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Anemia: Anemias are marked by abnormally low numbers
of RBC (red blood cell), a deficiency of hemoglobin, or a low volume of
packed RBCs per 100 ml of blood, stemming form an imbalance between blood
production and loss through injury or bleeding.  Such disorders include
aplastic anemia, folic acid deficiency anemia, sickle cell anemia,
iron deficiency anemia, and pernicious anemia.

Aplastic
anemia also called hypoplastic anemia:  results from a deficiency
of all of the blood’s formed elements, caused by the bone marrow’s failure
to generate an adequate supply of new cells.  Aplastic anemia usually
develops when damaged or destroyed stem cells inhibit RBC production. 
It also develops when damaged bone marrow microvasculature impairs cell
growth and maturation.

Often used interchangeably with other terms for bone marrow failure,
aplastic anemia properly refers to pancytopenia resulting from the decreased
functional capacity of a hypoplastic, fatty bone marrow.  Two forms
of idiopathic aplastic anemia are :  congenital hypoplastic anemia
(anemia of Blackfan and Diamond), which develops between ages 2 months
and 3 months; and Fanconi’s syndrome, in which chromosomal abnormalities
are usually associated with multiple congenital anomalies ; such as dwarfism
and hypoplasia of the kidneys and spleen. Mortality for aplastic anemia
with severe pancytopenia is 80% to 90%.  Death may result from bleeding
or infection.

Cause:  Aplastic anemia may result from drug use, toxic agents,
such as benzene and chloramphenicol., radiation, suspected but unconfirmed
immunologic factors, severe disease such as hepatitis, preleukemia and
neoplastic infiltration of bone marrow, congenital abnormalities, or induced
change in the development of the fetus (suspected as a cause in the absence
of a consistent familial or genetic history of aplastic anemia).

Symptoms:

Symptoms vary with the severity of pancytopenia, often develop insidiously,
and may include the following signs and symptoms:

Progressive weakness

Fatigue

Shortness of breath

Headache

Pallor

Tachycardia and congestive heart failure

Eccymosies

Petechiae

Hemorrhage, especially from the mucous membranes (nose, gums, rectum,
vagina) or into the retina or central nervous system

Treatment:

Eliminate any identifiable cause and provide vigorous supportive measures,
such as packed RBC, platelet, and experimental HLA matched leukocyte transfusions. 
Even after elimination of the cause, recovery can take months.  Bone
marrow transplantation is the preferred treatment for anemia stemming from
severe aplasia and for patients needing constant RBC transfusions.

Patients with low WBC counts may need reverse isolation to avoid infection. 
The infection itself may require specific antibiotics; however, these are
not given prophylactically because they tend to encourage resistant strains
of organisms.  Patients with low hemoglobin counts may need respiratory
support with oxygen, as well as blood transfusions.

Corticosteroids – to stimulate erythroid production (successful in children,
unsuccessful in adults)

Marrow stimulating agents, such as androgens

Immunosuppressive agents (if the patient does not respond to other therapy)

Note:  report any signs of infection to our doctor promptly.

Pernicious Anemia also called Addison’s anemia: progressive, megaloblastic, macrocytic anemia primarily
affecting persons of northern European ancestry.  Onset is typically
between ages 50 and 60, incidence rises with increasing age.  Pernicious
anemia causes serious neurologic, gastric, and intestinal abnormalities. 
Untreated, in may lead to permanent neurologic disability and death.

Cause: results from a deficiency of vitamin B12, which
may result from a genetic predisposition or an inherited autoimmune response.

Symptoms:

Pernicious anemia has an insidious onset but eventually causes an unmistakable
triad of symptoms including:

Weakness

Sore tongue

Numbness and tingling in the extremities

Pale lips, gums, and tongue and faintly jaundiced sclerae also occur.

Systemic signs may include: Pale to bright yellow skin
and indications of infection especially of the genitourinary tract.

GI symptoms:  nausea, vomiting, anorexia, weight loss, flatulence,
diarrhea, and constipation.  Gingival bleeding and tongue inflammation
may hinder eating and intensify anorexia.

CNS symptoms:  neuritis; weakness in extremities; peripheral
numbness and paresthesias; disturbed position sense; lack of coordination;
ataxia; impaired fine finger movement; positive Babinski’s and Romberg’s
signs; lightheadedness; altered vision; optic muscle atrophy; loss of bowel
and bladder control; irritability, poor memory, , headache, depression,
and delirium; and, in males, impotence.  Some of these symptoms are
temporary, irreversible CNS changes may have occurred before treatment.

Cardiovascular symptoms:  weakness, fatigue, light headedness,
palpitations, wide pulse pressure, dyspnea, orthopnea, tachycardia, premature
beats, and, eventually, congestive heart failure.

Treatment:

B12 injection

Iron replacement

May require blood transfusions, digitalis, a diuretic, and a low sodium
diet for CHF.

May require antibiotic therapy

Iron deficiency anemia:   Caused by an inadequate
supply of iron for optimal information of RBCs, this anemia results in
smaller cells with less color on staining.  Body stores or iron, including
plasma iron, decline, as do levels of transferring, which binds with and
transports iron.  Insufficient body stores of iron lead to a depleted
RBC mass an, in turn, to a diminished hemoglobin concentration and oxygen-carrying
capacity of the blood.

Iron deficiency anemia occurs most commonly in premenopausal women,
infants (particularly premature or low birth weight infants), children,
and adolescents (commonly girls).

Cause:  inadequate dietary intake of iron (less that 1 mg/day). 
This may occur during prolonged unsupplemented breast or bottle feeding
of infants or during periods of stress, such as rapid growth in children
and adolescents.  It may also result from iron malabsorption caused
by chronic diarrhea, partial or total gastrectomy, and malabsorption syndromes
such as celiac disease.

Symptoms:

Fatigue

Listlessness

Pallor

Inability to concentrate

Dyspnea on exertion

Irritability

Headache

For chronic iron deficiency:  may develop brittle, spoon shaped
nails and cracks at the corners of the mouth.

Treatment:

To determine the underlying cause of anemia

Oral iron and ascorbic acid

In some cases iron may be administer parenterally

Increase iron in diet

Folic Acid Deficiency Anemia:  A slowly progressive,
megaloblastic anemia, this common disorder occurs most often in infants,
adolescents, pregnant and lactating females, alcoholics, older adults,
and in persons with malignant or intestinal diseases.

Cause:  May result from alcohol abuse (alcohol may suppress
metabolic effects of folate); poor diet; impaired absorption; or bacteria
competing for available folic acid.

Other causes can include excessive cooking, which can destroy 
a high percentage of folic acid in foods; limited storage capacity in infants;
prolonged drug therapy; and increased folic acid requirement during pregnancy,
during rapid growth in infancy

Symptoms:

Progressive fatigue

Shortness of breath

Palpitations

Weakness

Glossitis

Nausea

Anorexia

Headache

Fainting

irritability

Forgetfulness

Pallor

Slight jaundice

Treatment:

Folic acid supplement and elimination of contributing causes.

Definition- anemia is a reduced number of circulating
red blood cells or a decrease in quality or quantity of hemoglobin (the
part of a red blood cell that carries oxygen, it is primarily made up of
iron).

Classification:

The most common classification system is based on the cell structure. 
This system focuses on the cells size and the content of hemoglobin. 
When describing cells “cytic” refers to the cell size, and  “chromic”
is used to describe hemoglobin content. In some animas the cell has different shapes, this is referred to as poikilocytosis.
There are 3 major types of anima, caused by the above mentioned cell abnormalities.

Macrocytic-normochromic:

Macro means large and normo means normal, so this is a large cell,
with normal contents. This problem is usually caused by defective DNA ( deoxyribonucleic
acid), which is like 1/2 of the brain of the cell, telling it what to do.Not
only are the cells unusually large in diameter, they also have increased
thickness and contents.  This defect is usually caused by a lack of
vitamin B12 or folate.  These are required by the cell for proper
growth and multiplication.  While the DNA is maturing at a slower
rate than normal the other 1/2 of the brain is working normally, but has
longer to work.  This causes  more contents and contributes to
the cell becoming larger and the increased thickness.  Due to their
increased size and their inability to change shape readily ( to go through
capillary beds, the most narrow part of the system of pipes used for blood
to travel through the body) they have a shorter than normal life. 
This causes a decrease in the number of red blood cells in the system. 
The body is unable to make enough new red blood cells (RBC), to replace
those being lost.  There are 2 types of anemia with this type of problem.

Pernicious anemia- which is caused by a lack of vitamin B12.

Treatment- usually B12 injections  to correct the deficiency.

Folate deficiency anemia- which is caused by a lack of folate.

Treatment-can be treated with diet if not severe, medication if more
severe.

Microcytic-hypochromic anemia:

Micro means small and hypo means less than normal, so we have a small
cell with less contents.  Their smaller size allows them to 
go through the system of pipes at a higher speed, which damages them and
they have shorter lives.  They also have less hemoglobin, which decreases the amount of oxygen they can carry. 
This condition can be caused by a variety of conditions. Iron must be broken
down into smaller pieces to be used by the body.  If the iron is not
being broken down, the RBC has none available for use.

Iron deficiency anemia- lack of iron for hemoglobin production, this
is usually caused by blood loss over a long period of time. The iron is
used up in an attempt to make new RBC’s. Another cause is pregnancy,
with an increased need for RBC’s for the fetus.

Treatment– Stop the bleeding and give more iron through diet
or medication.

Sideroblastic anemia (SA) –
cell unable to use iron available, it is not being broken down.  This
is caused by the iron not being used by the body to make hemoglobin. 
There are 2 reasons this may happen.

First, it can be inherited from a parent.

Second, it can be acquired.  The main cause of this is unknown.

Treatment- Pyridoxine therapy has been effective for both types. 
If Pyridoxine is effective, lifelong use of it is required.  If it
is not effective there is a chance of death.

Thalasemia – There are
two causes. Impaired production of hemoglobin is one. In the other, RBC’s
are being attacked by the body’s defense system because it does not recognize
them.  Both are caused by a congenital genetic defect.

Normocytic-normochromic:

The cells and their contents are normal, but there are not enough of
them.  These animas  are less common than the other 2 types. 
There are 5 types that share only the normal size and normal contents. 
They are caused by different problems and have different treatments as well as outcomes.

Aplastic Anemia – In the first stage, RBC’s fail
to develop completely, not at all, or they are defective.  This can
be caused by congenital abnormalities or by a large number of chemicals,
drugs, and radiation.

Hemolytic Anemia –
Mature RBC’s are destroyed prematurely.

Sickle Cell Anemia – The RBC’s are abnormally shaped
and the hemoglobin is also abnormal.  This causes the RBC’s to die
prematurely.  The abnormal shape has been selectively saved in a few
parts of the world.  People with Sickle Cell are not affected by malaria. This has to do with the shape of the RBC’s, they
look like saucers rather than round. This one redeeming quality is not
a good trade off.  People often die from this disease depending on
how many of their cells are abnormal. Large numbers of RBC’s dying at the same time can damage the liver and the
kidneys.

Treatment – Blood transfusions can be effective. Click here for more on
Sickle Cell Anemia.

Posthemmorrhagic Anemia –
This is caused by blood loss over a period of time.  This causes an
increased need for new RBC’s, which will cause the body to run out of iron,
because there is a limited amount of iron and is frequently the factor
that limits new RBC production.  The body can not function without
iron, either in reserve or in the blood system.

Treatment- Blood transfusions can be effective.

Anaphylaxis:  refers to an exaggerated hypersensitivity reaction
to a previously encountered antigen.  A severe reaction may precipitate
vascular collapse, leading to systemic shock and, sometimes, death.

Cause:  May results from exposure to sensitizing drugs or
other substances.  It may result from such drugs as penicillin (most
common), other antibiotics, serums, Vaccines, Injections, 
allergen extracts, enzymes, hormones, sulfonamides, local anesthetics,
salicylates, and polysaccharides.  The reaction may also result from
diagnostic chemicals, foods, Fresh Fruit, Sea Foods,
sulfites, insect venom such as Bee Sting and, rarely, a ruptured
hydatid cyst.

Symptoms:

Usually produces sudden distress within seconds or minutes after exposure
to an allergen.  ( a delayed or persistent reaction may occur up to
24 hours later.)  Allergic reaction may be mild to severe depending
on the original sensitizing dose of antigen, the amount and distribution
of antibodies, and the route of entry and the dose of antigen.

May have a feeling of impending doom or fright

Weakness

Sweating

Sneezing

Pruritus (itching)

Urticaria (hives)

Angioedema

Hypotension

Shock

Dysrhythmias (Irregularity in the rhythm of the brain waves) which
may precipitate circulatory collapse if not treated.

Nasal mucosal edema

Profuse watery rhinorrhea

Nasal congestion

Sneezing attacks

Hoarseness

Stridor

Dyspnea

Severe stomach cramps

Nausea

Diarrhea

Urinary urgency and incontinence

Tightening of the Throat

Treatment:

Anaphylaxis is always an emergency and requires Immediate
Medical Attention

Maintaining airway is important, Using an EPINEPHRINE Pen Injector.
Ask your Doctor about obtaining one.

Amyotrophic lateral sclerosis or ALS:  The most common motor
neuron disease of muscular atrophy, ALS results in degeneration of upper
motor neurons in the medulla oblongata and lower motor neurons in the spinal
cord.  This neurologic disease causes progressive physical degeneration
but doses not impair the patient’s mental status.  Onset usually occurs
between ages 40 and 70.  Most patients diagnosis with ALS die within
3 to 10 years after onset, usually due to aspiration pneumonia or respiratory
failure.

Precipitating factors for acute deterioration may include:  trauma,
viral ;infections, and physical exhaustion.  Disorders that must be
differentiated from ALS include CNS syphilis, multiple sclerosis, spinal
cord tumors, and syringomyelia.

Cause:  May be autosomal dominant inheritance, nutritional deficiency
of motor neurons related to a disturbance in enzyme metabolism, or autoimmune
disorders that affect immune complexes in the renal glomerulus and basement
membrane, or metabolic interference in nucleic acid production by the nerve
fibers.

Symptoms:

Atropy and weakness (especially in the muscles of the forearms and the
hands

Impaired speech

Difficulty chewing and swallowing

Difficulty breathing

Excessive drooling and possible choking

Does not impair mental status

Treatment:

No effective treatment exists for ALS

Management aims to control symptoms and provide emotional, psychological,
and physical support

Alcoholism or Alcohol Abuse:  Chronic, uncontrolled
intake of alcohol is the nation’s largest  substance abuse problem,. 
It cuts across all social and economic boundaries, involves both sexes,
and occurs at all stages of the life cycle.  It can state as early
as elementary school age, and alcoholic mothers pass the disease on to
their unborn child.  Alcoholism has no known cure.

Many Alcoholics are difficult to identify because most are able to
function adequately at work. 

Cause:  There is no definite cause that has been clearly identified. 
However, biologic, psychological, and socio-cultural factors contribute
to the disorder.  Studies shows that women become intoxicated more
readily than men because they metabolize alcohol more slowly.

Symptoms:

Characteristically, the alcoholic patient depends on daily or episodic
use of alcohol to function adequately.

Inability to discontinue or reduce alcohol intake

May experience episodes of anesthesia, amnesia, or violence during intoxication

Later stages of alcoholism:  unexplained traumatic injuries or
mood swings, unresponsiveness to sedatives, poor personal hygiene, and
secretive behavior.

The patient may attempt to consume alcohol in any form when deprived
of his usual supply.

May experience ‘black out’ where the patient does not remember any activity
he has done during intoxication

Treatment:

Total abstinence is the only effective treatment

Admitting that one has a drinking problem is a start

Detoxification

Rehabilitation

Support group such as AA programs

Acquired immunodeficiency syndrome/AIDS:  Progressive weakening
of cell mediated (T-cell) immunity,  AIDS heightens susceptibility
to opportunistic infections and unusual cancers.  Diagnosis rests
on correlation of the patient’s history and clinical features rather than
on laboratory criteria.  The time between probable exposure to the
causative human immunodeficiency virus (HIV) and diagnosis averages 1 to
3 years. Incubation time for children appears to be shorter.

Studies shows more than 75% of AIDS patients die within 2 years
of diagnosis.  Some patients, though, have AIDS-related complex (ARC). 
In this condition, the patient’s signs and symptoms suggest AIDS and laboratory
tests reveal HIV antibodies.  However, no opportunistic infections
or neoplasms exist.

Clinical profile differ between adults and children with AIDS. 
For instance, pediatric patients rarely develop Kaposi’s sarcoma, B-cell
lymphoma, or acute mononucleosis-like symptoms.  Children with AIDS
usually don’t develop hepatitis B or peripheral lymphopenia.

Pediatric AIDS patients do, however, experience problems that
are uncommon or milder in affected adults.  These include hypergammaglobulinemia,
lymphoid interstitial pneumonitis, serious bacterial infection, and progressive
neurologic disease caused by CNS infection.  Pediatric patients may
also have dysmorphic facial features.  They may exhibit a normal ratio
of T-helper to T-suppressor cells, although they will have fewer T-helper
cells than normal.

Causes:  The retrovirus HIV causes AIDS.  This virus
appears in body fluids, such as blood and semen.  Modes of transmission
include sexual contact, especially associated with trauma to the rectal
or vaginal mucosa; transfusion of contaminated blood or blood products;
and use of contaminated needles.  The virus can also be transmitted
perinatally from mother to fetus.

Risk factors include multiple sexual contacts with homosexual
and bisexual men, heterosexual contact with someone who has AIDS or is
at risk for it, present or past abuse of I.V. drugs, and transfusions of
blood or blood products, Multiple sex partners increases the risk of AIDS. 
Prenatal an perinatal exposure to AIDS also increases the risk of AIDS
in infants.  Breast feeding if the mother has AIDS or is at risk of
it.

Symptoms:

Symptoms vary widely.  Nonspecific ones often precede complications
and may include:

Fatigue

Afternoon fevers

Night sweats

Weight loss

Diarrhea

Cough

Patient may be asymptomatic until abrupt onset of complications, such
as opportunistic infections, HIV encephalopathy, and Kaposi’s sarcoma (see
below)

A child with AIDS may exhibit dysmorphic features.

Diagnostic tests:  two HIV antibody tests detect antibodies
to the virus responsible for AIDS:  the enzyme-linked immunosorbent
assay (ELISA) and the Western blot assay.

NOTE:  A positive result indicates previous exposure
to the virus and means the patient may be contagious and capable of transmitting
the virus; it doesn’t mean that he has or will get ARC or AIDS.

An antigen test, known as the HIVAGEN test, can detect antigens to HIV
(HIV p24 core protein) as early as 2 weeks after infection.  Patients
who test positive for HIV antibodies and carry the antigen may be more
apt to develop AIDS than patients who carry antibodies only.  The
presence of HIV antigen along with HIV antibody indicated that the virus
is actively replicating.

Treatment:

Currently no cure exists for AIDS.  However, researchers continue
to explore methods to arrest growth of HIV or to restore lost immune function.

Kaposi’s Sarcoma:  is characterized by purple or
blue patches, plaques, or nodular skin lesions that spread widely in patients
with AIDS.  The lesions occur most commonly in the skin, oral mucosa,
lymph nodes, GI tract, lungs, and visceral organs.  Although they
seldom drain or bleed, the lesions can cause other problems.  GI lesions
are associated with diarrhea, nausea, anorexia, and weight loss. 
Lung lesions are associated with congestion and difficulty breathing. 
Lymphatic system lesions are associated with severe facial and extremity
swelling with secondary pain.

Treatment:

Currently, many experimental protocols are being used to treat Kaposi’s
sarcoma.

Surgical incision may remove skin lesions, with no need for further
treatment.

Local irradiation usually has proved effective when tumors require further
treatment.

Chemotherapeutic agents, including doxorubicin, vinblastine, bleomycin,
interferon, and interleukin-2, are also used with some success.