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Janeway Type 3: 
also known as IgA deficiency:  is the most common immunoglobulin
deficiency.  The major immunoglobulin in human saliva, nasal and bronchial
fluids, and intestinal secretions, IgA guards against bacterial and viral
reinfections.  Ultimately, IgA deficiency leads to chronic sinopulmonary
(related to the paranasal sinuses and the airway of the lungs)  infections,
GI diseases, and other disorders. 

Causes:  IgA deficiency seems to be linked to autosomal
dominant or recessive inheritance.  The presence of normal numbers
of peripheral blood lymphocytes carrying IgA receptors and of normal amounts
of other immunoglobulins suggests that B cells may not be secreting IgA. 
In an occasional patient, T-suppressor cells appear to inhibit IgA. 
IgA deficiency is also link to  autoimmune disorders, since many patients
with rheumatoid arthritis or SLE ( systemic lupus erythematosus) are also
IgA deficient.  Some medications, such as anticonvulsants, may cause
transient IgA deficiency.

Symptoms:

May have the following signs and symptoms-

Chronic sinopulmonary 

Respiratory allergy (often triggered by infection

GI tract diseases, such as celiac disease, ulcerative colitis, and regional
enteritis

Autoimmune diseases, such as rheumatoid arthritis, SLE, hemolytic anemia,
and chronic hepatitis

Malignant tumors, such as squamous cell carcinoma of the lungs, reticulum
cell sarcoma, and thymoma

Some IgA deficient patients have no symptoms, possibly because they
have extra amounts of low-molecular-weight IgM, which takes over IgA function
and helps maintain immunologic defenses.

Diagnostic test:

Immunologic analyses of IgA deficient patients show serum IgA levels
below 5 mg/dl.  Although IgA is usually absent from secretions in
IgA deficient patients, levels may be normal in rare cases.

Test may also indicate auto antibodies and antibodies against IgG (rheumatoid
factor).

Treatment:

Selective IgA deficiency has no known cure.  Treatment aims to
control symptoms of associated diseases.

Influenza:  an acute viral infection of
the respiratory tract, occurring in isolated cases, epidemics, and pandemics,
with inflammation of the nasal mucosa, pharynx, and conjunctiva, headache,
and severe, often generalized, myalgia.

Symptoms:

Cough – initially nonproductive, – later, producing purulent sputum

Marked  cyanosis

Dyspnea (difficulty breathing)

High fever

Chills

Substernal pain and discomfort

Frontal headache

Myalgia

Treatment:

Antipyretics – for fever

For influenza A – amantadine

Endotracheal intubation and ventilator assistance

Also See Our Special Page on Flu: 
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Infertility:  diminution or absence of ability
to produce offspring.

Female infertility:  Studies shows approximately
10% to 15% of all couples in the United States cannot conceive after regular
intercourse for at least 1 year without contraception.  About 40$
to 50% of all infertility is attributed to the female.  After extensive
investigation and treatment, approximately 50% of infertile couples achieve
pregnancy.  Of the 50% who don’t, about 10% have no pathologic basis
for infertility; the prognosis for this group becomes extremely poor if
pregnancy is not achieved after 3 years.

Cause:  Infertility may be caused by any defect or malfunction
of the hypothalamic pituitary ovarian axis, such as certain neurologic
diseases.  Other causes include:

Ovarian factors related to anovulation or oligo ovulation

Uterine abnormalities, which may include congenitally absent, bicornuate,
or double uterus; leiomyomas; or Asherman’s syndrome, in which the anterior
and posterior uterine walls adhere because of scar tissue formation.

Tubal and peritoneal factors, such as tubal loss or impairment secondary
to ectopic pregnancy, or tubal occlusion due to salpingitis or peritubla
adhesions

Cervical factors, such as infection and possibly cervical antibodies
that immobilize sperm

Psychological problems.

Findings:

Diagnosis requires a complete physical examination and health history,
including questions about the patient’s reproductive and sexual function,
past diseases, mental state, previous surgery, types of contraception used
in the past, and family history.

Diagnostic tests:

The doctor may order tests to assess ovulation and the structural integrity
of the fallopian tubes, the ovaries, and the uterus as well as male-female
interaction studies.

Assessing ovulation:  Basal body temperature graph shows
a sustained elevation in body temperature after ovulation until just before
the onset of menses, indicating the approximate time of ovulation.

Endometrial biopsy done on or about day 5 after the basal
body temperature rises, provides histologic evidence that ovulation has
occurred.

Progesterone blood levels, measured when they should
be highest, can show a luteal phase deficiency.

Assessing structural integrity of female reproductive organs: Hysterosalpingography
provides radiologic evidence of tubal obstruction and abnormalities of
the uterine cavity after injection of a radiopaque contrast medium through
the cervix. 

Endoscopy confirms the results of hysterosalpingography
and visualizes the endometrial cavity by hysteroscopy or explores the posterior
surface of the uterus, fallopian tubes, and ovaries by culdoscopy. Laparoscopy
allows
visualization of the abdominal and pelvic areas.

Male-female interaction studies:  The postoital test also
known as Sims test examines the cervical mucus for motile
sperm cells after intercourse that takes place at midcycle (as close to
ovulation as possible).

Immunologic or antibody testing detects
spermicidal antibodies in the sera of the female.

Treatment:

Intervention aims to correct the underlying abnormality or dysfunction
with in the hypothalamic-pituitary-ovarian complex.  In cases of hyperactivity
or hypoactivity of the adrenal or thyroid gland, hormone therapy is necessary. 
Progesterone deficiency requires progesterone replacement.

Anovulation requires treatment with clomiphene citrate, human menopausal
gonadotropins, or HCG.  Ovulation usually occurs several days after
such administration.

Surgical restoration may correct certain anatomic causes of infertility,
such as fallopian tube obstruction.

Surgery may be required to remove tumors located within or near the
hypothalamus or pituitary gland.

Endometriosis requires drug therapy and or the combination of surgical
removal of areas of endometriosis.

* Artificial insemination has proven to be an effective alternative
strategy for dealing with infertility problems.

* In vitro (test tube) fertilization has also been successful.

---

Male infertility:  Studies show approximately
40% to 50% of infertility problems in the US are totally or partially attributed
to the male.

Assessment findings:  Clinical features of male infertility
include atrophied testes; empty scrotum; scrotal edema; varicocele or anteversion
of the epididymis; inflamed seminal vesicles; beading or abnormal nodes
on the spermatic cord and vas; penile nodes, warts, plaques, or hypospadias;
and prostatic enlargement, nodules, swelling, or tenderness.

Diagnostic test:  Patient history and physical examination.

Most conclusive test for male infertility is semen analysis.

Lab. test such as:  gonadotropin assay to determine the integrity
of the pituitary gonadal axis, serum testosterone levels to determine end
organ response to LH, urine 17-ketosteroid levels to measure testicular
function, and testicular biopsy to help clarify unexplained oligospermia
or azoospermia.

Vasography and seminal vesiculography may be necessary.

Cause:  Some of the factors that cause male infertility
include:

– Varicocele, a mass of dilated and tortuous varicose veins in the spermatic
cord

-Semen disorders, such as volume of motility disturbances or inadequate
sperm density

-Proliferation of abnormal or immature sperm, with variations in the
size and shape of the head

-Systemic diseases, such as diabetes mellitus, neoplasms, and mumps
orchitis

-Genital infection, such as gonorrhea, tuberculosis, and herpes

-Genetic defects

-Disorders of the testes

-Immunologic disorders

-Endocrine imbalance

-Chemicals and drugs that inhibit gonadotropins or interfere with spermatogenesis,
such as arsenic, methotrexate, some antihypertensives

-Sexual problems, such as errectile dysfunction, low libido

-Other factors: age, occupation, and trauma to the testes.

Treatment:

Aims to correct the underlying problem

Counseling or therapy (on sexual techniques, coital frequency, and reproductive
physiology)

Proper nutrition with vitamin supplements.

Decrease FSH levels may respond to vitamin B therapy

Decreased LH levels, to HCG therapy.

Elevated LH levels require low dosages of testosterone.  Decreased
testosterone levels, decreased semen motility, and volume disturbances
may respond to HCG.

Incontinence:  inability to control excretory functions.

Urge incontinence:  Related to decreased bladder
capacity, this diagnosis may be associated with conditions such as acute
bladder infection, obstruction, or interstitial cystitis.

Functional incontinence:  Related to sensory or mobility
deficits, this disorder is associated with alcohol abuse, Alzheimer’s disease,
closed head injuries, episodic loss of consciousness (such as:  seizures,
hypoglycemia, dementia), mental retardation, toxic confusional states (infection,
myxedema, uremia, hepatic dysfunction, and drug overdose).

Helpful ideas for treatment:

Medication therapy per doctors orders. Establish the underline problem.

Habit training:  by setting up regular toileting on an individual
basis, based on the patient’s own voiding pattern.

Try using the bathroom every 2 hours (during the day), and getting up
at least once at night.

Using protected pads and garments

Kegel exercise: (females)  to strengthen the pelvic floor muscles
by squeezing tight, let some urine flow, then hold it (count to 5) let
go and let urine flow. Do this 2-3 times a few times a day.

Impotence  also known as Erectile
Dysfunction:  it is a male reproductive disorder.  A
man with this disorder cannot attain or maintain penile erection sufficient
to complete intercourse.  The patient with primary impotence has never
achieved a sufficient erection; secondary impotence, more common and less
serious, implies that, despite present inability, the patient has succeeded
in completing intercourse in the past.  Transient periods of impotence
are not considered dysfunctional and probably occur in half of adult males. 
Erectile dysfunction affects all age groups but increases in frequency
with age.  This prognosis depends on the severity and duration of
impotence and on the underlying cause.

Cause:  May be caused by Psychogenic or Organic
factors.  Psychogenic factors may be intrapersonal  (such
as: depression, feelings of inadequacy) or interpersonal (such as: lack
of communication) . Organic factors may include chronic disorders, such
as MS or diabetes or drug or alcohol induced dysfunction. Impotence, though
rarely may stem from genital anomalies or CNS defects.

Symptoms:

Secondary erectile dysfunction is classified as follows:

Partial:  the patient cannot achieve a full erection.

Intermittent:  the patient is sometimes potent with
the same partner.

Selective:  the patient is potent only with certain
partners.

Some patients lose erectile function suddenly; others lose it gradually.
If the cause is not organic, erection may still be achieved through masturbation.

Patients with psychogenic impotence may appear anxious, with sweating
and palpitations, or they may become totally disinterested in sexual activity.

Patients with psychogenic or drug induce impotence may suffer extreme
depression, which may cause the impotence or result from it.

Treatment:

Sex therapy may be helpful

Treatment of organic impotence focuses on reversing the cause, if possible.

Certain patients suffering from organic impotence may benefit from surgically
inserted inflatable or non inflatable penile implants.

Patients with low testosterone levels may benefit from testosterone
injections.

Impetigo:  A contagious, superficial skin
infection.  It is cause by a beta-hemolytic streptococcus which produces
a non bullous impetigo.  Coagulase – positive Staphylococcus aureus
causes bullous impetigo. Poor hygiene, anemia, malnutrition,  impaired
skin integrity increase the risk of developing this disease. Impetigo spreads
most easily among infants, young children, and the elderly. It can complicate
other skin conditions marked by open lesions, such as chicken pox and 
eczema.

Symptoms:

Streptococcal  impetigo :  usually begins with a red spot
on the skin that is not raised above the surface (macula) then turns
into a blister like (vesicle), becoming pustular (pus containing
lesion) within a matter of hours.  When the vesicle breaks, a characteristic
thick, honey – colored crust forms from the exudate.

Pruritus (itching), burning, and regional lymphadenopathy. 

Staphylococcal impetigo:  begins with a thin – walled vesicle
opens and a thin, clear crust forms from the exudate. 
The lesion consists of a central clearing circumscribed by an outer rim,
much like a ringworm lesion, commonly appears on the face or other exposed
areas, and  painless pruritus.

Treatment:

Systemic antibiotic therapy

Removal of the exudate by washing the lesions 2 to 3 times a day with
soap and water

For stubborn crusts, warm soaks or compresses of normal saline or a
diluted soap solution may help.

Note:  Impetigo is bacterial infection, and is highly contagious,
see your doctor promptly for treatment and to prevent the spread of infection.

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Immune: being highly resistant to a disease because of the formation of humoral antibodies or the development of cellular immunity, or both, or as a result of some other mechanism, as interferon activity in viral infections.

Immunity: the condition of being immune; security against a particular disease.

Immunization: inoculation with specific antigen to induce an immune response.

Immune system: consist of specialized cells – lymphocytes and macrophages – and structures,
including lymph nodes, spleen, thymus, bone marrow, tonsils, adenoids, and appendix. Immune
system and blood are closely related, yet different. The blood includes plasma and numerous
kinds of blood cells. Their cells share a common origin in the bone marrow, and the immune system uses the bloodstream to transport its components.

The immune system includes organs and tissues in which lymphocytes predominate as well as cells that circulate in peripheral blood. Lymphoid organs includes: lymph nodes and vessels, spleen, tonsils, adenoids, appendix, bone marrow, thymus, and intestinal lymphoid tissue. The bone marrow and thymus play a role in developing the primary cells of the immune system: B cells and T cells.

Immunity: Refers to the body’s capacity to resist invading organisms and toxins. Preventing tissue and organ damage. The immune system’s cells and organs perform that function. The immune system uses three basic defense strategies: protective surface phenomena, general host defenses, and specific immune responses. It is designed to recognize, respond to, and eliminate foreign substances, such as bacteria, fungi, viruses, parasites,, and preserves the internal environment by scavenging dead or damaged cells and by performing surveillance.

Protective surface: Physical, chemical, and mechanical barriers work to prevent organism entry.
Intact and healing skin and mucous membranes provide the first line of defense against microbial invasion, preventing attachment of microorganisms. Skin desquamation and low pH further impede bacterial colonization. Seromucous surfaces, such as the conjunctiva of the eye and the oral mucous membranes, are protected by antibacterial substances, such as the enzyme lysozyme, found in tears, saliva, and nasal secretions.

The respiratory system requires special protection because microorganisms enter it easily from
outside. Nasal hairs and turbulent airflow through the nostrils filter foreign materials. Nasal
secretions contain an immunoglobulin (naturally produced antibody) that discourages microbe
adherence. A mucous layer that’s continuously sloughed off and replaced lines the respiratory
tract. The mucous layer, coupled with ciliary action, traps and expels inhaled particles and
microbes before they can damage delicate alveolar tissues.

The gastrointestinal system, saliva, swallowing, peristalsis, and defecation mechanically remove
bacteria. The low pH of gastric secretions is bactericidal, rendering the stomach virtually free of
viable bacteria. Resident bacteria prevent colonization by other microorganisms, protecting the
remainder of the gastrointestinal system (GI) through a process known as colonization resistance.

The urinary system is sterile except for the distal end of the urethra and the urinary meatus. When functioning together, urine flow, low urine pH, and immunoglobulin, and the bactericidal effects of prostatic fluid (in men) impede bacterial colonization. A series of sphincters also inhibits bacterial migration.

General host defenses: Once an antigen penetrates the skin or mucous membrane, the immune
system launches nonspecific cellular responses in a attempt to identify and remove the invader.
These nonspecific responses differentiate self from nonself but can’t distinguish specific antigens or respond to them differently. Inflammation, the first of these response against an antigen, causes four characteristic signs and symptoms: heat, redness, swelling, and pain. Neutrophils and
macrophages engulf, digest, and dispose of the antigen. Macrophages and lymphocytes move to
the site of insult and infection by two means: diapedesis (blood cell migration from the
intravascular compartment to tissue sites) and chemotaxis (movement toward a chemical attractor).

Specific immune responses: All foreign substances elicit the same response in general host
defenses. By contrast, particular microorganisms or molecules activate specific immune responses
and can initially involve specialized sets of immune cells. It is classified as either humoral or cell
-mediated immunity. Lymphocytes (B cells and T cells) produce the responses.

Humoral Immunity: In this specific response, an invasive antigen causes B cells to divide and
differentiate into Plasma cells that produce and secrete antigen-specific antibodies. There are five
types of antibodies, or immunoglobulins: IgA, IgD, IgE, IgG, and IgM. Each type serves a
particular function: IgA, IgG, and IgM protect against viral and bacterial invasion; IgD acts as an
antigen receptor of B cells; and IgE causes an allergic response.

After the body’s initial exposure to an antigen, a time lag occurs during which little or no antibody
can be detected. During this time, the B cell recognizes the antigen, and the sequence of division, differentiation, and antibody formation begins. This primary antibody response occurs 4 to 10 days after first time antigen exposure, during which immunoglobulin levels increase, then quickly dissipate, and IgM antibodies form.

Subsequent exposure to the same antigen initiates a secondary antibody response. In this
response, memory B cells manufacture antibodies (mainly IgG), achieving peak levels in 1 to 2
days. These elevated levels persist for months and then fall slowly. The secondary immune
response is, therefore, faster, more intense, and more persistent, and it amplifies with each
subsequent exposure to the same antigen.

An antigen-antibody complex forms after the antibody reacts to the antigen. It serves several
functions. First, a macrophage processes the antigen and presents it to antigen-specific B cells.
Then the antibody activates the complement system, causing an enzymatic cascade that destroys
the antigen. The activated complement system bridges humoral and cell-mediated immunity and
results in the arrival of phagocytic neutrophils and macrophages at the antigen site. This
combination of humoral and cell-mediated immune responses is common.

Cell-mediated immunity: protects the body against bacterial, viral, and fungal infections and
resists transplanted cells and tumor cells. In the cell-mediated response, a macrophage processes the antigen, which is then presented to T cells. Some T cells become sensitized and destroy the antigen; others release lymphokines, which activate macrophages that destroy the antigen. Sensitized T cells then travel through the blood and lymphatic systems, providing ongoing surveillance in their quest for specific antigens.

Diagnostic tests: The doctor may order several variation of tests to evaluate the patient’s immune response. Most common test studies include general cellular tests, such as T- and B lymphocyte assays, to aid diagnosis of primary and secondary immunodeficiency diseases; and general humoral test, such as complement assays, to help detect immuno-mediated disease. He may also order a scratch allergy tests and intrademal skin tests, to evaluate the cell-mediated immune response.

Lab studies such as: WBC or white blood cell count, ESR or Erythrocyte sedimentation rate, Platelet count, Direct antiglobullin test, immunoelectrophoresis, and ELISA enzyme-linked
immunosorbent.

Disorders: Immune disorders may result from hyperreactivity, as in allergic rhinitis; autoimmunity, as in SLE; or immunodeficiency, as in AIDS.

Symptoms: Symptoms varies with each disorder

Fatigue, dyspnea, malaise, frequent or recurrent infections, or slow would healing.

Treatment: Varies (search your disired disorder for info.)