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Good defense by Mind Map: Good defense

1. Lower respiratory tract

1.1. Consist of

1.1.1. Windpipe ( trachea)

1.1.2. Lung

1.2. Common infections

1.2.1. Tracheitis

1.2.2. Bronchitis

1.2.3. Pneumonia

1.2.4. Lung abscesses

2. Vaccines

2.1. Types

2.1.1. Live attenuated

2.1.2. Inactivated (killed)

2.1.3. Toxoids

2.1.4. Conjugated

2.1.5. Subunit

2.2. Routes of administration

2.2.1. SC

2.2.1.1. Measles

2.2.1.2. Yellow fever

2.2.2. ID

2.2.2.1. BCG

2.2.3. IM

2.2.3.1. D TwP, DTap, DT , Td, TT

2.2.3.2. Hepatitis B

2.2.3.3. IPV

2.2.3.4. Hib

2.2.3.5. PCV-7

2.2.4. Oral

2.2.4.1. OPV

2.2.4.2. Rotavirus

2.2.5. Intranasal

2.3. Contraindications

2.3.1. Live vaccines

2.3.1.1. Immunocompromised patients

2.3.1.2. Malignancy

2.3.1.3. Pregnancy

2.3.2. Toxoids

2.3.2.1. Encephalopathy

2.3.3. Haptitis B

2.3.3.1. Allergy to baker's yeast

2.3.4. HPV

2.3.4.1. Pregnancy

2.3.4.2. Allergy to yeast

2.3.5. MMR , Zoster & Varciella

2.3.5.1. Pregnancy

2.3.5.2. Immunodeficiency

2.3.5.3. Allergy to gelatin or neomycin

2.3.5.4. Untreated active tuberculosis ( only for varicella)

2.4. Complications

2.4.1. Injection site reactions

2.4.1.1. Pain

2.4.1.2. Swelling

2.4.1.3. Erythema

2.4.2. Retrovirus vaccine ( oral)

2.4.2.1. Mild diarrhea

2.4.2.2. Vomiting

2.4.3. Varicella & Zoster vaccines

2.4.3.1. Skin rash

2.4.4. Hepatitis A & B , human papilloma virus and meningococcal vaccine

2.4.4.1. Guillain - Barre syndrome ( GBS)

2.4.4.2. Autoimmune destruction of myelin sheath surrounding peripheral nerves

3. Whooping cough

3.1. Features of bordetella pertussis

3.1.1. Gram negative coccobacillus

3.1.2. Strict aerobe

3.1.3. Highly infectious

3.1.4. Human pathogen of ciliated respiratory epithelium

3.1.5. Transmitted by respiratory droplets from infected individuals

3.1.6. Occurs in primarily previously vaccinated individuals whose immunity has waned or unvaccinated ones

3.1.7. The most severe disease occurs in unvaccinated infants

3.2. Pathogenesis

3.2.1. Attachment

3.2.1.1. Pertactin and filamentous hemagglutinin

3.2.2. Tracheal cytotoxins

3.2.2.1. Mucus accumulation

3.2.3. Pertussis toxins and adenylate cyclades toxin

3.2.3.1. Inhibit early function of neutrophils & macrophages

3.2.4. Vasodilation

3.2.4.1. Narrowing air path

3.2.5. Pertussis toxins

3.2.5.1. Increase lymphocytosis

3.3. Complications

3.3.1. Pressure related from paroxysms

3.3.1.1. Subconjunctival hemorrhage

3.3.1.2. Rectal prolapse

3.3.1.3. Hernia

3.3.1.4. Epistaxis

3.3.2. Respiratory

3.3.2.1. Sinusitis

3.3.2.2. Pneumonia

3.3.2.3. Pneumothorax

3.3.3. Neurological

3.3.3.1. Seizures

3.3.3.2. Encephalitis

4. Levels of prevention

4.1. Primary

4.1.1. Preventing disease before it occurs

4.2. Secondary

4.2.1. Reduce the impact of a disease or injury

4.3. Tertiary

4.3.1. Soften the impact of ongoing illness or injury that has lasting effect

5. Azithromycin

5.1. WHO’s list of essential medicines

5.2. Class

5.2.1. protein synthesis inhibitors

5.3. Subclass

5.3.1. macrolide

5.4. Rout of administration

5.4.1. oral

5.4.2. IV

5.4.3. ophthalmic

5.5. Mainly bacteriostatic

5.5.1. with increased concentration it becomes bactericidal

5.6. Used to treat

5.6.1. Community-acquired pneumonia

5.6.1.1. Chlamydia pneumonia

5.6.1.2. mycoplasma pneumonia

5.6.1.3. streptococcus pneumonia

5.6.2. Urethritis

5.6.3. cervicitis

5.6.4. Pelvic inflammatory disease

5.6.5. Tonsillitis

5.6.6. Otitis media

5.7. Adverse Effects

5.7.1. CNS

5.7.1.1. vertigo

5.7.1.2. headache

5.7.1.3. fatigue

5.7.2. CV

5.7.2.1. palpitation

5.7.2.2. chest pain

5.7.3. GI

5.7.3.1. abdominal pain

5.7.3.2. vomiting

5.7.3.3. diarrhea

5.7.4. GU

5.7.4.1. candidiasis

5.7.4.2. vaginitis

5.7.4.3. nephritis

5.7.5. Skin

5.7.5.1. rash

5.7.5.2. photosensitivity

5.8. Work in 3 ways

5.8.1. Neutralization

5.8.1.1. Block the binding of toxins or the bacteria to host cells

5.8.2. Opsonisation

5.8.2.1. Coating antigens and allow it to be exposed to macrophages to be engulfed by phagocytosis process

5.8.3. Complement Activation

5.8.3.1. Enhance phagocytosis

6. Development of Disease

6.1. Incubation period

6.1.1. The interval between the initial infection and the first appearance of any signs or symptoms

6.2. Prodromal period

6.2.1. Appearance of early, mild symptoms. Relatively short

6.3. Period of illness

6.3.1. Most severe. Exhibition of overt signs and symptoms. WBC increase

6.4. Death

6.4.1. OR

6.4.1.1. Period of decline

6.4.1.1.1. Signs and symptoms subside. Patient is vulnerable to secondary infections

6.5. Period of convalescence

6.5.1. Regaining strength, recovery

7. Upper respiratory tract

7.1. Consist of

7.1.1. Nostril

7.1.2. Nasal cavity

7.1.3. Mouth

7.1.4. Throat ( pharynx)

7.1.5. Voice box ( larynx)

7.2. Common microbiota

7.2.1. Gram +ve bacteria

7.2.1.1. Staphylococcus spp.

7.2.1.2. Corynebacterium spp.

7.2.1.3. Streptococcus spp.

7.2.2. Gram -ve bacteria

7.2.2.1. Haemophilus spp.

7.2.2.2. Moraxella spp.

7.3. Common infections

7.3.1. Nasopharyngitis (common cold)

7.3.2. Laryngotracheitis

7.4. Bacteroides spp.

8. CAM

8.1. Abbreviation of Complementary and alternative medicine

8.2. Describes therapies that have typically not been part of conventional western medicine

8.3. Complementary Vs Alternative

8.3.1. Complementary

8.3.1.1. If a non-mainstream practice is used together with conventional medicine

8.3.2. Alternative

8.3.2.1. If a non-mainstream practice is used in place of conventional medicine

8.4. CAM can be divided into

8.4.1. Natural products

8.4.1.1. Dietary supplements

8.4.1.2. Herbal remedies

8.4.2. Mind and body practices

8.4.2.1. Meditation

8.4.2.2. Prayer

8.4.2.3. Art therapies

8.4.2.4. Osteopathic manipulation

8.4.2.5. Massage

8.4.2.6. Energy therapies

8.5. Other complementary health approaches

8.5.1. Ancient healing systems

8.5.1.1. Ex: Ayurveda

8.5.2. Homeopathy

8.5.2.1. Small doses of a drug that stimulate the body defense

8.5.3. Naturopathy

8.5.3.1. Noninvasive treatments that help body self- healing

8.6. Why are some doctors hesitant about CAM ?

8.6.1. Healthcare providers are not trained to use CAM

8.6.2. Not well studied

8.6.3. Some CAM practitioners make exaggerated claims about curing diseases

8.6.4. CAM practitioners may ask patients to forgo treatment from their conventional doctor

8.7. Cultural competence skills

8.7.1. It is the ability of the doctor to ask about various patients' beliefs and incorporate new awareness into diagnosis and treatment planning

8.7.2. It aims in building trust between the doctor and the patient relationship

9. Relative risk reduction

9.1. Proportion of risk reduction attributable to the intervention as compared to a control

9.2. Formula

9.2.1. RRR= (risk in controls - risk in treatment group) /risk in controls

9.2.2. Or

9.2.2.1. RRR= (1-RR )* 100 where RR= risk in exposed / risk in unexposed

10. Antibodies

10.1. Structure

10.1.1. Consist of 4 polypeptides

10.1.1.1. 2 heavy chains

10.1.1.2. 2 light chain

10.1.2. Variable region

10.1.2.1. Antigen binding site

10.1.2.2. Composed of 110 to 130 AA

10.1.3. Constant region

10.1.3.1. Differ from one class to the other

10.2. Classes of antibodies

10.2.1. IgG

10.2.1.1. Gamma H.chain

10.2.1.2. Most common

10.2.1.3. Found in serum

10.2.1.4. Categorized into 4 subclasses ranging from 1-4

10.2.1.5. Responsible for resistance against many kinds of viruses, bacteria and bacterial toxins

10.2.1.6. Crosses the placenta

10.2.1.7. Half life in serum around 23 days

10.2.2. IgM

10.2.2.1. Mu H. chain

10.2.2.2. First antibody type secreted after an an antigen arrives

10.2.2.3. Protects against blood-born pathogens

10.2.2.4. Binds complement

10.2.2.5. Have half life around 2-3 days

10.2.2.6. First Ig synthesized by the infants

10.2.3. IgD

10.2.3.1. Delta H. chain

10.2.3.2. Located on the surface of B cells

10.2.3.3. Monomer antibody

10.2.3.4. Mostly found as a part of B lymphocytes

10.2.3.5. Have immuno- regulatory function

10.2.4. IgA

10.2.4.1. Alpha H.chain

10.2.4.2. Found in serum and body secretions

10.2.4.3. Transported across the epithelium via transcytosis

10.2.4.4. Exists as a dimmer in the body secretions

10.2.4.5. Provides a protective coat for the mucous surface against microbial colonization and adherence

10.2.4.6. Transfer via breast milk

10.2.5. IgE

10.2.5.1. Epsilon H.chain

10.2.5.2. Monomer

10.2.5.3. Short half life of 2 days

10.2.5.4. Present respiratory & intestinal epithelia

10.2.5.5. Bind to mast cells

10.2.5.5.1. Release histamine

10.2.5.6. Plays a role in parasitic helminthic infections

11. Acquired immunity

11.1. B lymphocytes

11.1.1. Produced in bone marrow

11.1.2. Activate the humoral response

11.1.3. Produce plasma cells

11.1.3.1. Antibodies

11.1.3.1.1. Each B cell have only one type of antibodies on its surface

11.1.4. Memory B cells

11.1.5. Acts as antigen presenting cells

11.1.6. Produce cytokines

11.2. T lymphocytes

11.2.1. Matures in thymus

11.2.2. Mainly of 2 types

11.2.2.1. T helper cells ( CD4 )

11.2.2.1.1. Activated by antigen presenting cells

11.2.2.1.2. Secrets cytokines to activate other immune cells

11.2.2.2. T cytotoxic cells (CD8)

11.2.2.2.1. Binds to MHC1

11.2.2.2.2. Kill target cells by secreting a protein called perforin

12. Normal WBC count

12.1. Adults 4800-10800 Per microliter of blood

12.1.1. Differential count= % of each WBC in the blood

12.1.1.1. Neutrophils 40-75%

12.1.1.2. Lymphocytes 15-40%

12.1.1.3. Monocytes 2-10%

12.1.1.4. Eosinophils 1-6%

12.1.1.5. basophils 0-2%

12.2. Higher in neonate and children

13. Iceberg Phenomenon

13.1. Definition

13.1.1. It is the portion of disease that remains undetected or unrecorded despite physician’s diagnostic endeavors

13.2. Causes

13.2.1. Site of bacteria

13.2.2. Immune system

13.2.3. Genetics

13.2.4. Predisposing factors

13.2.4.1. sex

13.2.4.2. age

13.2.4.3. nutrition