THE IMMUNE SYSTEM

Protects body from harmful substances and micro-organisms.

Made up of complex collection of cells, proteins & various messengers.

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Classification
IMMUNE SYSTEM

Innate

Acquired

Active
Eg. Direct neutrophilic toxicity

Passive
Eg. Skin, tears

Active

Passive
Eg. Immunoglobulin transfer

Cell mediated (T cell)

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Antibody mediated (B cell)

Cells of Immune system

B-lymphocytes Lymphocytes that mature in bone marrow Mature Plasma cells antibodies Component of antibody mediated immune reaction T-lymphocytes Matures in Thymus Component of cell mediated immune reaction.
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Multiple Types of T Cells & their Functions

Cytotoxic T cells(Killer cells) Phagocytosis
Helper T cells (Th1 & Th2) activation of B cells, cytotoxic T cells, suppressor T cells & causes activation of macrophage system. Suppressor T cells (Regulatory T cells) Suppressing functions of both cytotoxic & helper T cells, regulates activity of other cells & keep them from causing excessive immune reactions that might be damaging to body.
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Cytokines
Group of extracellular factors produced by variety of cells including monocytes (monokines), lymphocytes (lymphokines). Cytokines include interleukins, some interferons & tumor necrosis factors (TNFs). Hormone-like proteins involved in cellular communication during immune responses

Act by binding to various receptors.

Cytokines are important in controlling local & systemic inflammatory response.
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Immune process

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Viruses
Viruses are primitive living cells also called as living chemicals. They form a link between nonliving and living world. Made up of a outer covering capsid and nucleic acid. Nucleic acid in viruses are only either DNA or RNA. Hence classified as DNA / RNA viruses.
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Life cycle of Virus

Step 7 : Release The bacterial cell lyses and releases many infective virions. Step 1 : Attachment Virus attaches to the cell wall. Step 2 : Penetration The viral DNA is injected into the cytoplasm.

Step 6: Assembly Viral components are assembled into mature virions.

Step 3 : Transcription Viral DNA is transcribed producing mRNA.

Step 5: Replication of Viral DNA and Synthesis of Proteins Viral coat proteins, other protein components, and DNA are produced separately, Host DNA degraded. Step 4 : Translation of viral proteins

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Human Papilloma Virus

Responsible for one of the most common disorders of the skin and mucous membranes warts. Plantar warts, common warts, and genital warts (condylomata acuminata) are all caused by different HPV types.

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Human Papilloma Virus

Family : Papovaviridae. The HPV virion is a small, nonenveloped icosahedral capsid that contains a single doublestranded circular DNA.

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Human Papilloma Virus

The viral capsid is made up of at least two proteins; the major structural protein accounts for more than 80% of the viral capsid.
Sexually transmitted disease (STD) common across all races and socioeconomic groups worldwide.
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Classification
At least 70 different HPV types have been identified; from 12 to 23 of these have been implicated in anogenital infections. These usually infect tissue of the internal and external genitalia and around the anus, although some types may also cause lesions on the oral mucosa, conjunctivae, and larynx.

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Classification
Classified into three groups:
Those causing benign, low-risk lesions (types 6 and 11) Those carrying a moderate risk of oncogenic potential (types 33, 35, 39, 40, 43, 51 through 56, and 58) Those associated with a high risk of oncogenic potential (types 16 and 18).
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Transmission and risk factors

Sexually transmitted: 73% of sexual partners of persons with clinically evident genital HPV infection manifest evidence of the infection at their initial examination.

Risk Factors: Initiation of sexual intercourse at an early age Multiple sex partners Persons with other STD`s Low cellular immunity.
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Pathogenesis
Trauma (e.g. abrasion during sexual contact) to the epithelial cells of the penis or vulva virus entry Infects the basal cell layer latent phase (from several months to year) Production of Viral DNA in basal cell nuclei (only dividing cells in epidermis) Expression of viral DNA leading to abnormal proliferation of keratinocytes and blood vessels Formation of warts Sales Training

Koilocytes
Mature squamous cells that display a ballooned cytoplasmic vacuole lying against the nucleus.
Due to a specific cytopathic effect of HPV infection.

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Clinical Features
Incubation period : may be as long as 9 months. Tends to persist or wax and wane for years.

Manifestations ranges from subclinical infection, in which there is no clinical presentation, to multiple, hyperplastic, exophytic lesions warts.

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Clinical Features

Penile Lesions

Warts on Labia Minora

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Clinical Features
Involve all genital areas, including the perianal area, perineum, and surrounding skin. Genital warts appear cauliflower-like and are usually hyperplastic, sessile, or pigmented papules.
Areas around warts are sub-clinically infected with the virions.
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Clinical Features
Hyperplastic warts (classic condylomata acuminata)
Are flesh-colored, pink, or hyperpigmented Papules and plaques Pointed projections on their surfaces

Sessile warts
Flat, nonexophytic lesions Flesh-colored or pink papules and plaques Smooth surface
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Clinical Features
In females:
vulva (introitus, labia minora / majora) the perianal area. vagina

In males:
Penile Shaft. the perianal area Glans penis

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Diagnosis
Usually the diagnosis is clinical.
Methods used to diagnose
visual inspection cytologic analysis (Papanicolaou [Pap] smear) colposcopy histologic analysis (biopsy) laboratory tests for HPV-DNA detection.
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Conventional Therapies
Patients and physicians, dissatisfaction is considerable. No one method has emerged as superior to any other. All existing modalities are based on tissue destruction.

NO THERAPY TO CONTROL THE INFECTING AGENT.

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Conventional Therapies
These therapies include either chemically induced cytotoxicity or physical destruction of infected tissue. Cell-mediated immunity appears to be the primary event responsible for wart regression . Currrently classified as: Provider-administered therapies Patient-administered therapies
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Conventional Therapies
Therapy Agent
1 Local Excision

Mechanism of Action
Surgical removal

2 Cryotherapy
3 CO2 Laser Vaporisation 4 Electrocautrey 5 Podophyllin

Physically Freeze/ thaw to destroy tissue. Vaporisation of tissue

Physical destruction of tissue Antimitotic

7 Podophyllotoxin 8 Trichloroacetic acid 9 Interferon

Antimitotic Chemical destruction Antiviral

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Genital Warts: Treatment

Podophyllin resin (10% to 25%):

Unstable- very wide range of clearance rates.

High recurrence rate Extremely neurotoxic Not be used on any mucosal surface (systemically absorbed) Erythematous and painful Must not be used in the vagina or the anus Carcinogenic
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Genital Warts: Treatment

Bichloro- or trichloroacetic acid (BCA/TCA) in an 80% to 90% concentration: Burning Contact with the surrounding epithelium may be extremely painful and may produce significant local erythema and swelling. Several weekly applications may be required. Large and keratinized condylomas are more refractory to BCA/TCA therapy
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Genital Warts: Treatment

Interferon Intra/sub lesional administration.
Frequent administrations. incidence of systemic S/E like flu-like symptoms, fever, body ache etc. Complete response rates from 36-63%. Costly therapy.
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Genital Warts: Treatment

Cryotherapy
effective against small, discrete genital and anal warts. involves freezing the wart and a small area of surrounding tissue with an agent such as nitrous oxide pain occasional ulceration secondary infection
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Genital Warts: Treatment Limitation

Cryotherapy: uncomfortable because of the extreme cold, secondary infections, repeated sittings, scarring. Surgical excision/ electrosurgery: low long-term clearance rates, postprocedure discomfort, superinfection. Laser vaporization: very expensive and require significant training, hypo- or hyperpigmentation or even scarring. Intralesional interferons:high cost, painful injections, systemic side effects and variable Sales Training efficacy.

Limitations of Current Therapies

No single method eradicates warts and eliminates the virus.
Variable efficacy.

Associated with high rates of wart recurrence.

Frequent cause of inconvenience and require repeated visits to physician.

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Limitations of Current Therapies

Surgical techniques
Painful Disfiguring Impractical for patients with disseminated infection.

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