Sunday, February 18, 2007

Learning issues wk 2 - part 1

GU(genitourinary) tract

hematocrit

classification of anemia

neuropathy

ROS(review of systems)

depression(symptoms)

depression(treatments)

dementia

delirium

delirium tremens

AMTS(abbreviated mental test score)

MMSE(mini-mental state examination)

syphilis(stages of)

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In anatomy, the genitourinary system is the organ system of all the reproductive organs and the urinary system. These are often considered together due to their common embryological origin.

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The hematocrit (Ht or HCT) and packed cell volume (PCV) are measures of the proportion of blood volume that is occupied by red blood cells. It is normally between 0.42 and 0.52 for males and between 0.36 and 0.48 for women



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Elevated hematocrit

In cases of dengue fever, where the full blood count is done daily, the hematocrit is monitored as a high hematocrit is a danger sign of an increased risk of dengue shock syndrome.

Polycythemia vera is associated with elevated hematocrit. PV is a myeloproliferative disorder in which the bone marrow produces excessive numbers of red cells, and reflects excessive numbers of rbc precursors in the bone marrow, as well as some abnormal forms. This condition is called erythroid hyperplasia. Excessive production of both rbcs and wbcs is called bilineage hyperplasia, and if there are excessive numbers of platelets also, trilineage hyperplasia. If PV is present, it is not uncommon to see the serum uric acid level elevated, reflecting an increase in the rate of cell turnover, reflecting increased pyridine metabolism.

Another myeloproliferative disorder is called essential thrombocythemia, in which primarily the platelets are elevated in number.

Chronic obstructive pulmonary disease (and other pulmonary conditions associated with hypoxia) may elicit an increased production of red blood cells. This increase is mediated by the increased levels of erythropoyetin by the kidneys in response to hypoxia.

[edit] Lowered hematocrit

Lowered hematocrit can imply significant hemorrhage (for example, in an ectopic pregnancy.)

The mean corpuscular volume (MCV) and the red cell distribution width (RDW) can be quite helpful in evaluating a lower-than-normal hematocrit, because it can help the clinician determine whether blood loss is chronic or acute. The MCV is the size of the red cells and the RDW is a relative measure of the variation in size of the red cell population. A low hematocrit with a low MCV with a high RDW suggests a chronic iron-deficient erythropoiesis, but a normal RDW suggests a blood loss that is more acute, such as a hemorrhage.

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Production vs. destruction or loss

The "kinetic" approach to anemia yields what many argue is the most clinically relevant classification of anemia. This classification depends on evaluation of several hematological parameters, particularly the blood reticulocyte (precursor of mature RBCs) count. This then yields the classification of defects by decreased RBC production versus increased RBC destruction and/or loss. Clinical signs of loss or destruction include abnormal peripheral blood smear with signs of hemolysis; elevated LDH suggesting cell destruction; or clinical signs of bleeding, such as guiaic-positive stool, radiographic findings, or frank bleeding.

Here is a simplified schematic of this approach:







Anemia









































Reticulocyte production index shows inadequate production response to anemia.



Reticulocyte production index shows appropriate response to anemia = ongoing hemolysis or blood loss without RBC production problem.




































No clinical findings consistent with hemolysis or blood loss: pure disorder of production.

Clinical findings and abnormal MCV: hemolysis or loss and chronic disorder of production*.

Clinical findings and normal MCV= acute hemolysis or loss without adequate time for bone marrow production to compensate**.




































Macrocytic anemia (MCV>100)

Normocytic anemia (80<100)


Microcytic anemia (MCV<80)





* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B12 and folate deficiency; and other instances of anemia with more than one cause. ** Confirm by repeating reticulocyte count: ongoing combination of low reticulocyte production index, normal MCV and hemolysis or loss may be seen in bone marrow failure or anemia of chronic disease, with superimposed or related hemolysis or blood loss.

[edit] Red blood cell size

In the morphological approach, anemia is classified by the size of red blood cells; this is either done automatically or on microscopic examination of a peripheral blood smear. The size is reflected in the mean corpuscular volume (MCV). If the cells are smaller than normal (under 80 fl), the anemia is said to be microcytic; if they are normal size (80-100 fl), normocytic; and if they are larger than normal (over 100 fl), the anemia is classified as macrocytic. This scheme quickly exposes some of the most common causes of anemia; for instance, a microcytic anemia is often the result of iron deficiency. In clinical workup, the MCV will be one of the first pieces of information available; so even among clinicians who consider the "kinetic" approach more useful philosophically, morphology will remain an important element of classification and diagnosis.

Here is a schematic representation of how to consider anemia with MCV as the starting point:










Anemia

























































Macrocytic anemia (MCV>100)





Normocytic anemia (80<100)





Microcytic anemia (MCV<80)












































High reticulocyte count





Low reticulocyte count





Other characteristics visible on the peripheral smear may provide valuable clues about a more specific diagnosis; for example, abnormal white blood cells may point to a cause in the bone marrow.

[edit] Microcytic anemia

  • Iron deficiency anemia is the most common type of anemia overall and it has many causes. RBCs on often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope.
    • Iron deficiency anemia is commonly caused by insufficient dietary intake or absorption of iron. Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red blood cells. In the United States, 20% of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men. The principal cause of iron deficiency anemia in premenopausal women is blood lost during menses. Studies have shown that iron deficiency without anemia causes poor school performance and lower IQ in teenage girls. Iron deficiency is the most prevalent deficiency state on a worldwide basis. Iron deficiency affects women from different cultures and ethnicities. Iron found in animal meats are more easily absorbed by the body than iron found in non-meat sources. In countries where animal meats are only occasionally available in the diet, iron deficiency anemia is six to eight times more prevalent than in North America and Europe. Iron deficiency is sometimes the cause of abnormal fissuring of the angular (corner) sections of the lips (angular cheilitis).
    • Iron deficiency anemia can also due to bleeding lesions of the gastrointestinal tract. Fecal occult blood testing, upper endoscopy and lower endoscopy are often performed to identify bleeding lesions. In elderly people the chances are higher that bleeding from the gastrointestinal tract could be due to a cancer.

Microcytic anemia is primarily a result of hemoglobin synthesis failure/insufficiency, which could be caused by several etiologies:

  • Heme synthesis defect
  • Globin synthesis defect
    • alpha-, and beta-thalassemia
    • HbE syndrome
    • HbC syndrome
    • and various other unstable hemoglobin diseases
  • Sideroblastic defect
    • Hereditary Sideroblastic anemia
    • Acquired Sideroblastic anemia including lead toxicity
    • Reversible Sideroblastic anemia

A mnemonic commonly used to remember causes of microcytic anemia is TAILS: T - Thalassemia, A - Anemia of chronic disease, I - Iron deficiency anemia, L - Lead toxicity associated anemia, S - Sideroblastic anemia.

[edit] Normocytic anemia

Normocytic anaemia is when the overall Hb levels are decreased, but the red blood cell size (MCV) remains normal. Causes include:

[edit] Macrocytic anemia

Macrocytic anemia can be further divided into "megaloblastic anemia" or "non-megaloblastic macrocytic anemia". The cause of megaloblastic anemia is primarily a failure of DNA synthesis with preserved RNA synthesis, which result in restricted cell division of the progenitor cells. The megaloblastic anemias often present with neutrophil hypersegmentation (6-10 lobes). The non-megaloblastic macrocytic anemias have different etiologies (i.e. there is unimpaired DNA synthesis,) which occur, for example in alcoholism.

The treatment for vitamin B12-deficient macrocytic and pernicious anemias was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and George Whipple then set about to chemically isolate the curative substance and ultimately were able to isolate the vitamin B12 from the liver. For this, all three shared the 1934 Nobel Prize in Medicine. Symptoms of vitamin B12 deficiency include having a smooth, red tongue.

[edit] Dimorphic anemia

Here there are two types of anemia simultaneously, e.g., macrocytic hypochromic, due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid [2] or following a blood transfusion. One hint that this kind of anemia may exist is a wide RBC distribution width (RDW), which suggests a wider-than-normal range of sizes of red blood cells.

[edit] Specific anemias

  • Fanconi anemia is an hereditary disorder or defect featuring aplastic anemia and various other abnormalities
  • Hemolytic anemia causes a separate constellation of symptoms (also featuring jaundice and elevated LDH levels) with numerous potential causes. It can be autoimmune, immune, hereditary or mechanical (e.g. heart surgery). It can result (because of cell fragmentation) in a microcytic anemia, a normochromic anemia, or (because of premature release of immature red blood cells from the bone marrow), a macrocytic anemia.
  • Hereditary spherocytosis is a hereditary defect that results in defects in the RBC cell membrane, causing the erythrocytes to be sequestered and destroyed by the spleen. This leads to a decrease in the number of circulating RBCs and, hence, anemia.
  • Sickle-cell anemia, a hereditary disorder, is due to the presence of the mutant hemoglobin S gene.
  • Warm autoimmune hemolytic anemia is an anemia caused by autoimmune attack against red blood cells, primarily by IgG
  • Cold Agglutinin hemolytic anemia is primarily mediated by IgM
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Neuropathy, strictly speaking, is any disease that affects the nervous system. In common usage, however, neuropathy is short for peripheral neuropathy, meaning a disease of the peripheral nervous system.

Types

The four major forms of nerve damage are polyneuropathy, autonomic neuropathy, mononeuropathy, and mononeuritis multiplex. The most common form is peripheral polyneuropathy, which mainly affects the feet and legs.

Often the form of neuropathy is further broken down as to cause (see below), or other type, such as small fiber peripheral neuropathy, which is idiopathic.

[edit] Causes

Aside from diabetes (see Diabetic neuropathy), the common causes of neuropathy are herpes zoster infection, HIV-AIDS, toxins, alcoholism, chronic trauma (such as repetitive motion disorders) or acute trauma (including surgery), various neurotoxins and autoimmune conditions such as celiac disease, which can account for approximately 16% of small fiber neuropathy cases. Neuropathic pain is common in cancer as a direct result of the cancer on peripheral nerves (e.g., compression by a tumor), as a side effect of many chemotherapy drugs, and as a result of electrical injury. In many cases no apparent causes can be found, in this case the neuropathy is "idiopathic" meaning no cause is found.

[edit] Symptoms

Neuropathy often results in numbness, abnormal sensations called dysesthesias and allodynias that occur either spontaneously or in reaction to external stimuli, and a characteristic form of pain, called neuropathic pain or neuralgia, that is qualitatively different from the ordinary nociceptive pain one might experience from stubbing a toe or hitting a finger with a hammer.

Neuropathic pain is usually perceived as a steady burning and/or "pins and needles" and/or "electric shock" sensations. The difference is due to the fact that "ordinary" pain stimulates only pain nerves, while a neuropathy often results in the firing of both pain and non-pain (touch, warm, cool) sensory nerves in the same area, producing signals that the spinal cord and brain do not normally expect to receive.

[edit] Treatment of neuropathic pain

Neuropathic pain can be very difficult to treat. Sometimes strong opioid analgesics may provide only partial relief. Opioid analgesics are to be considered only as a tertiary treatment. Several classes of medications not normally thought of as analgesics are often effective, alone or in combination with opioids and other treatments. These include tricyclic antidepressants such as amitriptyline (Elavil®), anticonvulsants such as gabapentin (Neurontin®) and pregabalin (Lyrica®).

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Clinical depression (also called major depressive disorder, or sometimes unipolar when compared with bipolar disorder) is a state of intense sadness, melancholia or despair that has advanced to the point of being disruptive to an individual's social functioning and/or activities of daily living. Although a low mood or state of dejection that does not affect functioning is often colloquially referred to as depression, clinical depression is a clinical diagnosis and may be different from the everyday meaning of "being depressed." Many people identify the feeling of being depressed as "feeling sad for no reason", or "having no motivation to do anything." One suffering from depression may feel tired, sad, irritable, lazy, unmotivated, and apathetic. Clinical depression is generally acknowledged to be more serious than normal depressed feelings. It often leads to constant negative thinking and sometimes substance abuse.

Without careful assessment, delirium can easily be confused with depression and a number of other psychiatric disorders because many of the signs and symptoms are conditions present in depression, as well as other mental illnesses including dementia and psychosis.[1]

Symptoms

According to the DSM-IV-TR criteria for diagnosing a major depressive disorder (cautionary statement) one of the following two elements must be present for a period of at least two weeks:

It is sufficient to have either of these symptoms in conjunction with five of a list of other symptoms over a two-week period. These include:

  • Feelings of overwhelming sadness and/or fear, or the seeming inability to feel emotion (emptiness).
  • A decrease in the amount of interest or pleasure in all, or almost all, daily activities.
  • Changing appetite and marked weight gain or loss.
  • Disturbed sleep patterns, such as insomnia, loss of REM sleep, or excessive sleep (Hypersomnia).
  • Psychomotor agitation or retardation nearly every day.
  • Fatigue, mental or physical, also loss of energy.
  • Intense feelings of guilt, helplessness, hopelessness, worthlessness, isolation/loneliness and/or anxiety.
  • Trouble concentrating, keeping focus or making decisions or a generalized slowing and obtunding of cognition, including memory.
  • Recurrent thoughts of death (not just fear of dying), desire to just "lie down and die" or "stop breathing", recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
  • Feeling and/or fear of being abandoned by those close to one.

Other symptoms often reported but not usually taken into account in diagnosis include:

  • Self-loathing.
  • A decrease in self-esteem.
  • Inattention to personal hygiene.
  • Sensitivity to noise.
  • Physical aches and pains, and the belief these may be signs of serious illness.
  • Fear of 'going mad'.
  • Change in perception of time.
  • Periods of sobbing.
  • Possible behavioral changes, such as aggression and/or irritability.

Depression in children is not as obvious as it is in adults. Here are some symptoms that children might display:

  • Loss of appetite.
  • Irritability.
  • Sleep problems, such as recurrent nightmares.
  • Learning or memory problems where none existed before.
  • Significant behavioral changes; such as withdrawal, social isolation, and aggression.

An additional indicator could be the excessive use of drugs or alcohol. Depressed adolescents are at particular risk of further destructive behaviours, such as eating disorders and self-harm.

One of the most widely used instruments for measuring depression severity is the Beck Depression Inventory, a 21-question multiple choice survey.

It is hard for people who have not experienced clinical depression, either personally or by regular exposure to people suffering it, to understand its emotional impact and severity, interpreting it instead as being similar to "having the blues" or "feeling down." As the list of symptoms above indicates, clinical depression is a serious, potentially lethal systemic disorder characterized by the psychiatric profession as interlocking physical, affective, and cognitive symptoms that have consequences for function and survival well beyond sad or painful feelings.

[edit] Mnemonics

Mnemonics commonly used to remember the DSM-IV criteria are SIGECAPS[6] (sleep, interest (anhedonia), guilt, energy, concentration, appetite, psychomotor, suicidality) and DEAD SWAMP[7] (depressed mood, energy, anhedonia, death (thoughts of), sleep, worthlessness/guilt, appetite, mentation, psychomotor).

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Treatment of depression

Treatment of depression varies broadly and is different for each individual. Various types and combinations of treatments may have to be tried, but without hope in a complete solution to the problem. There are two primary modes of treatment, typically used in conjunction: medication and psychotherapy. A third treatment, electroconvulsive therapy (ECT), may be used when chemical treatment fails.

Alternative treatments used for depression include exercise and the use of vitamins, herbs, or other nutritional supplements.[citation needed]

The effectiveness of treatment often depends on factors such as the amount of optimism and hope the sufferer is able to maintain, the control s/he has over stressors, the severity of symptoms, the amount of time the sufferer has been depressed, the results of previous treatments, and the degree of support of family, friends, and significant others.[citation needed]

Although treatment is generally effective[citation needed], in some cases the condition does not respond. Treatment-resistant depression warrants a full assessment, which may lead to the addition of psychotherapy, higher medication dosages, changes of medication or combination therapy, a trial of ECT/electroshock, or even a change in the diagnosis, with subsequent treatment changes. Although this process helps many, some people's symptoms continue unabated.

In emergencies, psychiatric hospitalization is used simply to keep suicidal people safe until they cease to be dangers to themselves. Another treatment program is partial hospitalization, in which the patient sleeps at home but spends the day, either five or seven days a week, in a psychiatric hospital setting in intense treatment. This treatment usually involves group therapy, individual therapy, psychopharmacology, and academics (in child and adolescent programs).

[edit] Medication

Medication that relieves the symptoms of depression has been available for several decades. These drugs are listed in order of historical development. Typical first-line therapy for depression is the use of an selective serotonin reuptake inhibitor, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). Under some circumstances, medication and psychotherapy may be more effective than either treatment separately.[20]

Monoamine oxidase inhibitors (MAOIs) such as Nardil may be used if other antidepressant medications are ineffective. Because there are potentially fatal interactions between this class of medication and certain foods and drugs, they are rarely prescribed anymore. MAOI's are used to block the enzyme monoamine oxidase which breaks down neurotransmitters such as serotonin and norepinephrine (noradrenaline). MAOI's are as effective as tricyclics, if not slightly more effective [citation needed]. A new MAOI has recently been introduced. Moclobemide (Manerix), known as a reversible inhibitor of monoamine oxidase A (RIMA), follows a very specific chemical pathway and does not require a special diet.

Tricyclic antidepressants are the oldest and include such medications as amitriptyline and desipramine. Tricyclics block the reuptake of certain neurotransmitters such as norepinephrine (noradrenaline) and serotonin. They are used less commonly now because of their side effects, which include increased heart rate, drowsiness, dry mouth,constipation, urinary retention, blurred vision,dizziness, confusion, and sexual dysfunction. Most importantly, they have a high potential to be lethal in moderate overdose. However, tricyclic antidepressants are still used because of their high potency, especially in severe cases of clinical depression.

Selective serotonin reuptake inhibitors (SSRIs) are a family of antidepressant considered to be the current standard of drug treatment. It is thought that one cause of depression is an inadequate amount of serotonin, a chemical used in the brain to transmit signals between neurons. SSRIs are said to work by preventing the reabsorption of serotonin by the nerve cell, thus maintaining the levels the brain needs to function effectively, although two researchers recently demonstrated that the advertised connection between seratonin deficiency and symptoms of depression is a marketing technique rather than a scientific portrayal of how the drugs actually work. [4]. Recent research indicates that these drugs may interact with transcription factors known as "clock genes"[5], which may be important for the addictive properties of drugs of abuse and possibly in obesity[6][7].

This family of drugs includes fluoxetine (Prozac), paroxetine (Paxil), escitalopram (Lexapro), citalopram (Celexa), and sertraline (Zoloft). These antidepressants typically have fewer adverse side effects than the tricyclics or the MAOIs, although such effects as drowsiness, dry mouth, nervousness, anxiety, insomnia, decreased appetite, and decreased ability to function sexually may occur. Some side effects may decrease as a person adjusts to the drug, but other side effects may be persistent.

Norepinephrine (noradrenaline) reuptake inhibitors (NRIs) such as reboxetine (Edronax) act via norepinephrine (also known as noradrenaline). NRIs are thought to have a positive effect on concentration and motivation in particular.[citation needed]

Norepinephrine-dopamine reuptake inhibitors such as bupropion (Wellbutrin, Zyban) inhibit the neuronal reuptake of dopamine and norepinephrine (noradrenaline)[8].

Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta) are a newer form of antidepressant that works on both noradrenaline and serotonin. They typically have similar side effects to the SSRIs, although there may be a withdrawal syndrome on discontinuation that may necessitate dosage tapering.

Noradrenergic and specific serotonergic antidepressants (NASSAs) form a newer class of antidepressants which purportedly work to increase norepinephrine (noradrenaline) and serotonin neurotransmission by blocking presynaptic alpha-2 adrenergic receptors while at the same time minimizing serotonin related side-effects by blocking certain serotonin receptors. The only example of this class in clinical use is mirtazapine (Avanza, Zispin, Remeron).

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Dementia (from Latin de- "apart, away" + mens (genitive mentis) "mind") is the progressive decline in cognitive function due to damage or disease in the brain beyond what might be expected from normal aging. Particularly affected areas may be memory, attention, language and problem solving, although particularly in the later stages of the condition, affected persons may be disoriented in time (not knowing what day of the week, day of the month, what month or even what year it is), place (not knowing where they are) and person (not knowing who they are). Symptoms of dementia can be classified as either reversible or irreversible depending upon the etiology of the disease. Less than 10% of all dementias are reversible. Dementia is a non-specific term that encompasses many disease processes, just as fever is attributable to many etiologies.

Diagnosis

Proper differential diagnosis between the types of dementia (see below) will require, at the least, referral to a specialist, e.g. a geriatric internist, geriatric psychiatrist, neurologist, neuropsychologist or geropsychologist. However, there are some brief (5-15 minutes) tests that have good reliability and can be used in the office or other setting to evaluate cognitive status. Examples of such tests include the abbreviated mental test score (AMTS) and the mini mental state examination (MMSE).

An AMTS score of less than six and an MMSE score under 24 suggests a need for further evaluation. Of course, this must be interpreted in the context of the person's educational and other background, and particular circumstances. Routine blood tests are usually performed to rule out treatable causes. These tests include vitamin B12, folic acid, thyroid-stimulating hormone (TSH), C-reactive protein, full blood count, electrolytes, calcium, renal function and liver enzymes. Abnormalities may suggest vitamin deficiency, infection or other problems that commonly cause confusion or disorientation in the elderly. Chronic use of substances such as alcohol can also predispose the patient to cognitive changes suggestive of dementia.

A CT scan or magnetic resonance imaging (MRI scan) is commonly performed. This may suggest normal pressure hydrocephalus, a potentially reversible cause of dementia, and can yield information relevant to other types of dementia, such as infarction (stroke) that would point at a vascular type of dementia. Sometimes neuropsychological testing is helpful as well.

The final diagnosis of dementia is made on the basis of the clinical picture. For research purposes, the diagnosis depends on both a clinical diagnosis and a pathological diagnosis (ie, based on the examination of brain tissue, usually from autopsy).

[edit] Types

The most common types of dementia are as follows and vary according to the history and the presentation of the disease: (Where available the ICD-10 codes are provided. The first code refers to the dementia, and the second to the underlying condition.)

[edit] Most common causes

[edit] Less common causes

It can also be a consequence of:

[edit] Treatable causes

Less than 5% of a sample of dementia cases have a potentially treatable cause. These include:

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Delirium is a medical term used to describe an acute (i.e. relatively recent) decline in attention-focus, perception, and cognition. Because it represents a change in cognitive function, the diagnosis cannot be made without knowledge of the affected person's baseline level of cognitive function.

Without careful assessment, delirium can easily be confused with a number of psychiatric disorders because many of the signs and symptoms are conditions present in dementia, depression, and psychosis.

Differential

Differential points from other processes and syndromes that cause cognitive dysfunction:

  • Delirium may be distinguished from psychosis, in which consciousness and cognition may not be impaired (however, there may be overlap, as some acute psychosis, especially with mania, is capable of producing delirium states).
  • Delirium is distinguished from dementia (chronic organic brain syndrome) which describes an "acquired" (non-congenital) and usually irreversible intellectual impairment. Dementia usually results from an identifiable degenerative brain disease (for example Alzheimer disease or Huntington's disease).
  • Delirium is distinguished by time-course from the confusion and lack of attention which result from long term learning disorders and varieties of congenital brain dysfunction. Delirium has been also referred to as 'acute confusional state' or 'acute brain syndrome'. The key word in both of these descriptions is "acute" (meaning: of recent onset), since delirium may share many of the clinical (i.e., symptomatic) features of dementia, developmental disability, or attention-deficit hyperactivity disorder, with the important exception of symptom duration.

It is a corollary of the above differential criteria that a diagnosis of delirium cannot be made without a previous assessment or knowledge of the affected person's baseline level of cognitive function.

[edit] Causes

Delirium may be caused by severe physical or mental illness, or any process which interferes with the normal metabolism or function of the brain. For example, fever, pain, poisons (including toxic drug reactions), brain injury, surgery, traumatic shock, severe lack of food or water or sleep, and even withdrawal symptoms of certain drug and alcohol dependent states, are all known to cause delirium.

In addition, there is an interaction between acute and chronic symptoms of brain dysfuction; delirious states are more easily produced in people already suffering with underlying chronic brain dysfunction.

[edit] Commonly concuring mental symptoms, with a note on severity

Since delirium may occur in relative states of severity, all symptoms may occur with varying degrees of intensity. For example, a mild disability to focus attention may result in only a disability in solving more complex problems. However, delirium may be so severe that it borders on unconsciousness. In this state a person may be awake and immediately aware and responsive, but unable to perform any meaningful mental task at all.

[edit] Inability to focus attention, confusion and disorientation

The delirium-sufferer loses the capacity for clear and coherent thought. This may be apparent in disorganised or incoherent speech, the inability to concentrate (focus attention), or in a lack of any goal-directed thinking.

Disorientation (another symptom of confusion, and usually a more severe one) describes the loss of awareness of the surroundings, environment and context in which the person exists. It may also appear with delerium, but it is not required, as noted below. Disorientation may occur in time (not knowing what time of day, day of week, month, season or year it is), place (not knowing where you are) or person (not knowing who you are).

Cognitive function may be impaired enough to make medical criteria for delirium, even if orientation is preserved. Thus, a patient who is fully aware of where they are and who they are, but cannot think because they cannot concentrate, may be medically delirious. The state of delirium most familiar to the average person is that which occurs from extremes in pain, lack of sleep, or emotional shock.

Because most high level mental skills are required for problem solving, including ability to focus attention, this ability also suffers in delirium. However, this is a secondary phenomenon, since problem-solving involves many sub-skills and basic mental abilities, any of which may be imipaired in a delirious patient.

[edit] Memory formation disturbance

Impairments to cognition may include reduction in the function of ability to form short or long term memory. Reduction in formation of new long-term memory (that which survives immediate attention) is more common, because it generally requires a higher degree of attention.

Previously formed long-term memories (i.e., those formed before the period of delirium) are usually preserved in all but the most severe cases of delirium.

[edit] Abnormalities of awareness and affect

Hallucinations (perceived sensory experience with the lack of an external source) or distortions of reality may occur in delirium. Commonly these are visual distortions, and can take the form of masses of small crawling creatures (particularly common in delirium tremens, caused by severe alcohol withdrawal) or distortions in size or intensity of the surrounding environment.

Strange beliefs may also be held during a delirious state, but these are not considered fixed delusions in the clinical sense as they are considered too short-lived (i.e., they are temporary delusions). Interestingly, in some cases sufferers may be left with false or delusional memories after delirium, basing their memories on the confused thinking or sensory distortion which occurred during the episode of delirium.

Abnormalities of affect which may attend the state of delirium may include many distortions to perceived or communicated emotional states. Emotional states may also fluctuate, so that a delirious person may rapidly change between, for example, terror, sadness and jocularity.

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Delirium tremens (colloquially, the DTs, "the horrors", "the shakes" or "rum fits") is an acute episode of delirium that is usually caused by withdrawal or abstinence from alcohol following habitual excessive drinking. Delirium tremens can also appear after a rapid reduction in the amount of alcohol being consumed by heavy drinkers, or as a complication of withdrawal from benzodiazepines or barbiturates. It only occurs in individuals with a history of constant, long-term alcohol consumption. Delirium tremens typically manifests about 18 to 24 hours after discontinuation of alcohol consumption, but can appear two or three days after.

Symptoms

The main symptoms are confusion and agitation. Other common symptoms include intense hallucinations such as visions of insects, snakes or rats. These may be related to the environment, e.g., drawings on wallpaper that the patient would perceive as giant spiders attacking her or him. Unlike hallucinations associated with schizophrenia, delirium tremens hallucinations are primarily visual, but associated with tactile hallucinations such as sensations of something crawling on the subject - a phenomenon known as formication. Delirium tremens can sometimes be associated with severe, uncontrollable tremors of the extremities and secondary symptoms such as anxiety, panic attacks and paranoia.

Delirium tremens (DT) should be distinguished from alcoholic hallucinosis, the latter occurring in approximately 20% of hospitalized alcoholics and not carrying a significant mortality. In contrast, DT occurs in 5-10% of alcohol-dependent people and carries up to 5% mortality with treatment and up to 35% mortality without treatment. DT is characterized by the presence of altered sensorium--i.e. complete hallucination without any recognition of the real world. DT has extreme autonomic hyperactivity (high pulse, blood pressure, and rate of breathing), and 35-60% of patients have a fever.

Treatment

Pharmacotherapy is symptomatic and supportive. Typically the patient is kept sedated with benzodiazepines, such as diazepam (Valium), lorazepam (Ativan) or oxazepam (Serax) and in extreme cases low-levels of antipsychotics, such as haloperidol until symptoms subside. If status epilepticus is present, seizures are treated accordingly. Controlling environmental stimuli can also be helpful, such as a well-lit but relaxing environment to minimise visual misinterpretations such as the visual hallucinations mentioned above.

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The abbreviated mental test score (AMTS) was introduced by Hodkinson in 1972 to rapidly assess elderly patients for the possibility of dementia. Its uses in medicine have become somewhat wider, e.g. to assess for confusion, although it has mainly been validated in the elderly.

The following questions are put to the patient. Each question correctly answered scores one point. A score of less than 6 suggests dementia, although further and more formal tests are necessary to confirm the diagnosis.

An alternative to the AMTS is the 30 point mini-mental state examination (MMSE).

Question Score
What is your age?
What is the time to the nearest hour?
Give the patient an address, and ask him or her to repeat it at the end of the test
What is the year?
What is the name of the hospital or number of the residence where the patient is situated?
Can the patient recognize two persons (the doctor, nurse, home help, etc.)?
What is your date of birth?
In which year did the First World War begin (adjust this for a world event the patient would have known during childhood)?
What is the name of the present monarch (head of state, etc.)?
Count backwards from 20 down to 1.



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The mini-mental state examination (MMSE) or Folstein test is a brief 30-point questionnaire test that is used to assess cognition. It is commonly used in medicine to screen for dementia. In the time span of about 10 minutes, it samples various functions, including arithmetic, memory and orientation. It was introduced by Folstein et al in 1975,[1] and is widely used with small modifications.

The test

Interlocking pentagons used for the last question
Interlocking pentagons used for the last question

The MMSE test includes simple questions and problems in a number of areas: the time and place of the test, repeating lists of words, arithmetic, language use and comprehension, and copying a drawing.

[edit] Interpretation

Any score over 24 (out of 30) is effectively normal. The normal value is also corrected for degree of schooling and age.[3] Low to very low scores correlate closely with the presence of dementia, although other mental disorders can also lead to abnormal findings on MMSE testing. The presence of purely physical problems can also interfere with interpretation if not properly noted; for example, a patient may be physically unable to hear or read instructions properly, or may have a motor deficit that affects writing and drawing skills.

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Syphilis is a sexually transmitted disease (STD) caused by a spirochaete bacterium, Treponema pallidum. Syphilis has many alternate names, including "syph", "Cupid's Disease", "the Pox" (or "great pox", to distinguish it from smallpox), "lues" (hence luiphobia, or fear of syphilis), and the "French disease."

The route of transmission of syphilis is typically by sexual contact; however, there are examples of:

The signs and symptoms of syphilis are myriad; before the advent of serological testing, diagnosis was more difficult and the disease was dubbed the "Great Imitator" because it was so often confused with other diseases.

Syphilis can be treated with penicillin or other antibiotics. Statistically, oral treatment is dramatically less effective than other treatments because patients tend not to complete the course. The oldest, and still most effective, method is to inject benzathine penicillin into each buttock (procaine is added to make the pain bearable); the dose must be given half in each buttock because the amount given would be too painful if given in a single injection.

Another treatment is to administer several tablets of azithromycin (which has a long duration of action) orally under observation. This latter course may soon be obsolete, as strains of syphilis resistant to azithromycin have developed, and accounted for 56% of San Francisco infections in 2004.[1] Other treatments are less effective as the patient is required to take pills several times a day.


Stages of syphilis

Different manifestations occur at each stage of the disease:-

[edit] Primary syphilis

Chancres on penis due to primary syphilitic infection
Chancres on penis due to primary syphilitic infection

Primary syphilis is manifested after an incubation period of 10-90 days (the average is 21 days) with a primary sore. During the initial incubation period, individuals are asymptomatic. The sore, called a chancre, is a firm, painless skin ulceration localized at the point of initial exposure to the bacterium, often on the penis, vagina or rectum. Local lymph node swelling can occur. The primary lesion may persist for 4 to 6 weeks and then heal spontaneously.

[edit] Secondary syphilis

Secondary syphilis manifested on labia
Secondary syphilis manifested on labia

Secondary syphilis is characterized by a skin rash that appears 1-6 months (commonly 6 to 8 weeks) after the primary infection. This is a symmetrical reddish-pink non-itchy rash on the trunk and extremities, which unlike most other kinds of rash involves the palms of the hands and the soles of the feet; in moist areas of the body the rash becomes flat broad whitish lesions called condylomata lata. Mucous patches may also appear on the genitals or in the mouth. A patient with syphilis is most contagious when he or she has secondary syphilis.

Other symptoms common at this stage include fever, sore throat, malaise, weight loss, headache, meningismus, and enlarged lymph nodes. Rare manifestations include an acute meningitis that occurs in about 2% of patients, hepatitis, renal disease, hypertrophic gastritis, patchy proctitis, ulcerative colitis, rectosigmoid mass, arthritis, periostitis, optic neuritis, iritis, and uveitis.

[edit] Tertiary syphilis

Tertiary syphilis occurs from as early as one year after the initial infection but can take up to ten years to manifest - though cases have been reported where this stage has occurred fifty years after initial infection. This stage is characterised by gummas, soft, tumor-like growths, readily seen in the skin and mucous membranes, but which can occur almost anywhere in the body, often in the skeleton. Other characteristics of untreated syphilis include Charcot's joints (a degeneration of joint surfaces resulting from loss of proprioception), and Clutton's joints (bilateral knee effusions). The more severe manifestations include neurosyphilis and cardiovascular syphilis.

Neurological complications at this stage include generalized paresis of the insane which results in personality changes, changes in emotional affect, hyperactive reflexes, and Argyll-Robertson pupils, a diagnostic sign in which the small and irregular pupils constrict in response to focusing the eyes, but not to light; Tabes dorsalis, also known as locomotor ataxia, a disorder of the spinal cord, often results in a characteristic shuffling gait.

Cardiovascular complications include syphilitic aortitis, aortic aneurysm, aneurysm of sinus of Valsalva, and aortic regurgitation, and are a frequent cause of death. Syphilitic aortitis can cause de Musset's sign (a bobbing of the head that de Musset first noted in Parisian prostitutes).

[edit] Latent syphilis

Latent syphilis is defined as having serologic proof of infection without signs or symptoms of disease. Latent syphilis is further described as either early or late. Early latent syphilis is defined as having syphilis for two years or less from time of initial infection without signs or symptoms of disease. Late latent syphilis, then, is infection for greater than two years but having no clinical evidence of disease. The distinction is important for two reasons, therapy and risk for transmission.

In practice, the time of initial infection is often not known and in this case should then be presumed to be late for the purpose of therapy. Early latent syphilis may be treated with a single IM injection of a long-acting penicillin. Late latent syphilis, however, requires three such injections, each a week apart. For infectiousness, however, late latent syphilis is not considered contagious while early latent is. Thus, if the duration of infection is not known, one should presume the patient is early and contagious.

[edit] Neurosyphilis

Neurosyphilis refers to a site of infection involving the neurologic system. As such, neurosyphilis may occur at any stage of syphilis. Neurosyphilis in patients with HIV infection is well described. Reports of neurosyphilis in HIV-infected persons are similar to cases reported before the HIV pandemic. The precise extent and significance of neurologic involvement in HIV-infected patients with syphilis, reflected by either laboratory or clinical criteria, remain incompletely characterized. Furthermore, the alteration of host immunosuppression by ART in recent years has further complicated such characterization.

There are four clinical types.

  • Asymptomatic Neurosyphilis
  • Meningovascular Syphilis
  • Tabes Dorsalis
  • General Paresis [3]

Approximately 35% to 40% of persons with secondary syphilis have asymptomatic CNS involvement, as demonstrated by any of these on CSF examination:-

  • An abnormal cell count, protein level, or glucose level;
  • Demonstrated reactivity to Venereal Disease Research Laboratory (VDRL) antibody test.

Acute syphilitic meningitis usually occurs within the first 2 years of infection; 10% of cases are diagnosed at the time of the secondary rash. Patients present with headache, meningeal irritation, and cranial nerve abnormalities, typically involving cranial nerves at the base of the brain. Meningovascular syphilis occurs a few months to 10 years (average, 7 years) after the primary infection. Unlike the sudden onset of thrombotic or embolic stroke syndromes, meningovascular syphilis is associated with prodromal symptoms lasting weeks to months before focal deficits of a vascular syndrome are identifiable. Prodromal symptoms include unilateral numbness, paresthesias, extremity weakness, headache, vertigo, insomnia, and psychiatric abnormalities such as personality changes. The focal deficits initially are intermittent or progress slowly over a few days.

Current treatment

The first choice treatment for primary, secondary, and early latent infection remains penicillin, in the form of Benzathine penicillin G, 2.4 MU IM in a single dose. Individuals who have severe allergic reactions to penicillin (e.g., anaphylaxis) may be effectively treated with oral tetracyclines (100 mg orally twice a day for 14 days). Ceftriaxone may be considered as an alternative therapy, although the optimal dose is not yet defined and close clinical and serologic follow-up is essential. If ceftriaxone is used for the treatment of early syphilis, some experts recommend 1 g daily, given intramuscularly or intravenously, for 8 to 10 days. (47,159,160)

Late latent and infections of unknown duration If CSF examination yields no evidence of neurosyphilis, then a total of 7.2 million units of benzathine penicillin G is recommended (administered as 3 doses of 2.4 million units by intramuscular injection weekly for 3 successive weeks). If allergic, then tetracyclines may be used for this stage also, but for 28 days instead of the normal 14.

For patients diagnosed with neurosyphilis (including ocular or auditory syphilis with or without positive LP results), aqueous crystalline penicillin G is the treatment of choice (administered as 18-24 million units intravenously per day; ie, 3-4 million units every 4 hours or continuous infusion for 10-14 days). If intravenous administration is impossible, then aqueous procaine penicillin G is an alternative (administered as 2.4 million units intramuscularly daily plus probenecid 500 mg by mouth 4 times daily for 14 days). Procaine injections are painful, however, and patient compliance may be difficult to ensure. To approximate the 21-day course of therapy for late latent disease and to address concerns about slowly dividing treponemes, most experts now recommend 3 weekly doses of benzathine penicillin G (total 7.2 million units intramuscularly) after the completion of a 14-day course of aqueous crystalline or aqueous procaine penicillin G for neurosyphilis. No oral antibiotic alternatives are recommended for the treatment of neurosyphilis, but in special circumstances the only alternative that has been studied is ceftriaxone 2 g intramuscularly for 14 days.

Alternative regimens (eg, tetracyclines) are not well studied in HIV infection and a careful follow-up is recommended. Tetra-cyclines are contraindicated in pregnancy. Skin testing or desensitization to facilitate therapy with penicillin is recommended in pregnant patients and for treatment of latent syphilis and neurosyphilis in other patients with HIV infection. Follow-up includes clinical evaluation at 1 to 2 weeks followed by clinical and serologic evaluation at 3, 6, 9, 12, and 24 months after treatment.

Oral Azithromycin given as a single dose of 2 g has been used successfully to treat syphilis in a pilot study of 328 patients in Tanzania (Riedner 2005), but resistance to azithromycin (eg, as high as 56% in San Francisco in 2004)[2] has made it an unacceptable alternative.

HIV-infected patients with early syphilis may have a higher risk of neurologic complications and a higher rate of treatment failure with currently recommended regimens. The magnitude of these risks, however, although not precisely defined, is probably small.

Before administering any treatment, clinicians should warn all patients about the possibility of a Jarisch-Herxheimer reaction, which occurs most often in secondary syphilis and with penicillin therapy, and may be more common in HIV-infected patients.[3] This reaction is characterized by fever, fatigue, and transient worsening of any mucocutaneous symptoms, and usually subsides within 24 hours. These symptoms can be alleviated with acetaminophen and should not be mistaken for drug allergy. In addition, clinicians should inform HIV-infected patients that currently recommended regimens may be less effective for them than for patients without HIV infection and that close serologic follow-up is therefore essential.

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