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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

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.

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.

Aneurysm: a sac formed by localized dilatation of an
artery or vein

Thoracic aortic aneurysm:    In this disorder,
the ascending, transverse, or descending part of the aorta widens abnormally. 
A dissecting aneurysm indicates a hemorrhagic separation in the
aortic wall, usually within the medial layer. A saccular aneurysm
describes an outpouching of the arterial wall, with a narrow neck. 
A fusiform aneurysm is a spindle shaped enlargement encompassing
the entire aortic circumference.  Thoracic aortic aneurysms are most
common in men between ages 50 and 70.  Some aneurysms progress to
serious and eventually lethal complications.

Cause:  Usually this disorder occurs a s a consequence of
atherosclerosis.  Other possible causes include infection of the aortic
arch and descending segments, congenital defects, trauma, and syphilis. 
Intimal tear in the ascending aorta as well as hypertension can initiate
a dissecting aneurysm.

Symptoms:

Pain – In a dissecting aneurysm, pain usually occurs suddenly, with a tearing
or ripping sensation in the thorax or anterior chest.  Pain may extend
to the neck, shoulder, lower back, or abdomen but rarely reaches the jaw
and arms.

Temporary loss of consciousness (syncope)

Pallor

Sweating

Shortness of breath

Tachycardia

Cyanosis

Leg weakness

Transient paralysis

Effects of saccular or fusiform aneurysms varies according to the aneurysm’s
size and location and degree of compression, distortion, or erosion of
surrounding structures.

The patient may develop aortic valve insufficiency; diastolic murmur;
substernal ache in his shoulders, lower back, or abdomen; marked respiratory
distress, with dyspnea, brassy cough, or wheezing; hoarseness or loss of
voice.

Treatment:

An extreme emergency: dissecting aortic aneurysm requires
immediate attention.

To prevent further dissection, the doctor may order administration of
antihypertensives, such as nitroprusside; negative inotropic agents that
decrease contractile force, such as propranolol; oxygen for respiratory
distress; narcotic for pain; I.V. fluids; and, if necessary, whole blood
transfusions.

Depending on the extent of damage and the vessels involved, the patient
may undergo vascular surgery.

Abdominal aortic aneurysm:  an abnormal
dilation in the arterial wall, most commonly occurs in the aorta between
the renal arteries and iliac branches.  More that 50% of all patients
with untreated abdominal aneurysms die, primarily from aneurysmal rupture,
within 2 years of diagnosis.  More than 85% die within 5 years

Causes:  Usually abdominal aortic aneurysm results from
artherosclerosis.  Other possible causes include cystic medial necrosis,
trauma, syphilis, and infection.

Symptoms:

When aneurysmal rupture isn’t imminent, you may be able to see an asymptomatic
pulsating mass in the periumbilical area.  Auscultation may reveal
a systolic bruit over the aorta, and tenderness may be present on deep
palpation.

Pressure on lumbar nerves may lead to lumbar pain that radiates to the
flank and groin.

If the aneurysm ruptures into the peritoneal cavity, it causes severe,
persistent abdominal and back pain, mimicking renal or ureteral colic. 
The patient may hemorrhage; however, retroperitoneal bleeding may make
such signs and symptoms as weakness, sweating, tachycardia, and hypotension
appear rather subtle.

Treatment:

Usually, abdominal aneurysm requires resection of the aneurysm and replacement
of the damaged aortic section with a Dacron graft.

If the aneurysm appears small and asymptomatic, the doctor may delay
surgery.  However,  small aneurysms may rupture.  The patient
must undergo regular physical examination and ultrasound checks to detect
enlargement, which may forewarn rupture.

Femoral and popliteal aneurysms:  Progressive
atherosclerotic changes in the medial layer of the femoral and popliteal
arteries may lead to aneurysm.  Aneurysmal formations may be fusiform
(spindle -shaped) or saccular (pouchlike).  Fusiform aneurysms occur
three times more frequently.

Femoral and popliteal aneurysm may occur as single or multiple segmental
lesions, in many cases affecting both legs, and may accompany aneurysms
in the abdominal aorta or iliac arteries.  Elective surgery before
complications arise greatly improves prognosis.

Causes:  Femoral and popliteal aneurysms usually occur secondary
to atherosclerosis, although in rare cases they may result from congenital
weakness in the arterial wall. Other possible causes include blunt or penetrating
trauma, bacterial infection, or peripheral vascular reconstructive surgery.

Symptoms:

Pain in the popliteal space.

Edema

Venous distention

Treatment:

Femoral and popliteal aneurysms requires surgical bypass and reconstruction
of the artery, usually with an autogenous saphenous vein graft replacement.

Arterial occlusion that causes severe ischemia and gangrene may require
leg amputation.

Angina:  spasmodic, choking, or suffocation
pain.  The episodic pain of angina occurs when the supply of oxygen
to the heart can’t meet the heart’s needs.

Physical or emotional stress activates the sympathetic nervous system,
causing vasoconstriction and increased heart rate, contractility, and blood
pressure.  These heighten the hearts oxygen needs.

Angina may occur during stress, exertion (pain will be relieved by rest),
or dreaming, or after a heavy meal or exposure to cold.

Symptom:

Increase heart rate

Increase blood pressure

Retrosternal or substernal pain that’s described as a feeling of tightness,
pressure, heaviness, squeezing, or burning.

Pain that radiates to the lower jaw, neck, shoulder, arm, or hand, usually
on the left side.  This pain is generally felt with the retrosternal
or substernal pain.

Dyspnea

Diaphoresis

GI distress

Pulmonary congestion

Increase need to void

Bradycardia or tachycardia

Pallor

Treatment:

Nitroglycerin:  IV or Sublingual

Chest pain should be reported to your doctor immediately

Angina

Angina: is usually described as chest pain, and is referred to as
angina pectoris.  The cause of this pain is the heart not getting
enough oxygen.  To understand how this works, we need to take a brief
and over simplified look at the lungs, blood, and the cells of the body. First, the lungs function is to take oxygen from
the air we breath and put it into the blood.  The blood then carries
the oxygen to all the cells in our bodies.  The cells then use the
oxygen to produce energy to complete their various tasks. The pain or discomfort is usually of short duration, lasting
3 to 5 minutes.  The pain goes away when the heart starts getting
enough oxygen again.  The effects of a temporary reduction of oxygen
is reversible, that is, the cells are not permanently damaged.

Symptoms- the most common is discomfort of the chest, ranging
from a feeling of pressure to moderate pain. It is sometimes mistaken for
indigestion.  Other common sites are, the lower jaw and the left shoulder
and arm.  A person may describe the discomfort with a clenched fist.  White or pale skin, sweating,
and difficulty breathing are frequently seen with this disease.

Types:

Stable angina is brought on by increased demands but on the heart. 
Physical exertion brings it on.  An individual generally knows what
activity level will cause the discomfort.

Unstable angina cannot be predicted, it may happen while a person
is at rest.  Unstable angina usually indicates a more advanced disease
than stable angina.  The arteries carrying blood are no longer able
handle enough blood for the heart even at rest.  This is sometimes
caused by the arteries of the heart going into spasm.  This is most
frequently a result of Atherosclerosis.

Treatment- Nitrates are usually the first line of defense. 
They cause the blood vessels to expand and this in turn decreases demand
on the heart.  It is easier for the heart to push blood through the
expanded vessels. Other medications are often used to decrease blood pressure, decrease heart rate and contractility,
and decrease blood volume in the left ventricular chamber of the heart.