. In general, delusions can form about anything or anyone, and may not fit into any particular type of
delusion.

❍ How is concentration assessed on a mental status examination?
By patient report, behavioral observation, serial 7’s (or 3’s if there are educational or developmental deficits noted),
or by spelling the word “world” backward.

❍ In a patient who is disoriented, which sphere is the last to be affected; which is the first?
Orientation to person; orientation to time.

❍ What is the best way to infer a patient’s level of intellectual functioning?
By considering the patient’s vocabulary and ability to interpret proverbs.

❍ What is considered to be a normal digit span?
The majority of people are able to recall seven digits forward and five to seven digits backward.

❍ What are the essential differences between delirium and dementia?
Delirium is characterized by an acute state of confusion, disorientation, and varying levels of consciousness, while
dementia is a gradual or step-wise decline in intellectual functioning.

❍ What are the characteristic features and course of delirium?
Delirium is characterized by an acute onset of impaired consciousness, with global impairment of cognitive
functions. The course is usually brief and fluctuating, and rapid improvement occurs when the underlying etiology
resolves.

❍ How can agitation be distinguished from anxiety in the geriatric population?
Agitated individuals do not generally complain of a sense of impending doom or dread.

❍ In distinguishing between schizophrenia and bipolar disorder, what single finding on mental status examination would most likely lead to a diagnosis of schizophrenia?
Flat affect.