Understanding the human immune system. Includes discussions about Allergy, Rheumatology and Non-infectious skin diseases (acne and psoriasis)

1. IMMUNOLOGY:
A BACKGROUND
Reported by:
MA. LOURDES L. MOJARES, R. Ph.
CEU Graduate School
Ph. D. in Pharmacy

2. IMMUNOLOGY: DEFINITION
Study of;
1. the protection of the human
body from foreign
macromolecules or invading
organisms.
2 responses of the human body
to them.

3. OUR FIRST LINE OF DEFENSE:
These cells include;
1. macrophages
2. neutrophils
that engulf foreign organisms and
kill them without the need for
antibodies.

4. OUR SECOND LINE OF DEFENSE:
 The specific or adaptive immune
system
Which may take days to respond
to a primary invasion (that is
infection by an organism that has
not hitherto been seen).

5. THE IMMUNE SYSTEM
1. Innate or Non-specific
Immune System
1. Adaptive or Specific Immune
System

6. OVERVIEW OF THE IMMUNE
SYSTEM

7. DEVELOPMENT OF THE CELLS OF
THE IMMUNE SYSTEM

8. CELLS OF THE IMMUNE SYSTEM

9. MAIN FUNCTION OF THE IMMUNE
SYSTEM
The ability to distinguish
between self and non-self is
necessary to protect the
organism from invading
pathogens and to eliminate
modified or altered cells (e.g.
malignant cells).

10. MAIN FUNCTION OF THE IMMUNE
SYSTEM
 It is important to remember
that infection with an organism
does not necessarily mean
diseases, since the immune
system in most cases will be
able to eliminate the infection
before disease occurs.

11. CAUSES OF A DISEASE:
When the bolus of infection is

high.
The virulence of the microrganism
is great.
When immunity is compromised.

12. NON – SPECIFIC SPECIFIC
IMMUNITY IMMUNITY
Response is antigen- Response is antigen-
dependent dependent
There is immediate There is lag time between
maximal response exposure and maximal
response
Non-antigen specific Antigen - specific
Exposure results in no Exposure results in
immunologic memory immunologic memory

13. INNATE / NON-SPECIFIC
IMMUNITY
The elements of the innate
(non-specific) immune system
include;
1. anatomical barriers
2. secretory molecules
3. cellular components

14. ANATOMICAL BARRIERS TO
INFECTIONS
1. MECHANICAL FACTORS
The skin acts as our first line of
defense against invading
organisms.
Movement due to cilia or
peristalsis helps to keep air
passages and the gastrointestinal
tract free from microorganisms.

15. ANATOMICAL BARRIERS TO
INFECTIONS
1. MECHANICAL FACTORS
The flushing action of tears and
saliva helps prevent infection of
the eyes and mouth.
The trapping effect of mucus that
lines the respiratory and
gastrointestinal tract helps protect
the lungs and digestive systems
from infection.

16. ANATOMICAL BARRIERS TO
INFECTIONS
2. CHEMICAL FACTORS
Fatty acids in sweat inhibit the growth of
bacteria.
Lysozyme and phospholipase found in
tears, saliva and nasal secretions can
breakdown the cell wall of bacteria
and destabilize bacterial membranes.

17. ANATOMICAL BARRIERS TO
INFECTIONS
2. CHEMICAL FACTORS
The low pH of sweat and gastric
secretions prevents growth of
bacteria.
Defensins (low MW proteins) found in the
lung and gastrointestinal tract have
antimicrobial activity.

18. ANATOMICAL BARRIERS TO
INFECTIONS
3. BIOLOGICAL FACTORS
The normal flora of the skin and in the
gastrointestinal tract can
prevent the colonization of pathogenic
bacteria by;
1. secreting toxic substances
2. competing with pathogenic bacteria
for nutrients or attachment to cell
surfaces.

19. HUMORAL BARRIERS TO
INFECTIONS
Humoral factors play an important role
in inflammation, which is
characterized by edema and the
recruitment of phagocytic cells.
These humoral factors are found in
serum or they are formed at the site
of infection.

20. HUMORAL BARRIERS TO
INFECTIONS
1. Complement System
The complement system is the major
humoral non-specific defense
mechanism.

21. HUMORAL BARRIERS TO
INFECTIONS
1. Complement System
Once activated complement can lead
to;
a. increased vascular permeability
b. recruitment of phagocytic cells, c.
lysis
d. opsonization of bacteria

22. HUMORAL BARRIERS TO
INFECTIONS
2. Coagulation System
Some products of the coagulation
because of their ability to;
a. increase vascular permeability b.
act as chemotactic agents for
phagocytic cells.

23. HUMORAL BARRIERS TO
INFECTIONS
2. Coagulation System
In addition, some of the products of
the coagulation system are directly
antimicrobial.
For example, beta-lysin, a protein
produced by platelets during
coagulation can lyse many Gram
positive bacteria by acting as a
cationic detergent.

24. HUMORAL BARRIERS TO
INFECTIONS
2. Lactoferrin and Transferrin
By binding iron, an essential nutrient
for bacteria, these proteins limit
bacterial growth.

25. HUMORAL BARRIERS TO
INFECTIONS
3. Interferons
Interferons are proteins that can limit
virus replication in cells.
4. Lysozyme
Lysozyme breaks down the cell wall of
the bacteria.

26. HUMORAL BARRIERS TO
INFECTIONS
5. Interleukin – 1
Il-1 induces fever and the production of
acute phase proteins, some of which
are antimicrobial because they can
opsonize bacteria.

27. PHYSICO-CHEMICAL BARRIERS
TO INFECTIONS
SYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISM
SKIN SQUAMOUS CELLS / DESQUAMATION
SWEAT FLUSHING
ORGANIC ACIDS
GI TRACT COLUMNAR CELLS PERISTALSIS
LOW pH
BILE ACID
FLUSHING
THIOCYANATE
LUNGS TRACHEAL CILIA MUCOSCIALARY ELEVATOR
SURFACTANT
NASOPHARYNX MUCUS, SALIVA, FLUSHING
AND EYE TEARS LYSOZYME

28. PHYSICO-CHEMICAL BARRIERS
TO INFECTIONS
SYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISM
CIRCULATION PHAGOCYTIC CELLS PHAGOCYTOSIS
AND AND
LYPHOID ORGANS INTRACELLULAR KILLING
NK CELLS DIRECT
AND AND
K CELLS ANTIBODY DEPENDENT
CYTOLYSIS
LAK IL – 2 ACTIVATED CYTOLYSIS

29. PHYSICO-CHEMICAL BARRIERS
TO INFECTIONS
SYSTEM / ACTIVE COMPONENT EFFECTOR MECHANISM
ORGAN
SERUM LACTOFERRIN IRON BINDING
AND
TRANSFERRIN
INTERFERONS ANTIVIRAL PROTEINS
TNF - ALPHA ANTIVIRAL,
PHAGOCYTE ACTIVATION

30. PHYSICO-CHEMICAL BARRIERS
TO INFECTIONS
SYSTEM / ORGAN ACTIVE COMPONENT EFFECTOR MECHANISM
SERUM LYSOZYME PEPTIDOGLYCAN
HYDROLYSIS
FIBRONECTIN OPSONIZATION
AND
PHAGOCYTOSIS
COMPLEMENT OPZONIZATION,
ENHANCED
PHAGOCYTOSIS,
INFLAMMATION

31. CELLULAR BARRIERS TO
INFECTIONS
Part of the inflammatory
response is the recruitment of
polymorphonucleareosinophile
s and macrophages to sites of
infection.

32. CELLULAR BARRIERS TO
INFECTIONS
1. NeutrophilsPolymorphonuclear cells
are recruited to the site of infection
where they phagocytose invading
organisms and kill them intracellularly.
In addition, PMNs contribute to collateral
tissue damage that occurs during
inflammation.

33. CELLULAR BARRIERS TO
INFECTIONS
2. Macrophages and Newly
Recruited Monocytes
Differentiate into macrophages,
also function in phagocytosis
and intracellular killing of
microorganisms.

34. CELLULAR BARRIERS TO
INFECTIONS
3. Natural Killers
(NK)andLymphokine Activated
Killer (LAK) cells
NK and LAK cells can nonspecifically kill virus
infected and tumor cells.
These cells are not part of the inflammatory
response but they are important in
nonspecific immunity to viral infections
and tumor surveillance.

35. NK CELLS AND ITS ACTIVATION

36. CELLULAR BARRIERS TO
INFECTIONS
4. Eosinophils
They have proteins in granules
that are effective in killing
certain parasites.

37. KILLER (K) CELLS
Killer(K) cells are not a
morphologically distinct type of
cell.
Rather a K cell is any cell that
mediates antibody-dependent
cellular cytotoxicity (ADCC).

38. KILLER (K) CELLS
InADCC antibody acts as a link to
bring the K cell and the target cell
together to allow killing to occur.
K cells have on their surface an Fc
receptor for antibody and thus they
can recognize, bind and kill target
cells coated with antibody.

39. KILLER (K) CELLS
Killercells which have Fc receptors
include NK, LAK, and macrophages
which have an Fc receptor for IgG
antibodies and eosinophils which
have an Fc receptor for IgE
antibodies.

40. KILLING OF OPSONIZED
TARGET BY THE K CELL

41. PHAGOCYTOSIS AND
INTRACELLULAR KILLING
A. PHAGOCYTIC CELLS
1. Neutrophiles / Polymorphonuclear (PMN)
Cells
1.1 primary or azurophilic granules, which are
abundant in young newly formed PMNs, contain
cationic proteins and defensins that can kill
bacteria, proteolytic enzymes like elastase, and
cathepsin G to breakdown proteins, lysozyme to
break down bacterial cell walls, and
characteristically, myeloperoxidase, which is
involved in the generation of bacteriocidal
compounds.

42. PHAGOCYTOSIS AND
INTRACELLULAR KILLING
A. PHAGOCYTIC CELLS
1. Neutrophiles / Polymorphonuclear (PMN)
Cells
1. 2 secondary or specific granule
These contain lysozyme, NADPH oxidase
components, which are involved in the generation
of toxic oxygen products, and characteristically
lactoferrin, an iron chelating protein and B12-
binding protein.

43. PHAGOCYTOSIS AND
INTRACELLULAR KILLING
A. PHAGOCYTIC CELLS
2. Monocytes / Macrophages
Macrophages are phagocytic cells that have a
characteristic kidney-shaped nucleus.
They can be identified morphologically or by
the presence of the CD14 cell surface marker.

44. OXYGEN –INDEPENDENT MECHANISMS
OF INTRACELLULAR KILLING
EFFECTOR FUNCTION
MOLECULE
Cationic Proteins Damage to microbial
(including cathepsin) membranes
Lysozyme Splits mucopeptide in
the bacterial cell wall
Lactoferrin Deprives proliferating
bacteria of iron
Proteolytic and Digestion of killed
Hydrolytic Enzymes organisms

45. RESPONSE OF PHAGOCYTES TO
INFECTION
 Circulating PMNs and monocytes respond to
danger (SOS) signals generated at the site of an
infection.
 SOS signals include;
1. N-formyl-methionine containing peptides
released by bacteria
2. clotting system peptides
3. complement products
4. cytokines released from tissue macrophages
that have encountered bacteria in tissue

46. RESPONSE OF PHAGOCYTES TO
INFECTION
Some of the SOS signals stimulate
endothelial cells near the site of the
infection to express cell adhesion
molecules such as;
1. ICAM-1
2. selectins
which bind to components on the surface
of phagocytic cells and cause the
phagocytes to adhere to the endothelium.

47. RESPONSE OF PHAGOCYTES TO
INFECTION
Vasodilators produced at the site of
infection cause the junctions between
endothelial cells to loosen and the
phagocytes then cross the endothelial
barrier by “squeezing” between the
endothelial cells in a process called
“DIAPEDESIS.”

48. CHEMOTACTIC RESPONSE TO
INFLAMMATORY STIMULUS

49. RESPONSE OF PHAGOCYTES TO
INFECTION
Once in the tissue spaces some of the
SOS signals attract phagocytes to the
infection site by chemotaxis (movement
toward an increasing chemical
gradient).

50. RESPONSE OF PHAGOCYTES TO
INFECTION
The SOS signals also activate the
phagocytes, which results in;
1. increased phagocytosis
2. intracellular killing of the invading
organisms.

51. DISEASES OF THE
IMMUNE SYSTEM
ALLERGIES:
Asthma (Bronchial, Exercise Induced)
Dermatitis (Contact and Atopic)
Arthritis (Rheumatoid and Reactive)

52. ALLERGY: DEFINITION
An immune response or
reaction to substances that are
usually not harmful.
Allergies are pretty common.
Both genes and environment
play a role.

53. COMMON ALLERGENS:
 Drugs
 Dust
 Food
 Insect venom
 Mold
 Pet and other animal dander
 Pollen

54. RARE ALLERGENS:
 Hot or Cold Temperatures
 Sunlight
Friction (clothing
/garters, rubbing or stroking the
skin)

55. ALLERGY: SYMPTOMS
Allergens that one breathes
1. stuffy nose
2. itchy nose and throat
3. mucus production
4. cough
5. wheezing

56. ALLERGY: SYMPTOMS
Allergens that touch the eyes
1. itchy
2. watery
3. red
4. swollen

57. ALLERGY: SYMPTOMS
Allergens that one gets from
foods eaten / drugs taken.
1. nausea and vomiting
2. abdominal pain
3. cramps
4. diarrhea
5. life-threatening reaction

58. ALLERGY TESTING:
 Complete Blood Count (CBC)
Eosinophil WBC Count
An absolute eosinophil count is a
blood test that measures the
number of white blood cells called
eosinophils.

59. ALLERGY TESTING:
Eosinophil WBC Count
This test may help diagnose:
1. Acute hypereosinophilic syndrome (a
rare but sometimes fatal leukemia-like
condition)
2. An allergic reaction (can also reveal
how severe the reaction is)
3. Early stages of Cushing's disease
4. Infection by a parasite

60. ABNORMALLY HIGH
EOSINOPHIL WBC COUNT:
 Asthma
 Autoimmune diseases
 Eczema
 Hay fever
 Leukemia

61. ABNORMALLY LOW
EOSINOPHIL WBC COUNT:
CAUSES
 Alcohol intoxication
 Over production of certain steroids
in the body (such as cortisol)

62. ALLERGY: TREATMENT
Anaphylaxis - treated with
epinephrine
 Avoid exposure to ―triggers‖
Anthihistamines

63. ALLERGY: TREATMENT
Decongestants – used with
caution in patients with;
1. hypertension
2. heart problems,
3. prostate enlargement

64. ALLERGY: TREATMENT
Leukotriene inhibitors such as
Zafirlukast (Accolate) and
(Monteleukast) Singulair.
For treatment of indoor and
outdoor allergies and asthma.

65. ALLERGY: TREATMENT
 Allergy Shots or
Immunotherapy

66. ALLERGY: PROGNOSIS
 Most
allergies can be easily treated with
medication.
 Some children may outgrow an
allergy, especially food allergies.
However, once a substance has triggered an
allergic reaction, it usually continues to
affect the person.

67. ALLERGY: PROGNOSIS
 Allergyshots / Immunology are most
effective when used to treat people with hay
fever symptoms and severe insect sting
allergies.
 Theyare not used to treat food allergies
because of the danger of a severe reaction.

68. ALLERGY: PROGNOSIS
 Allergy shots may need years of treatment,
but they work in most cases.
However, they may cause uncomfortable
side effects;
 hives and rash
 Anaphylaxis (life-threatening allergic
reaction)
 Breathing problems and discomfort during
the allergic reaction
 Drowsiness and other side effects of
medicines

69. ALLERGY: PREVENTION
Breastfeeding babies for 4 to 6
months.
 Hygiene Hypothesis
Involves exposure of an infant
to ―allergens‖ during the first
year of life.

70. ALLERGY: SYMPTOMS
Allergens that touch the skin
1. rash
2. hives
3. itching
4. peeling

71. DISEASES OF THE
IMMUNE SYSTEM
ASTHMA:
BRONCHIAL
EXERCISE -INDUCED

72. ASTHMA: DEFINITION
A disorder that causes the
airways of the lungs to swell
and narrow, leading to;
1. wheezing
2. shortness of breath
3. chest tightness
4. coughing

73. ASTHMA: CAUSES
 Inflammation in the airways.
When an asthma attack
occurs, the muscles
surrounding the airways
become tight and the lining of
the air passages swells.

74. PATHOLOGY OF ASTHMA

75. ASTHMA TRIGGERS:
 Animals (pet hair or dander)
 Dust
 Changes in weather (most often cold
weather)
 Chemicals in the air or in food
 Exercise
 Mold and Pollen
 Respiratory infections, such as the
common cold
 Strong emotions (stress)
 Tobacco smoke

76. ASTHMA DRUG TRIGGERS:
Aspirin
NSAIDs
These drugs act as a deregulator
of leukotrienes.
Leukotrienes are substances in the
body that cause inflammation and
many of the symptoms in asthma.

77. ASTHMA: SYMPTOMS
Cough with or without sputum
(phlegm) production
Pulling in of the skin between the
ribs when breathing (intercostal
retractions)
Shortness of breath that gets
worse with exercise or activity

78. ASTHMA: SYMPTOMS
 Wheezing, which:
 Comes in episodes with symptom-free periods
in between
 May be worse at night or in early morning
 May go away on its own
 Gets better when using drugs that open the
airways (bronchodilators)
 Gets worse when breathing in cold air
 Gets worse with exercise
 Gets worse with heartburn (reflux)
 Usually begins suddenly

79. ASTHMA: EMERGENCY SYMPTOMS
 Bluish color to the lips and face
 Decreased level of alertness, such as
severe drowsiness or confusion,
during an asthma attack
 Extreme difficulty breathing
 Rapid pulse
 Severe anxiety due to shortness of
breath
 Sweating

80. ASTHMA: OTHER SYMPTOMS THAT MAY
OCCUR
 Abnormal breathing pattern --
breathing out takes more than twice
as long as breathing in
 Breathing temporarily stops
 Chest pain
 Tightness in the chest

81. ASTHMA:
EXAMINATIONS AND TESTS
 Skin Prick Test
 Placing a small amount of substances
that may be causing your symptoms
on the skin, most often on the
forearm, upper arm, or back.
 Then, the skin is pricked so the
allergen goes under the skin's
surface.

82. ASTHMA:
EXAMINATIONS AND TESTS
 Skin Prick Test
 Thehealth care provider closely
watches the skin for swelling and
redness or other signs of a reaction.
Results are usually seen within 15-20
minutes.
 Several
allergens can be tested at the
same time.

83. ASTHMA:
EXAMINATIONS AND TESTS
 Intradermal Skin Test:
 Injecting a small amount of allergen
into the skin.
 Then the health care provider watches
for a reaction at the site.
 This test is more likely to be used to
find out if you are allergic to
something specific, such as bee
venom or penicillin

84. ASTHMA:
EXAMINATIONS AND TESTS
 Patch Testing
 Used to diagnose the cause of skin
reactions that occur after the
substance touches the skin.
 Possible allergens are taped to the
skin for 48 hours.
 The health care provider will look at
the area in 72 - 96 hours.

85. ASTHMA:
EXAMINATIONS AND TESTS
 ArterialBlood Gas
 Performed by collecting a sample of
blood through a needle from an artery.
 The test is used to
1. evaluate respiratory diseases and
conditions that affect the lungs,
2. to determine the effectiveness of
oxygen therapy.

86. ASTHMA:
EXAMINATIONS AND TESTS
 Arterial Blood Gas
 3. The acid-base component of the
test also gives information on how
well the kidneys are functioning.

87. ASTHMA:
EXAMINATIONS AND TESTS
 Blood Tests
Measure;
1. eosinophil count (a type of white
blood cell)
2. IgE (a type of immune system
protein called an immunoglobulin)

88. ASTHMA:
EXAMINATIONS AND TESTS
 Chest X-Rays
 Lung Function Tests
(by Spirometry)
Painless study of air volume and flow
rate within the lungs.
Peak Flow Measurements

89. SPIROMETRY:

90. ASTHMA: GOALS OF TREATMENT
Control swelling of the airways.
Stay away from the substance
triggers.

91. KINDS OF MEDICATION IN
TREATING ASTHMA
Control drugs to PREVENT
attacks
Quick-relief
(rescue) drugs for
use DURING attacks

92. LONG-TERM CONTROL DRUGS
FOR ASTHMA
 Inhaled  Leokotriene Modifiers
Corticosteroids (Singulair, Accolate)
 LA – beta agonist  Cromolyn Sodium (Intal)
Inhalers
 Nedocromil Sodium
 Omalizumab (Xolair)
(Tilade)
 Combination Therapy
 Alternate Names
(Combination of all
fours)

93. QUICK RELIEF (RESCUE)
DRUGS for ASTHMA
These work fast to control asthma symptoms.
You take them when you are coughing, wheezing,
having trouble breathing, or having an asthma
attack.
 Short-Acting Bronchodilators
(Proventil, Ventolin,Xopenex)
 Oral Steroids (Corticosteroids)

94. ASTHMA: PROGNOSIS
 There is no cure for asthma,
although symptoms sometimes
improve over time.
With proper self management and
medical treatment, most people
with asthma can lead normal
lives.

95. ASTHMA ACTION PLAN:
A plan for taking asthma
medications when your condition
is stable.
A list of asthma triggers and how
to avoid them.
How to recognize when your
asthma is getting worse, and
when to call your doctor or nurse

96. ASTHMA:
POSSIBLE COMPLICATIONS
 Death
 Decreased ability to exercise and take
part in other activities
 Lack of sleep due to nighttime
symptoms
 Permanent changes in the function of
the lungs
 Persistent cough
 Trouble breathing that requires
breathing assistance (ventilator)

97. ASTHMA: PREVENTION
Cover bedding with "allergy-
proof" casings to reduce exposure
to dust mites.
Remove carpets from bedrooms
and vacuum regularly.
Use only unscented detergents
and cleaning materials in the
home.

98. ASTHMA: PREVENTION
Keep humidity levels low and fix
leaks to reduce the growth of
organisms such as mold.
Keep the house clean and keep
food in containers and out of
bedrooms -- this helps reduce the
possibility of cockroaches, which
can trigger asthma attacks in
some people.

99. ASTHMA: PREVENTION
 If a person is allergic to an animal
that cannot be removed from the
home, the animal should be kept
out of the bedroom.
Place filtering material over the
heating outlets to trap animal
dander.

100. ASTHMA: PREVENTION
Eliminate tobacco smoke from the
home.
This is the single most important
thing a family can do to help a
child with asthma.

101. DISEASES
OF THE
IMMUNE SYSTEM
CONTACT DERMATITIS
ALLERGIC TYPE
IRRITANT TYPE

102. CONTACT DERMATITIS:
DEFINITION
 A condition in which the skin
becomes red, sore, or inflamed
after direct contact with a
substance.
Two kinds of contact dermatitis:
1. irritant dermatitis
2. allergic dermatitis

103. IRRITANT CONTACT
DERMATITIS:
The most common type.
It's caused by contact with acids,
alkaline materials such as soaps,
detergents, fabric softeners,
solvents, or other chemicals.
The reaction usually looks like a
burn.

104. IRRITANTS INCLUDE:
Cement
Hairdyes
Long-term exposure to wet
diapers
Pesticides or weed killers
Rubber gloves
Shampoos

105. ALLERGIC CONTACT
DERMATITIS: DEFINITION
This is caused by exposure to a
substance or material to which
one have become;
1. extra sensitive
2. allergic

106. COMMON ALLERGENS:
 Adhesives, including  Balsam of Peru (used
those used for false in many personal
eyelashes or toupees products and
cosmetics, as well as
in many foods and
 Antibiotics such as
drinks)
neomycin rubbed on
the surface of the
skin  Fabrics and clothing

107. COMMON ALLERGENS:
 Fragrances in  Nickel or other metals
perfumes, cosmetics, (found in jewelry,
soaps, and watch straps, metal
moisturizers zips, bra hooks,
buttons,
pocketknives, lipstick
 Nail polish, hair dyes,
holders, and powder
and permanent wave
compacts)
solutions

108. COMMON ALLERGENS:
 Poison ivy, poison oak, poison sumac, and other
plants
 Rubber or latex gloves or shoes
 Coal Tar Products, Sulfa Ointments, Shaving
Lotions, Sun Screens, Lime Oil ( due to
photosensitivity)
 Air-borne allergens (Ragweed, Insecticides)

109. POISON IVY NICKEL
RASH ERYTHEMA

110. CONTACT DERMATITIS:
SYMPTOMS
 ALLERGIC DERMATITIS  IRRITANT
1. Itching DERMATITIS
1. Burning and Pain
2. Red, Streaky, Patchy
Rash 2. Dry, red, rough skin
3. Warm and Tender Skin 3. Cuts and Fissures
on Hands
4. Scaly, Crusty, Raw and
Thickened Skin

111. LABORATORY EXAMS AND
TESTS: DERMATITIS
Allergy Testing / Skin Patch
Testing
It determine which allergen is
causing the reaction.
Patch testing is used for certain
patients who have long-term,
repeated contact dermatitis.

112. LABORATORY EXAMS AND
TESTS: DERMATITIS
Allergy Testing / Skin Patch
Testing
It requires three office visits
and must be done by a health
care provider with the
experience and skill to interpret
the results correctly.

113. LABORATORY EXAMS AND
TESTS: DERMATITIS
Skin Lesion Biopsy
The removal of a piece of skin to
diagnose or rule out an illness.
Shave biopsy
Punch biopsy
Excisional biopsy
Incisional biopsy

114. SKIN LESION BIOPSY: PROCEDURES

115. LABORATORY EXAMS AND
TESTS: DERMATITIS
Skin or Nail Culture
A laboratory test to look for and
identify germs that cause
problems with the skin or nails.
It is called a mucosal culture if the
sample involves the mucous
membranes.

116. LABORATORY EXAMS AND
TESTS: DERMATITIS
Skin or Nail Culture
This test may be done to diagnose the
cause of:
1. A fungus infection of the skin, finger
or toenail
2. A skin rash or sore that appears to
be infected
3. A skin ulcer that is not healing

117. DERMATITIS: TREATMENT
 Washing with lots of water to remove any traces
of the irritant that may remain on the skin. Avoid
further exposure to known irritants or allergens.
 In some cases, the best treatment is to do
nothing to the area.
 Emollients or moisturizers help keep the skin
moist, and also help skin repair itself. They
protect the skin from becoming inflamed again.
They are a key part of preventing and treating
contact dermatitis.

118. DERMATITIS: TREATMENT
 Corticosteroid
ointments and
creams – reduce inflammation
 Tacrolimus
ointment or
Pimecrolimus cream
 Corticosteroid pills or shots
 Wet Dressings / Antipruritic lotions

119. DERMATITIS: PROGNOSIS
Contact dermatitis usually clears
up without complications in 2 or 3
weeks.
However, it may return if the
substance or material that caused
it cannot be found or avoided.

120. DERMATITIS: PROGNOSIS
There may be a need to change
your job or job habits if the
disorder is caused by
occupational exposure.

121. RHEUMATOLOGY
Rheumatoid Arthritis
Osteoarthritis
Gout
Rheumatic Fever

122. RHEUMATOLOGY: DEFINITION
 Deals with the diagnosis and
therapy of rheumatic diseases.
 Deals mainly with clinical problems
involving joints, soft tissues,
autoimmune diseases, vasculitis,
and heritable connective tissue
disorders.

123. RHEUMATISM: DEFINITION
A non-specific term used to
describe any painful disorder
affecting the loco-motor system
including joints, muscles,
connective tissues, soft tissues
around the joints and bones

124. RHEUMATISM: DEFINITION
Also used to describe
rheumatic fever affecting heart
valves.
 Rheumatoid arthritis
Alkylosingspondylitis
 Gout
 Systemic LE

125. ARTHRITIS: DEFINITION
 Inflammation of one or more joints.
A joint is the area where two bones
meet.
 There are over 100 different types of
arthritis.

126. ARTHRITIS: CAUSES
Breakdown of cartilage
 Joint inflammation, due to;
1. autoimmune disease (the body's
immune system mistakenly attacks
healthy tissue)
2. Broken bone
3. General "wear and tear" on joints
Infection, usually by bacteria or virus

127. ARTHRITIS: SYMPTOMS
 Joint pain
 Joint swelling
 Reduced ability to move the joint
 Redness of the skin around a joint
 Stiffness, especially in the morning
 Warmth around a join

128. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
 GOAL: to reduce pain, improve
function, and prevent further joint
damage.
The underlying cause cannot
usually be cured.

129. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
LIFESTYLE CHANGES
Lifestyle changes are the
preferred treatment for
osteoarthritis and other types of
joint inflammation.
Diet and Exercise

130. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
 Exercise programs may include:
Low-impact aerobic activity (also
called endurance exercise)
Range of motion exercises for
flexibility
Strength training for muscle tone

131. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
Physical Therapy:
1 Heat or ice compress
2. Splints or orthotics to support
joints and help improve their
position; this is often needed for
rheumatoid arthritis
3. Water therapy / Hydrotherapy
4. Massage

132. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
 8 to 10 hours of sleep
 Avoid staying in one position for
too long.
 Avoid positions or movements that
place extra stress on your sore
joints.
 Meditation, Yoga, Tai-chi
 Eat your fruits and vegetables

133. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
Eat foods rich in omega-3 fatty
acids, such as cold water fish
(salmon, mackerel, and herring),
flaxseed, rapeseed (canola) oil,
soybeans, soybean oil, pumpkin
seeds, and walnuts.

134. ARTHRITIS: NON-
PHARMACOLOGICAL TREATMENT
 Change your home to make
activities easier.
 Example, install grab bars in the
shower, the tub, and near the toilet.
 Lose the excess weight.
 Apply capsaicin liniment over
painful joints.

135. ARTHRITIS: -PHARMACOLOGICAL
TREATMENT
Acetaminophen is usually tried
first. Take up to 4 grams a day (two
arthritis-strength every 8 hours).
Do not take more than the
recommended dose or take the drug
along with a lot of alcohol. Doing so
may damage your your liver.

136. ARTHRITIS: -PHARMACOLOGICAL
TREATMENT
 Aspirin, Ibuprofen, or Naproxen are
nonsteroidal anti-inflammatory
drugs (NSAIDs)
Potential side effects include heart
attack, stroke, stomach
ulcers, bleeding from the digestive
tract, and kidney damage.

137. ARTHRITIS: -PHARMACOLOGICAL
TREATMENT
Biologics are used for 5. rituximab (Rituxan)
the treatment of  6. golimumab
autoimmune arthritis. (Simponi)
1. etanercept (Enbrel)  7. certolizumab
2. infliximab (Cimzia)
(Remicade)  8. tocilizumab
3. adalimumab (Actemra)
(Humira)
4. abatacept (Orencia)

138. ARTHRITIS:-PHARMACOLOGICAL
TREATMENT
 Corticosteroids ("steroids") help
reduce inflammation. They may be
injected into painful joints or given
by mouth.
 Disease-modifyinganti-rheumatic
drugs (DMARDs) are used to treat
autoimmune arthritis.

139. ARTHRITIS:-PHARMACOLOGICAL
TREATMENT
 DMARD’s include;
1. methotrexate
2. gold salts
3. penicillamine
4. sulfasalazine
5. hydroxychloroquine

140. ARTHRITIS:-PHARMACOLOGICAL
TREATMENT
Immunosuppressants such as
azathioprine or
cyclophosphamide are used to
treat patients with rheumatoid
arthritis when other medications
have not worked.

141. ARTHRITIS:
SURGICAL TREATMENT
 Arthroplasty to rebuild the joint

142. ARTHRITIS:
SURGICAL TREATMENT
 Joint
Replacement such as, total
knee joint replacement.

143. ARTHRITIS: PROGNOSIS
A few arthritis-related disorders
can be completely cured with
proper treatment.
Most forms of arthritis however
are long-term (chronic)
conditions.

144. ARTHRITIS: PROGNOSIS
Complications of arthritis
include:
Long-term (chronic) pain
Disability
Difficulty performing daily
activities

145. ARTHRITIS: PREVENTION
Early diagnosis and treatment
can help prevent joint damage. If
you have a family history of
arthritis, tell your doctor, even if
you do not have joint pain.
Avoiding excessive, repeated
motions may help protect against
osteoarthritis.

146. RHEUMATOID ARTHRITIS
 Or RA, is a form of arthritis that
causes pain, swelling, stiffness and
loss of function in the joints.
 It can affect any joint but is common in
the wrist and fingers.
 More women than men get
rheumatoid arthritis. It often starts
between ages 25 and 55.

147. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Antinuclear antibody (ANA)
Commonly found in the blood of people
who have lupus, ANAs (abnormal
antibodies directed against the cells’
nuclei) can also suggest the presence
of polymyositis, scleroderma, Sjogren’s
syndrome, mixed connective tissue
disease or rheumatoid arthritis.

148. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Antinuclear antibody (ANA)
Tests to detect specific subsets of
these antibodies can be used to
confirm the diagnosis of a particular
disease or form of arthritis.

149. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Rheumatoid factor (RF)
Designed to detect and measure the
level of an antibody that acts against
the blood component gamma globulin.
This test is often positive in people with
rheumatoid arthritis.

150. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Uric acid Measurement
By measuring the level of uric acid in
the blood, this test helps doctors
diagnose gout, a condition that occurs
when excess uric acid crystallizes and
forms deposits in the joints and other
tissues, causing inflammation and
severe pain.

151. LABORATORY EXAMS and
TESTS: ARTHRITIS
 HLA tissue typing
This test, which detects the presence of
certain genetic markers in the blood,
can often confirm a diagnosis of
ankylosingspondylitis (a disease
involving inflammation of the spine and
sacroiliac joint) or Reiter’s syndrome (a
disease involving inflammation of the
urethra, eyes and joints).

152. LABORATORY EXAMS and
TESTS: ARTHRITIS
 HLA tissue typing
The genetic marker HLA-B27 is almost
always present in people with either of
these diseases.

153. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Erythrocyte sedimentation rate
 Also called ESR or ―sed rate,‖ this test
measures how fast red blood cells cling
together, fall and settle (like sediment)
in the bottom of a glass tube over the
course of an hour.
 The higher the rate, the greater the
amount of inflammation.

154. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Lyme Serology
This test detects an immune response
to the infectious agent that causes
Lyme disease and thus can be used to
confirm a diagnosis of the disease.

155. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Skin Biopsy
Taking small samples of skin and
examining them under a microscope
can help doctors diagnose forms of
arthritis that involve the skin, such as
lupus, vasculitis (inflammation of the
blood vessels) and psoriatic arthritis.

156. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Muscle biopsy
By going a little deeper into the tissue
than with the skin biopsy, the surgeon
can take a sample of muscle to be
examined for signs of damage to the
muscle fibers.
Findings can confirm a diagnosis of
polymyositis or vasculitis.

157. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Joint fluid tests
In this procedure, which is similar to drawing
blood, the doctor inserts a needle into a joint
space and removes fluid.
An examination of the fluid may reveal uric
acid crystals, confirming a diagnosis of gout
or bacteria, suggesting that the joint
inflammation is caused by infection.

158. LABORATORY EXAMS and
TESTS: ARTHRITIS
 Muscle Enzymes Test ( CPK, Aldolase)
Such tests can measure the amount of
muscle damaged as well as how
effective medication has been in
reducing the inflammation that caused
the muscle damage.

159. RHEUMATOID ARTHRITIS
 An autoimmune disease in which
the body's immune system attacks
itself.
 The pattern of joints affected is
usually symmetrical, involves the
hands and other joints and is worse
in the morning.

160. RHEUMATOID ARTHRITIS
 Rheumatoid arthritis is also a
systemic disease, involving other
body organs, whereas osteoarthritis
is limited to the joints.
 Overtime, both forms of arthritis
can be crippling.

161. RHEUMATOID ARTHRITIS:
CAUSES
 Causeof RA is unknown. It is an
autoimmune disease, which means
the body's immune system
mistakenly attacks healthy tissue.
 RA
can occur at any age, but is
more common in middle age.
Women get RA more often than
men.

162. RHEUMATOID ARTHRITIS:
CAUSES
 Infection,
genes, and hormone
changes may be linked to the
disease.

163. RHEUMATOID ARTHRITIS:
SYMPTOMS
1. Morning stiffness, which lasts
more than 1 hour, is common.
Joints may feel warm, tender, and
stiff when not used for an hour.
2. Joint pain is often felt on the
same joint on both sides of the
body.

164. RHEUMATOID ARTHRITIS:
SYMPTOMS
3. Chest pain when taking a breath (pleurisy)
4. Dry eyes and mouth (Sjogren syndrome)
5. Eye burning, itching, and discharge
6. Nodules under the skin (usually a sign of
more severe disease)
7. Numbness, tingling, or burning in the
hands and feet
8. Sleep difficulties

165. RHEUMATOID ARTHRITIS:
TREATMENT
RA usually requires lifelong
treatment, including medications,
physical therapy, exercise,
education, and possibly surgery.
Early, aggressive treatment for RA
can delay joint destruction.

166. OSTEOARTHRITIS: DEFINITION
 Associated with the aging process
and can affect any joint.
 The cartilage of the affected joint is
gradually worn down, eventually
causing bone to rub against bone.
 Bony spurs develop on the
unprotected bones causing pain and
inflammation.

167. OSTEOARTHRITIS: DEFINITION

168. OSTEOARTHRITIS: HANDS

169. OSTEOARTHRITIS: CAUSES
 Aging.
The water content of the cartilage
increases and the protein makeup of
cartilage degenerates.
Repetitive use of the joints over the
years causes damage to the cartilage
that leads to joint pain and swelling.

170. OSTEOARTHRITIS: CAUSES
 Heredity.
The genetic basic cause of this
condition.

171. OSTEOARTHRITIS: RISK FACTORS
 Older age
 Sex
 Bone deformities
 Joint injuries
 Obesity
 Sedentary lifestyles
 Diseases, like diabetes,
hypothyroidism, gout, Paget’s
disease
 Certain occupations

172. OSTEOARTHRITIS: SYMPTOMS
 Pain
 Tenderness
 Stiffness
 Loss of flexibility
 Grating sensation
 Bone spurs

173. GOUT: DEFINITION
 It can cause an attack of
sudden burning pain, stiffness,
and swelling in a joint, usually a
big toe.
These attacks can happen over
and over unless gout is treated.

174. GOUT: DEFINITION
Over time, they can
harm the joints,
tendons, and other
tissues.
Gout is most common in
men.

175. GOUT: CAUSES AND RISK FACTORS
 High levels of uric acid in the
blood, which crytallize in the joints.
 Overweight
 High alcohol consumption
 Diet rich in fish and meat (due to
purine content)
 Diuretics

176. GOUT: THE THREE STAGES
 Stage One: High Blood Acid levels
The uric acid level in the blood may be higher
than normal, but there are no symptoms of
gout.
High uric acid in the blood (hyperuricemia)
may never progress beyond this stage, and
symptoms of gout may never develop.
Some people may have kidney stones before
having their first attack of gout.

177. GOUT: THE THREE STAGES
 Stage Two: Episodes of acute gouty
arthritis separated by periods without
symptoms.
This stage is also called intercritical or interval
gout.
Uric acid crystals begin to form in the joint
fluid, usually in one joint-most commonly the
big toe-and the body often responds with a
sudden inflammatory reaction: a gout attack.

178. GOUT: THE THREE STAGES
 Stage Two: Episodes of acute gouty
arthritis separated by periods without
symptoms.
Although the big toe is the most common site
for a gout attack, gout may develop in other
joints, including the knee, ankle, and joints in
the foot, wrist, and fingers.
After the gout attack is over, the affected joint
and surrounding tissues feel normal within
days until the next attack, which often occurs
within 2 years

179. GOUT: THE THREE STAGES
 Stage Two: Episodes of acute gouty
arthritis separated by periods without
symptoms.
For many people this period becomes
progressively shorter as attacks occur
more often.
Later attacks may be more severe, last
longer, and involve more than one joint.

180. GOUT: THE THREE STAGES
 Stage Three: Chronic Tophaceous Gout
If gout symptoms have occurred off and
on without treatment for several years,
they may become ongoing (chronic)
and frequently affect more than one
joint.
There may no longer be periods of time
between attacks.

181. GOUT: THE THREE STAGES
 Stage Three: Chronic Tophaceous Gout
By this time, enough uric acid crystals have
accumulated in the body to form gritty
nodules called tophi.
When located just under the surface of the
skin, these deposits are usually firm and
movable. The overlying skin may be thin and
red. Tophi that are very near the skin may
appear cream-colored or yellow.

182. GOUT: THE THREE STAGES
 Stage Three: Chronic Tophaceous Gout
At first, tophi are usually found on or near the
elbow, over the fingers and toes, or on the
outer edge of the ear.

183. GOUT: THE THREE STAGES
 Stage Three: Chronic Tophaceous Gout
Progressive crippling and destruction of
cartilage and bone is possible.
This stage of gout is uncommon because of
advances in the early treatment of gout.

184. GOUT: NON-PHARMACOLOGICAL
MANAGEMENT
 Eat
moderate amounts of a healthy
mix of foods.
 Avoid regular daily intake of meat,
seafood, and alcohol (especially
beer).
 Drink plenty of water and other
fluids.

185. RHEUMATIC FEVER: DEFINITION
 An inflammatory disease that
may develop after an infection
with group A Streptococcus
bacteria (such as strep throat or
scarlet fever).
 The disease can affect the
heart, joints, skin, and brain.

186. RHEUMATIC FEVER: CAUSES,
INCIDENCE, RISK FACTORS
 Common worldwide and is
responsible for many cases of
damaged heart valves.
Rheumatic fever mainly affects
children ages 5 -15, and occurs
approximately 14-28 days after
strep throat or scarlet fever.

187. RHEUMATIC FEVER: SYMPTOMS
 Abdominal pain
 Fever
 Heart (cardiac) problems, which may
not have symptoms, or may result in
shortness of breath and chest pain
 Joint pain, arthritis (mainly in the
knees, elbows, ankles, and wrists)
 Joint swelling; redness or warmth

188. RHEUMATIC FEVER: SYMPTOMS
 Nosebleeds (epistaxis)
 Skin nodules
 Skin rash (erythemamarginatum)
1. Skin eruption on the trunk and
upper part of the arms or legs
2. Eruptions that look ring-shaped or
snake-like

189. RHEUMATIC FEVER: SYMPTOMS
 Sydenham chorea (emotional
instability, muscle weakness and
quick, uncoordinated jerky movements
that mainly affect the face, feet, and
hands)

190. RHEUMATIC FEVER: MAJOR
CRITERIAS FOR DIAGNOSIS
1. Arthritis in several large joints
(polyarthritis)
2. Heart inflammation (carditis)
3. Nodules under the skin (subcutaneous skin
nodules)
4. Rapid, jerky movements (chorea,
Sydenham chorea)
5. Skin rash (erythemamarginatum)

191. RHEUMATIC FEVER: MINOR
CRITERIAS FOR DIAGNOSIS
6. Fever
7. High ESR
8. Joint pain
9. Abnormal EKG

192. RHEUMATIC FEVER: LABORATORY
EXAMS AND TESTS
Blood test for recurrent strep infection (such as an
ASO test)
Antistreptolysin O (ASO) titer is a blood test to
measure antibodies against streptolysin O, a
substance produced by group A Streptococcus
bacteria.
 Complete blood count
 Electrocardiogram
 Sedimentation rate (ESR)

193. RHEUMATIC FEVER: LABORATORY
EXAMS AND TESTS
 Sedimentation rate (ESR)
Normal Values
Adults (Westergren method):
Men under 50 years old: less than 15 mm/hr
Men over 50 years old: less than 20 mm/hr
Women under 50 years old: less than 20 mm/hr
Women over 50 years old: less than 30 mm/hr

194. RHEUMATIC FEVER: LABORATORY
EXAMS AND TESTS
Children (Westergren method):
Newborn: 0 to 2 mm/hr
Newborn to puberty: 3 to 13 mm/hr

195. RHEUMATIC FEVER: TREATMENT
 Low doses of antibiotics (such as
penicillin, sulfadiazine, or
erythromycin) over the long term to
prevent strep throat from returning.
 Anti-inflammatory (Aspirin or
Corticosteroids)

196. RHEUMATIC FEVER: PROGNOSIS
 If rheumatic fever returns, the
doctor may recommend the patient
take low-dose antibiotics
continually, especially during the
first 3 -5 years after the first episode
of the disease.
 Heart complications may be severe,
particularly if the heart valves are
involved.

197. RHEUMATIC FEVER:
COMPLICATIONS
 Arrhythmias
 Damage to heart valves (in particular, mitral
stenosis and aortic stenosis)
 Endocarditis
 Heart failure
 Pericarditis
 Sydenham chorea

198. RHEUMATIC FEVER: PREVENTION
The most important way to
prevent rheumatic fever is by
getting quick treatment for
strep throat and scarlet fever.

199. NON-INFECTIOUS
TOPICAL
DISEASES
ACNE
(VULGARIS, CYSTIC, ROSACEA)
PSORIASIS

200. SKIN ANATOMY:

201. ACNE: DEFINITION
 Common skin disease that causes
pimples.
 Pimples form when hair follicles under
the skin clog up.
 Most pimples form on the face, neck,
back, chest and shoulders.
 Anyone can get acne, but it is common
in teenagers and young adults. It is not
serious, but it can cause scars.

202. ACNE: BODY PARTS AFFECTED
Acne typically appears on your
face, neck, chest, back and
shoulders, which are the areas
of the skin with the largest
number of functional oil glands.

203. ACNE: CAUSES
Hormonal changes (during puberty
and pregnancy.
Overproduction of sebum / oil
Irregular shedding of dead skin cells
resulting in irritation of the hair
follicles of skin
Buildup of bacteria

204. ACNE: HOW IT DEVELOPS

205. ACNE: FACTORS THAT WORSENS IT
 Hormones
Androgens are hormones that
increase in boys and girls during
puberty and cause the sebaceous
glands to enlarge and make more
sebum.
Hormonal changes related to
pregnancy and the use of oral
contraceptives can also affect
sebum production.

206. ACNE: FACTORS THAT WORSENS IT
 Certain medications
Drugs containing;
1. corticosteroids
2. androgens
3. lithium
are known to cause acne.

207. ACNE: FACTORS THAT WORSENS IT
 Diet
Studies indicate that certain dietary
factors, including dairy products
and carbohydrate-rich foods —
such as bread, bagels and chips,
which increase blood sugar — may
trigger acne.

208. ACNE: DIFFERENT FORMS
 NON-INFLAMMATORY LESIONS
1. Comedones (Whiteheads and
Blackheads)
Created when the openings of hair
follicles become clogged and blocked
with oil secretions, dead skin cells
and sometimes bacteria.

209. ACNE: DIFFERENT FORMS
 NON-INFLAMMATORY LESIONS
1. Comedones (Whiteheads and
Blackheads)
When comedones are open at the skin
surface, they're called blackheads
because of the dark appearance of the
plugs in the hair follicles.

210. ACNE: DIFFERENT FORMS
 NON-INFLAMMATORY LESIONS
1. Comedones (Whiteheads and
Blackheads)
When comedones are closed, they're
called whiteheads — slightly raised,
skin-colored bumps.

211. ACNE: DIFFERENT FORMS
 INFLAMMATORY LESIONS
1. Papules - small raised bumps that
signal inflammation or infection in the
hair follicles. Papules may be red and
tender.

212. ACNE: DIFFERENT FORMS
 INFLAMMATORY LESIONS
2. Pustules (pimples) - are red, tender
bumps with white pus at their tips.

213. ACNE: DIFFERENT FORMS
 INFLAMMATORY LESIONS
3. Nodules - are large, solid, painful
lumps beneath the surface of the skin.
They're formed by the buildup of
secretions deep within hair follicles.

214. ACNE: DIFFERENT FORMS
 INFLAMMATORY LESIONS
4. Cysts - painful, pus-filled lumps
beneath the surface of the skin. These
boil-like infections can cause scars.

215. ACNE ROSACEA: DEFINITION
A long-term disease that affects
the skin and sometimes the eyes.
It causes redness and pimples.
Rosaceais most common in
women and people with fair skin.
It usually starts between age 30
and 60.

216. ACNE ROSACEA: SYMPTOMS
 Frequent redness (flushing) of the face.
Most redness is at the center of the
face (forehead, nose, cheeks, and chin).
 A burning feeling and slight swelling.
 Small red lines under the skin.

217. ACNE ROSACEA: SYMPTOMS
 Constant redness along with bumps on
the skin. Sometimes the bumps have
pus inside (pimples), but not always.
Solid bumps on the skin may later
become painful.
 Inflamed eyes/eyelids.
 Swollen, red, large bumpy nose.

218. ACNE ROSACEA: SYMPTOMS
 Thicker skin.
The skin on the
forehead, chin, cheeks, or other areas
can become thicker because of
rosacea.

219. ACNE ROSACEA: CAUSES
 When blood vessels expand too
easily, causing flushing.
People who blush a lot may be more
likely to get rosacea.
 Hereditary

220. ACNE ROSACEA: CAUSES
 Patients’skin with rosacea were to
have high levels of cathelicidins,
peptides with antimicrobial and pro-
inflammatory properties that protect
the skin against infection.

221. ACNE ROSACEA: CAUSES
 Levelsof stratum corneumtryptic
enzyme or SCTE — the enzyme
responsible for cleaving the inactive
cathelicidins into their active form —
were also elevated in people with the
disease.
A flaw in the immune system
contributes to this disease.

222. ACNE ROSACEA: FACTORS THAT
MAKE IT WORSE
 Heat (including hot baths)
 Heavy exercise
 Sunlight
 Winds
 Very cold temperatures
 Hot or spicy foods and drinks
 Drinking alcohol
 Menopause
 Emotional stress
 Long-term use of steroids on the face

223. ACNE ROSACEA: TREATMENT
Adapalene Cream or Gel (Differin)
A moderator of differentiation of
follicular epithelial
cells, keratinization, and
inflammatory processes.
It has both exfoliating and anti-
inflammatory effects.

224. ACNE ROSACEA: TREATMENT
 Electro surgery and Laser
surgery
Improves skin appearance with
less scarring.

225. ACNE ROSACEA: TREATMENT
 Scraping off the excess skin
tissue from a swollen, bumpy
nose.
Application of green-tinted
foundation or make-up to conceal
the skin redness.

226. ACNE: RISK FACTORS
 Teenagers
 Women and girls, two to seven days
before their periods
 Pregnant women
 People using certain medications,
including those containing
corticosteroids, androgens or
lithium

227. ACNE: RISK FACTORS
 Direct skin contact with greasy or oily
substances, or to certain cosmetics
applied directly to the skin
 A family history of acne
 Friction or pressure on the skin
caused by various items, such as
telephones or cellphones, helmets,
tight collars and backpacks

228. ACNE: NON-PHARMACOLOGICAL
TREATMENTS
 Wash problem areas with a gentle
cleanser.
 Avoid irritants (greasy
cosmetics, oily hairstyling
products, oil-based sunscreens)
 Keep hair away from your face
 Avoid tight-fitting clothes
 Don’t prick or squeeze!

229. ACNE: PHARMACOLOGICAL
TREATMENTS
 OTC topical medications
containing salicylic acid, benzoyl
peroxide, sulfur, resorcinol.
 Prescription medications such as
retinoids, adapalene, tazarotene

230. ACNE: PHARMACOLOGICAL
TREATMENTS
 Antibiotics – for moderate to
severe acne.
 Isotretinoin – for deep, cystic acne.
 Oral Contraceptives -a combination
of norgestimate and ethinylestradiol
(Ortho Tri-Cyclen, Previfem), can
improve acne in women.

231. ACNE: COSMETIC / SURGICAL
TREATMENTS
 Laser / Light Therapy
Laser treatment – damages the oil
glands, to produce lesser oil.
Light therapy – targets the bacteria
that causes acne inflammation

232. ACNE: COSMETIC / SURGICAL
TREATMENTS
 Chemical Peels /
Microdermabrasion
Lessen the appearance of fine
lines, sun damage and minor facial
scars — are most effective when
used in combination with other
acne treatments.

233. ACNE: COSMETIC / SURGICAL
TREATMENTS
 Acne Scar Treatment
1. Dermabrasion
2. Microdermabrasion (such as
Diamond Peeling)
3. Soft Tissue (Collagen) Fillers
4. Chemical Peels
5. RadioFrequency Treatments
6. Skin Surgery ( by Punch Excision)

234. ACNE: PREVENTION
 Wash acne-prone areas only twice a
day.
 Avoid heavy make-up / foundation.
 Wear loose-fitting clothes.
 Shower after excersizing or after
doing strenous work.

235. PSORIASIS

236. PSORIASIS: DEFINITION
A skin disease that causes scaling and
inflammation (pain, swelling, heat, and
redness).
 Skincells grow deep in the skin and
slowly rise to the surface.

237. PSORIASIS: DEFINITION
 Thisprocess is called cell turnover,
and it takes about a month.
 Withpsoriasis, it can happen in just a
few days because the cells rise too fast
and pile up on the surface.

238. PSORIASIS: DEFINITION
A chronic, autoimmune disease that
appears on the skin.
 Itoccurs when the immune system
sends out faulty signals that speed up
the growth cycle of skin cells.
 Psoriasis is not contagious.

239. PSORIASIS: FIVE TYPES
 Plaque Psoriasis (psoriasis vulgaris)
The most prevalent form of the disease.
About 80 percent of those who have
psoriasis have this type.
It is characterized by raised, inflamed, red
lesions covered by a silvery white scale.
It is typically found on the elbows, knees,
scalp and lower back.

240. PSORIASIS: FIVE TYPES
 Plaque Psoriasis (psoriasis vulgaris)

241. PSORIASIS: FIVE TYPES
 Guttate Psoriasis
Aform of psoriasis that often starts in
childhood or young adulthood.
This form of psoriasis appears as small,
red, individual spots on the skin.
Guttatelesions usually appear on the trunk
and limbs. These spots are not usually
as thick as plaque lesions.

242. PSORIASIS: FIVE TYPES
 Guttate Psoriasis

243. PSORIASIS: FIVE TYPES
 Inverse Psoriasis
Found in the armpits, groin, under the
breasts, and in other skin folds around
the genitals and the buttocks.
This type of psoriasis appears as bright-
red lesions that are smooth and shiny.
Inverse psoriasis is subject to irritation
from rubbing and sweating because of
its location in skin folds and tender
areas.

244. PSORIASIS: FIVE TYPES
 Inverse Psoriasis

245. PSORIASIS: FIVE TYPES
 Pustular Psoriasis
Primarily seen in adults, pustular psoriasis is
characterized by white blisters of
noninfectious pus (consisting of white blood
cells) surrounded by red skin.

246. PSORIASIS: FIVE TYPES
 Pustular Psoriasis
Triggers include irritating topical agents,
overexposure to UV light, pregnancy,
systemic steroids, infections, stress and
sudden withdrawal of systemic medications
or potent topical steroids.

247. PSORIASIS: FIVE TYPES
 Erythrodermic Psoriasis
An inflammatory form of psoriasis that
affects most of the body surface.
It may occur in association with von
Zumbuschpustular psoriasis.
The reddening and shedding of the skin are
often accompanied by severe itching and
pain, heart rate increase, and fluctuating
body temperature.

248. PSORIASIS: FIVE TYPES
 Erythrodermic Psoriasis
Triggers include;
a. abrupt withdrawal of a systemic psoriasis
treatment including cortisone
b. allergic reaction to a drug resulting in the
Koebnerresponse
c. severe sunburn
d. infection
e. medications such as lithium, anti-malarial
drugs
f. strong coal tar products.

249. PSORIASIS: FIVE TYPES
 Erythrodermic Psoriasis

250. PSORIASIS: CAUSES
 Stress
 Injury / Trauma to skin – Koeb-
ner phenomenon
 Medications, such as;
lithium
antimalarials
inderal
quinidine
indomethacin

251. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Corticosteroids – most frequent
 Anthralin,synthetic Vitamin D3, and
Vitamin A are also used in
prescription topical treatments to
control psoriasis lesions.
 OTC topicals containing salicylic
acid and coal tar.

252. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Phototherapy / Light Therapy with
Psoralen
It involves exposing the skin to
ultraviolet light on a regular basis
and under medical supervision.
Consistency is the key for the
success of this treatment.

253. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Sunlight
Start with five to 10 minutes of
noontime sun daily.
Gradually increase exposure time
by 30 seconds if the skin tolerates
it.
To get the most from the sun, all
affected areas should receive equal
and adequate exposure.

254. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Laser treatments
1. Excimer Laser – FDA approved for
chronic, localized psoriasis plaques.

255. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Laser treatments
2. Pulsed Laser - uses a dye and
different wavelength of light than the
excimer laser or other UVB-based
treatments, pulsed dye lasers destroy
the tiny blood vessels that contribute
to the formation of psoriasis lesions.

256. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Traditional Systemic Medications
Acitretin (Psoriatane)
Cyclosporin
Methotrexate
Off-lablesystemics
(hydroxyurea, isotretinoins,
sulfasalazine, 6-thioguanine,
mycophenolatemofetil)

257. PSORIASIS: PHARMACOLOGICAL
TREATMENT
Biologics – moderate to severe
psoriasis
1. T-cell blockers – Amevive (Alefacept),
Raptiva (Efalizumab)
2. Tumor necrosis factor-alpha (TNF-
alpha) blockers - Enbrel (etanercept),
Humira (adalimumab), Remicade
(infliximab) and Simponi (golimumab)

258. PSORIASIS: PHARMACOLOGICAL
TREATMENT
 Biologics – moderate to severe
psoriasis
3. Interleukin 12/23
Stelara(ustekinumab) works by
selectively targeting the cytokines
interleukin-12 (IL12) and interleukin 23
(IL23).

259. PSORIASIS: NON -
PHARMACOLOGICAL TREATMENT
A. Lifestyle changes
1. diet – avoid gluten (wheat and red
meat) and fatty acids.
2. take fish oil supplements
EAT WELL….LOSE WEIGHT
3. Anti-inflammatory Diet
Heart-Healthy Diet

260. PSORIASIS: NON -
PHARMACOLOGICAL TREATMENT
B. Mind –Body medicine
1. meditation
2. cognitive behavioral therapy

261. PSORIASIS: NON -
PHARMACOLOGICAL TREATMENT
C. Whole Medical Systems
1. TCM - acupunture
2. Ayurveda - Yoga
3. Naturopathy
4. Homeopathy