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