CHRIST THE KING COLLEGE

College of Nursing and IHAP

Calbayog City

October 12, 2020

BSN 3

 Please research the following topics and write them in them in the
notebook.

1. The Anatomy and Physiology of the Immune System.

The immune system is one of the most complex systems within the human body,
made up of both physical structures and processes, comprising a network of
organs, tissues, and cells that protect the body from disease and foreign invaders.
Its main function is to keep us healthy and prevent illness.

The major component of the immune system is the lymphatic system, composed

of the bone marrow, spleen, and thymus gland, as well as the lymph nodes and
ducts. In addition, there are specialized blood cells (lymphocytes and leukocytes)
that work within the immune system.

The human immune system acts as the guardian of our physical health by
providing safeguards to the outside invasion of pathogens, which include viruses
and bacteria. Over the past 100 years, many organisms have been recognized by
clinical researchers as pathogens, with the ability to cause harm to humans. This
has led to the creation of biologics (drugs and immunizations) to fight these
invaders at the cellular level.

One of the deadliest invaders of the past 50 years is the human

immunodeficiency virus (HIV), which causes acquired immune deficiency
syndrome (AIDS), a disease in which there is a severe loss of the body’s cellular
immunity, greatly lowering the resistance to infection and malignancy.

Since the late 1970s, more than 70 million people have been infected worldwide,
with over 35 million deaths and approximately 38 million living with HIV. The
disease has caused both cultural upheaval and economic devastation in many
countries.

The Immune response is the body's ability to stay safe by affording protection against harmful
agents and involves lines of defense against most microbes as well as specialized and highly
specific response to a particular offender. This immune response classifies as either innate which
is non-specific and adaptive acquired which is highly specific. The innate response, often our
first line of defense against anything foreign,  defends the body against a pathogen in a similar
fashion at all times. These natural mechanisms include the skin barrier, saliva, tears, various
cytokines, complement proteins, lysozyme, bacterial flora, and numerous cells including
neutrophils, basophils, eosinophils, monocytes, macrophages, reticuloendothelial system, natural
killer cells (NK cells), epithelial cells, endothelial cells, red blood cells, and platelets.
The adaptive acquired immune response will utilize the ability of specific lymphocytes and their
products (immunoglobulins, and cytokines) to generate a response against the  invading
microbes and its typical features are[1][2][3]:

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 1. Specificity: as the triggering mechanism is a particular pathogen, immunogen or
antigen.  
2. Heterogeneity: signifies the production of millions of different effectors of the immune
response (antibodies) against millions of intruders.
3. Memory: The immune system has the ability not only to recognize the pathogen on its
second contact but to generate a faster and stronger response.  
The inflammatory immune response is an example of innate immunity as it blocks the entry of
invading pathogens through the skin, respiratory or gastrointestinal tract. If pathogens can breach
the epithelial surfaces, they encounter macrophages in the subepithelial tissues that will not only
attempt to engulf them but also produce cytokines to amplify the inflammatory response.
Active immunity results from the immune system's response to an antigen and therefore is
acquired. Immunity resulting from the transfer of immune cells or antibodies from an immunized
individual is passive immunity.
The immune system has evolved for the maintenance of homeostasis, as it can discriminate
between foreign antigens and self; however, when this specificity is affected an autoimmune
reaction or disease develops.

2. Discuss the nature, mode of transmission, prevention, and signs and

symptoms of COVID-19.

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 3. Management of Patients With Immunodeficiency
Treatment

 Avoidance of live vaccines and exposure to infection

 Antibiotics and sometimes surgery

 Replacement of missing immune components

Treatment of immunodeficiency disorders generally involves preventing infection, managing acute

infection, and replacing missing immune components when possible.

Infection prevention
Infection can be prevented by advising patients to avoid environmental exposures and not giving
them live-virus vaccines (eg, varicella, rotavirus, measles, mumps, rubella, herpes zoster, yellow
fever, oral polio, intranasal influenza vaccines) or BCG (bacille Calmette-Guérin). Pneumococcal,
meningococcal, and Haemophilus influenzae type b (Hib) vaccines are the recommended risk-
specific vaccines, but their effectiveness varies with the degree of immunodeficiency.
Patients at risk of serious infections (eg, those with SCID, chronic granulomatous disease,
Wiskott-Aldrich syndrome, or asplenia) or of specific infections (eg, with Pneumocystis jirovecii in
patients with T-cell disorders) can be given prophylactic antibiotics
(eg, trimethoprim/sulfamethoxazole 5 mg/kg orally twice a day).
To prevent graft-vs-host disease  after transfusions, clinicians should use blood products from
cytomegalovirus-negative donors; the products should be filtered to remove white blood cells and
irradiated (15 to 30 Gy).

Management of acute infection

After appropriate cultures are obtained, antibiotics that target likely causes should be given
promptly. Sometimes surgery (eg, to drain abscesses) is needed.

Usually, self-limited viral infections cause severe persistent disease in immunocompromised

patients. Antivirals (eg, oseltamivir, peramivir, or zanamivir for influenza; acyclovir for herpes
simplex and varicella-zoster infections; ribavirin for respiratory syncytial virus or parainfluenza 3
infections) may be lifesaving.

Replacement of missing immune components

Such replacement helps prevent infection. Therapies used in more than one primary
immunodeficiency disorder include the following:

 IV immune globulin (IVIG) is effective replacement therapy in most forms of antibody

deficiency. The usual dose is 400 mg/kg once a month; treatment is begun at a low infusion
rate. Some patients need higher or more frequent doses. IVIG 800 mg/kg once a month
helps some antibody-deficient patients who do not respond well to conventional doses,
particularly those with a chronic lung disorder. High-dose IVIG aims to keep IgG trough
levels in the normal range (> 600 mg/dL [> 6 g/L]).
 Subcutaneous immune globulin (SCIG) can be given instead of IVIG. SCIG can be given
at home, usually by patients themselves. The usual dose is 100 to 150 mg/kg once a week.
Because SCIG and IVIG differ in bioavailability, the dose of SCIG may need to be adjusted
if patients are switched from IVIG. With SCIG, local site reactions are a risk, but SCIG
seems to have fewer systemic adverse effects.

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  Hematopoietic stem cell transplantation  using bone marrow, umbilical cord blood, or
adult peripheral blood stem cells is effective for lethal T-cell and other immunodeficiencies.
Pretransplantation chemotherapy is unnecessary in patients without T cells (eg, those with
SCID). However, patients with intact T-cell function or partial T-cell deficiencies (eg, Wiskott-
Aldrich syndrome, combined immunodeficiency with inadequate but not absent T-cell
function) require pretransplantation chemotherapy to ensure graft acceptance. When a
matched sibling donor is unavailable, haploidentical bone marrow from a parent can be
used. In such cases, mature T cells that cause graft-vs-host disease must be rigorously
depleted from parental marrow before it is given. Umbilical cord blood from an HLA-matched
sibling can also be used as a source of stem cells. In some cases, bone marrow or umbilical
cord blood from a matched unrelated donor can be used, but after transplantation,
immunosuppressants are required to prevent graft-vs-host disease, and their use delays
restoration of immunity.

4. Primary Immunodeficiencies
 B cell deficiencies
 T cell deficiencies
 Combined B-cell and T-cell deficiencies
5. Secondary Immunodeficiencies
 HIV-AIDS
6. Compare the causes of immediate and delayed type of immune
responses.
7. Describe the immune mechanism involved in type I, type II, type III, and
type IV hypersensitivity reactions.
8. State the difference between an atopic and nonatopic hypersensitivity
response.
9. Describe the pathogenesis of allergic rhinitis, food allergy, serum
sickness, arthus reaction, contact dermatitis, and hypersensitivity
pneumonitis.
10. Characterize the differences in latex allergy caused by type I, Ig E
– mediated response and that caused by type IV, cell – mediated
hypersensitivity response.

Please prepare for an oral recitation.

***NOTHING FOLLOWS***

Thank You,

Atty. JOSEPH G. DINOY

Professor