INTRODUCTION TO PATHOPHYSIOLOGY

- Understanding causes of diseases

- Also in changes of cells, tissues, and organs that are associated to the disease
- Give rise to the presenting signs and symptoms to a patient

SIGN
- Subjective
- Only you can tell

SYMPTOM
- Objective
- Something that the other person can see

ETIOLOGY
- Causes and modifying causes that are responsible for the initiation and
progression of a disease
- Why a disease happens

PATHOGENESIS
- Mechanisms of development and progression of a disease
- Accounts for the cellular and molecular changes which arises the functional and
structural abnormalities of a disease
- How a disease develops

CAUSES OF CELL INJURY

1. HYPOXIA
- Oxygen deficiency
- Most common: ischemia resulting from blockage (arterial obstruction)
- Arterial obstruction, or inadequate oxygenation
- Affects the oxygen carrying organ
- Anemia: impaired carrying capacity of RBC
- Carbon monoxide poisoning: RBC favors carbon monoxide than oxygen 200/ 20
times more
2. ISCHEMIA
- Reduced blood supply
- Most common

3. TOXINS
- Air pollutants, insecticides, carbon monoxides, asbestos, drugs, cigarettes,
ethanol,
- Drugs/ pharmaceutical medicines: can cause cell injuries in susceptible patients
or if used in high dosages (meant to be taken for therapeutic benefit)
- Innocuous substances can be toxic in high levels (glucose, water, salt, oxygen)
- Anything in excess can cause damage (hyperglycemia for glucose, hyponatremic
or hypertensive for salt, and metabolic alkalosis for oxygen)

4. INFECTIOUS AGENTS
- Disease causing pathogens (viruses, bacteria, protozoans)
- Not all bacteria are harmful (stomach bacteria = normal flora for digestion)

5. IMMUNOLOGIC RESPONSE
- Elicit inflammatory reactions that damages the tissues
- Autoimmune reaction against own tissues (autoimmune disease attacks its own
body)
- Allergic reaction against environmental substances
- Chronic immune response to microbes (anaphylaxis through chronic allergic
reactions to allergens which are life threatening and damages cells)

6. GENETIC ABNORMALITIES
- Conspicuous genetical malformation
- Results to down syndrome or sickle cell anemia (amino acid substitution)
- Deficiency of a protein resulting to problems with metabolism
- Accumulation of damaged DNA or misfolded proteins that triggers cell death
when beyond repair
- Can be inherited and acquired
- Issue of thalidomide = when pregnant woman took the drug, their babies suffer
from genetic malformation

7. NUTRITIONAL IMBALANCES
- Protein calorie insufficiency = major cause of cell injury in poverty community
 - Specific vitamin deficiency (most common even in developed countries with high
standards of living)
- Excessive dietary intake = obesity
- Obesity = ground factor for underlying diseases (diabetes mellitus and
atherosclerosis)

Developing countries:
a. Kwashiorkor
- Nutrional imbalances
- Not receiving enough protein when a child is growing

b. Marasmus
- Severely underweight
- Insufficient energy in all forms including protein
- Pediatric patients

Developed Countries:
a. Diabetes Mellitus
- Is now a lifestyle illness
- Intake of excess sugar/ carbohydrates resulting in insulin resistance

b. Hypertension
- Lifestyle illness
- Eating excess amount of fat or salt resulting blockages in blood vessels which
consequently raises blood pressure

8. PHYSICAL AGENTS
- Physically damages tissues
- Trauma, extreme temperature change (too hot/ too cold), radiation, electric
shock, sudden change of atmospheric pressure

9. AGING
- Cellular senescence: stable cell cycle arrest in which proliferating cells become
resistant to growth-producing stimuli (diminishing the cell’s ability to response
from stress and later on results to cell death)
- Aging = all of us age
- Old = unable to fight infection, susceptible to diseases, and those infectants that
are not harmful for middle and adolescent ages are now lethal
ADAPTATIONS TO CELL INJURY
- Adaptation: response of a cell to prolonged stress and to protect and prevent
occurrent injuries
- Either physical or functional
- Main marker of an individual = ability to adapt

ETIOLOGIES OF CELLULAR ADAPTATION

1. PATHOLOGIC ATROPHY
- Decrease of size or number of cells
- Decline of blood flow, hormone supply, and nutrition
- Physiologic (thymus shrinks as we grow) or pathologic (response to stress)

2. HYPERTROPHY
- Increase cell size
- Due to increase workload, exercise, or hormone supply
- Physiologic (exercise) or pathologic (enlargement of heart due to prolonged
hypertension)
- Though the heart enlarges even in exercise, the only difference is the chambers
of the heart is congruent to the heart muscles

3. HYPERPLASIA
- Increased of number of cells
- Physiologic (lining of uterus during menstruation) or pathologic (hypothyroidism
forms goiter due to increased thyroid cells)

4. METAPLASIA
- Inflammatory change due to hormonic response
- Change of one type of a cell to another
- Benign reversible cellular change
- Pathologic (reflux diseases turn the esophagus’ epithelial cells into squamous
cells)

5. DYSPLASIA
- Change of mature cell type to immature cell type
- Abnormal cell differentiation
- Partially reversible and considered primarily pre-malignant
- Many etiologies: smoking, chronic exposure
 - If metaplasia persistent  results to cancerous cells
- Morphologically, dysplasia results in abnormal cellular and nuclear features
- Human papilloma virus (HPV): attacks the cervix (squamous columnar) and if
untreated, lining changes and becomes precursor to cervical cancer

CELL INJURY AND DEATH

- Cell death: failure to adapt
- Cell injury can be reversible or irreversible

CELL INJURY
1. REVERSIBLE
- Swelling of organelles (endoplasmic reticulum and mitochondria)
- Swelling of entire cell
- Hyperchromatic nucleus (looks darker due to the clumping of nuclei chromatin)
- Cytoplasmic densities, membrane blebbing/ cell blebbing (bulging of plasma
membrane), detachment of ribosomes

2. IRREVERSIBLE
- If damage is chronic
- Injury that leads to cell death by necrosis or apoptosis

CELL DEATH
1. NECROSIS
- Death of group of cells due to injury
- Always pathologic
- Never occurs in normal tissues
- Results to the release of multiple cell components that triggers an inflammatory
reaction
- Cellular component leakage
- Increase in cell volume
- Loss of plasma membrane integrity/ bursting  precursor to arachidonic acid
metabolism  gives rise to inflammation
Forms of Necrosis
a. Coagulation
- Due to hypoxia
- Denaturing of cells and maintain architecture composition for several days
 - Ex. Myocardial infarction (no morphological changes)

b. Liquefactive
- Transformation of cells into a thick liquid
- Loss of complete structure
- Ex. Brain (bacterial infections)

c. Caseous
- Loss of architectural structure of cells
- Turns amorphous
- Ex. fungal infections and tuberculosis

d. Fat
- Enzymatic necrosis
- Seen in fat tissues
- Most common: pancreas (acute pancreatitis)
- Blood supply compromised

e. Fribinoid
- Deposition or staining of fibrin and antigen-antibody complexes in the blood cell
- Ex. autoimmune diseases

2. APOPTOSIS
- Programmed cell death
- Ex. RBC (reached lifespan)
- Normal process
- Cell shrinkage
- Formation of apoptotic bodies (function to enclose cellular organelles so it will not
leak to the bloodstream)

INFLAMMATION
- Protective response to something foreign or non-physiological
- Intended to eliminate initial cell injury and/or cell necrosis and necrotic tissues

1. ACUTE
- Early response to injury
- Within hours to days
- Vascular changes (dilation of blood vessels, increased permeability of blood
vessels causing leakage)
- Cellular changes (leukocytes accumulation)
 - Meant to confine the injury to a specific site and limit ng injure
- Goal: limit injury and restore tissue
- Start of acute inflammation: exiting of leukocytes from blood vessels through
margination  rolling  adhesion  transmigration  and start of chemotaxis
- Vascular and cellular changes leads to classical and clinical signs and symptoms
(redness, increase in temperature, swelling, pain, and limited function)
- Outcome: complete resolution (completely disappear), abscess formation (nana,
leukocytes specifically neutrophils gather around the infection), regenerate
(healed completely) and develop scar tissue/ formation
- Neutrophils are the main cell components
- Ex. bacterial and viral infections

2. CHRONIC
- If infection not confined
- Prolong inflammation
- Months to years
- Tissue injury (on and off repair)
- Usually preceded by acute inflammation
- Ex. tuberculosis, autoimmune diseases
- Treatments are available to confine the infection
- Necrosis  parenchymal damage  granulation tissue formation  and
eventually scar formation
- Main cells: lymphocytes
- Other cells present: macrophages, plasma cells, monocytes, eosinophils

TISSUE REPAIR
- Follows after the two inflammations
- Intention to restore the normal tissue function
- Require the cells on the inflammation site to be viable and regenerate in order to
proceed to tissue repair
- Severe case: loss of cell function leading to necrosis

Cells Involved in Tissue Repair

1. LABILE CELLS
- Stem cells, hemopoietic cells
- Replicate throughout their whole lives to replace the lost cells

2. STABLE CELLS
 - Fibroblasts (mainly found in tissues)
- Can only replicate when activated to replace lost cells
- Activated for scar tissue formation
3. PERMANENT CELLS
- Myocardium cells and striated muscle cells
- Cannot replicate
- Lost cells replaced by scar tissue
- Liver: can regenerate tissues
- Brain: neuroplasticity (can repair damaged brain tissues but are no longer
functional)

4. GRANULATION TISSUE
- Main tissue in tissue repair
- Consists of blood vessels, fibroblasts, collagen
- Tissue repair and collagen = stimulated by several genes and chemical
mediators (PDGF/ platelet-derived growth factor, TGF beta/ transforming growth
factor beta, FGF/ fibroblastic growth factor, VEGF/ vascular epithelial growth
factor)
- Langid

THE IMMUNE SYSTEM

PATHOGEN
- An organism that can cause a disease

PATHOGENICITY
- Ability of an organism to cause a disease

VIRULENCE
- Degree of pathogenicity

OPPURTUNISTIC PATHOGEN
- Bacteria that cause disease in a compromise host
- Usually not disease causing (depends on route entry, number of pathogens, and
immune status of host)
 - Normal flora: normal bacteria in a host but can be harmful if with other pathogens
cause an inflammation to a host

DEFENSES OF THE BODY

1. INNATE/ NON-SPECIFIC
- Body’s foot soldiers
- Already in birth
- Always prepared
- Response in minutes
- Protects the body from all foreign substances
- Sufficient to ward off invading pathogens
- Essential reduces the workload of adaptive immune system

1st Line of Defense of Innate Immune System

- Surface barriers
- Prevents pathogens from entering

a. Skin
- Stratified squamous epithelial cells
- Keratinized or non-keratinized
- The more keratinized the better

b. Mucous Membranes
- Lysozyme enzyme (saliva, tears, sticky mucous)
- Goblet cells: produce mucous that traps the foreign materials excreted by a
cough or digested by the stomach
- Cilia: nasal and respiratory track to sweep the bacteria in the mouth to swallow
- Acid secretion in skin, vagina, stomach to kill microbes

2nd Line of Defense of Innate Immune System

- Internal defenses

a. Phagocytes
- Macrophages (large phagocytic cells)

b. Granulocytes
- Possesses cytoplasmic granules
 - Neutrophils: release toxic chemicals in the extracellular fluid which both kills the
pathogen and itself
- Eosinophils: kills parasitic worms
- Basophils: allergic reactions
c. Fever
- Leukocytes and macrophages secrete pyrogens (fever producing substance) to
increase thermal temperature, speeds up metabolic repair, and kills microbes
- Reliable sign of a foreign invasion

d. Natural Killer Cells

- Can kill cancer cells and virus infected cells
- Target all cells that lack cell surface receptors (non-specific)
- Latch to invaders and begins aqua cytosis
- Secrete chemicals that promote inflammation

e. Antimicrobial Proteins
- Attack microbes directly or reduce its reproductive ability
- Includes interferons and complement system

f. Inflammation
- Response to physical trauma, intense heat, and chemical infection
- Prevent the damage from spreading to nearby tissues
- Dispose/ confine cell degree and pathogens
- Sets a stage for repair

2. ADAPTIVE/ SPECIFIC
- Elite special cells
- Equipped with ‘high-tech weapons’
- Called in for reinforcements
- Take more time to mobilize (due to gene translation)
- Attack specific foreign substances (antigens and abnormal body cells)
- If low count = you are immunocompromise
- Tremendously amplifying the immune response
- Systematic (immunity is not restricted to initial infected site)
- Mounts stronger attacks to previous encountered pathogens (has memory)
- Same mechanism for booster vaccines
3rd Line of Defense of Innate Immune System
a. Humoral Immunity
- Antibody-mediated immunity
- Can be transfer from person to person via serum
- Ex. blood transfusion
 - B-cells (makes antibodies for antigens)
- Antibodies: immunoglobulins that circulate freely in blood and lymph and
neutralizes bacteria, toxins, and viruses which marks for the destruction of
phagocytes or complements
b. Cellular-Cell Mediated Immunity
- Transferred from person to person via blood cell
- Activated by antigens
- Macrophages and natural killer cells: destroy intracellular pathogens
- T-cells: induce apoptosis body cells with viruses, bacteria, and cancerous traits
- Cytokines: enhance inflammatory response and/or activate other lymphocytes
macrophages
- Activated cells destroy the infected foreign cells

THE INTEGUMENTARY SYSTEM

COMMON SKIN INFECTIONS
I. DERMATOPHYTOSIS
- Infection the skin, hair, and nails
- Caused by a specie of dermatophyte (fungi that live within dead epidermal
keratin and do not penetrate deeper structures)
- Fungal infection
- Dermatophyte included: Mircosporum, Epidermophyton, Trichonphyton
Pathophysiology
- Digestion of keratin by a dermatophyte
- Results to a scaly skin, broken hair, and crumbling of nails

Investigations
- Fungi live as molds so look for hyphae and mycelia
- Hyphae: masses of branched, tubular, thread-like filaments that penetrates into
substrates and absorb nutrients
- Mycelia: expanding network of hyphae
- Common microbiological test

 Skin Scrapings
 Hair and Nail Clippings (analyzed with a potassium hydroxide preparation)
Management
1. Topical
- Medication that is applied in a particular place on or in the body
- Interdigital ointments/ applied between the fingers of hands and/or feet
- Applied 2x a day and continued for a week until complete resolution of lesion
Examples:
 Clotrimazole Cream
 Terbinafine Hydrochloride

Used For First Line Agents For:

 Tinea pedis (athlete’s foot)
 Tinea corporis/ cruris (ringworm of the body/ jock itch)

2. Oral Therapy
- If infected part spread throughout the body
- Oral preparation (anti-fungal)

Examples:
 Terbinafine Hydrochloride
 Itraconazole (Sporanox)
- P450 inhibitor
- Alters metabolism of:
o Non-sedating antihistamines
o Cisapride (medicine that increases motility in the upper gastrointestinal tract),
digoxin/for heart conditions
o HMG CoA reductase inhibitors (interrupts first step of cholesterol synthesis)

Used For:
 Onychomycosis (fungal infection of nail)
 Tinea capitis (scalp/ ‘blackdot’ ringworm)
FUNGI INVOLVED IN DERMATOPHYTOSIS
A. TINEA CAPITIS
- Non-scarring alopecia (loss of hair) with scale
Etiology
- Caused by Trichophyton tonsurans and Microsporum species

Epidemiology
- Affects children and black immunocompromised adults
- Very contagious
- May be transmitted from barber cuts, hats, theatre seats, and pets

Signs and Symptoms

 Round scaly patches of alopecia
 May see broken off hairs
 If tissue reaction is acute: Kerion (boggy, elevated, purulent inflamed
nodule/plaque) may form due to secondarily infection by bacteria and result in
scarring
Kerion (left) and round alopecia (right)
Examination

 Bulb Light Examination of Hair

- Green fluorescence only for microsporum infections

 Culture of Scale and Hair Shaft

- Done on Sabouraud agar

 Microscopic Examination
- Potassium hydroxide (KOH) preparation
- Preparation of scales or infected hair shafts
- Reveal characteristic hyphae
- Easiest examination

Management (Additional Learnings)

 Griseofulvin
- 15-15 mg/kg/ per day
- For 8 weeks

 Terbinafine (Lamisil)
- 250 mg
 - Once a day
- 2-4 weeks
- Dosage varies by weight

B. TINEA CORPORIS
- Pruritic/ itchy scaling round oval plaque
- With erythematous margin/ red skin rash and a central clearing
- Single or multiple lesions
- Found on peripheral limbs, face, trunk,
- Sometimes enlarge in size
Etiology
- Caused by:
 Trichophyton rubrum
 Epidermophyton floccosum
 Mircosporum cannis
 Trichophyton cruris

Epidemiology
- Most common in children and with infected pets

Sign and Symptoms

 Pruritic/ itchy scaling round oval plaque
 With erythematous margin/ red skin rash and a central clearing
 Single or multiple lesions

Examination
 Microscopic Examination
- Potassium hydroxide (KOH) preparation of skin scraps
- Margin shows hyphae
- Better option
  Culture of Scale
- Done on Sabouraud agar
- Most preferred but takes time
Management (Additional Learnings)
 Clotrimazole
 Fluconazole
 Lamisil Cream

C. TINEA CRURIS
- Jock Itch/ hadhad
- Scaly patch/plaque with a well-defined curve border and central clearing
- On the medial thighs
- Does not involve the scrotum
- Pruritic erythematous with dry/ macerated borders
Etiology
- Caused by:
 Trichophyton rubrum
 Trichophyton mentagrophytes
 Epidermophyton floccosum

Epidemiology
- Most common with adult males

Examination
- Same as tinea corporis
 Microscopic Examination
- Potassium hydroxide (KOH) preparation of skin scraps
- Margin shows hyphae
- Better option

 Culture of Scale
- Done on Sabouraud agar
- Most preferred but takes time
Differential Diagnosis
- Distinguishing of a disease/ condition from other presenting with similar signs
and symptoms
 Candidiasis (involvement of scrotum and with satellite lesion)
 Erythrasma (coral-red fluorescence with Wood’s lamp)
 Contact dermatitis

D. TINEA PEDIS
- Athlete’s Foot
- Pruritic, scaling or maceration of the web spaces and powdery scaling of soles
- Interdigital
- White vesicles, bullae/ fluid-filled skin lesions, scale maceration
Etiology
- Caused by:
 Trichophyton rubrum
 Trichophyton mentagrophytes
 Epidermophyton floccosum

Epidemiology
- Chronic infections are common in atopics
- Heat, humidity, and occlusive footwear (predisposing factors)
- Fungi found adequate heat as something suitable for reproduction

Signs and Symptoms

i. Acute
- May present as a flare up of chronic tinea pedis
- May be frequently become secondarily infected by bacteria (because of constant
itching)
- Epidermis exposed
 Red/white scales
 Vesicles
 Bullae
 Often with maceration

ii. Chronic
  Non-pruritic (prolong exposure made the skin adapt the change)
 Pink, scaling keratosis on soles and sides of foot (often in a moccasin
distribution)
 Interdigital (especially in the fourth web space)
Examination
 Microscopic Examination
- Potassium hydroxide (KOH) preparation of scales
- From roof of a vesicle or powdery scaling area

 Culture of Scale
- Done on Sabouraud agar
- Most preferred but takes time

E. TINEA MAUUM
- 1 hand 2 feet syndrome
- Primary fungal infection of the hand is quite rare
- Usually associated with tinea pedis with one hand and two feet affected
Etiology
- Same as tinea pedis
 Trichophyton rubrum
 Trichophyton mentagrophytes
 Epidermophyton floccosum

Signs and Symptoms

i. Acute
 Blisters at edge of red areas on hands
ii. Chronic
 Single dry scaly patch

Differential Diagnosis
 Contact dermatitis
 Atopic dermatitis
 Psoriasis
- All mistaken as fungal infections
  Granuloma annulare (annular)

F. TINEA UNGUIUM
- Onychomycosis
- Crumbling, distally dystrophic nail
- Yellow, opaque with subungual herpekeratotic debris
- Toenail infections usually precede fingernail infections
Etiology
- Caused by:
 Trichophyton rubrum (culprit for 90% toenail infections)

Examination
 Microscopic Examination
- Potassium hydroxide (KOH) preparation of scales
- From subungual scraping
- Shows hyphae

 Culture of Subungual Scraping

- Done on Sabouraud agar
- Most preferred but takes time

II. CANDIDIASIS
A. CUTANEOUS CANDIDIASIS
- Overgrowth of normal commensal (parasitic organism that causes no harm to the
host) of mouth, vagina, or lower gastrointestinal tract
- Only infects outer epithelium mucous membrane or skin
Etiology
- Caused by:
 Candida albicans

Presentation
 Red macerated area with glistening surface
 Scaling along with advancing borders
 Lesions grow in size
  Initial lesion is papule/ red lump that can become a pustule (with pus inside)

Clinical Feature
 Presence of satellite pustule beyond the border of the main infection

Management
 Topical Therapy

B. ORAL CANDIDIASIS
- Candida Albicans
- In some cases: will imitate a leukoplakia (difficult to scrap off and if possible,
bleeding will occur)
Etiology
- Caused by:
 Candida albicans

Presentation
 White patches easily scraped off that leaves a red raw base
 Chronic red, raw gums, tongue, and buccal mucosa

Management
 Topical therapy
 Systemic therapy of anti-fungal
 C. PITYRIASIS VERSICOLOR
- Caused by normal commensals (yeasts)
- Common superficial fungal induced rash
- Like a form of cutaneous candidiasis but presentation is different
Etiology
- Caused by:
 Candida albicans

Presentation
 Flaky discolored patches on the chest, back
 Small and well-defined slightly flaky patches
 Can either be hypopigmented or hyperpigmented

III. ECTOPARASITIC
A. SCABIES
- Human infestations originating from pigs, horses, and dogs = mild and self-
limiting
- From other humans = never cure without intervention/ hard to treat and never go
away by itself
Etiology
 - Caused by:
 Sarcoptes scabiei

Ecology
- Mites live in stratum corneum (do not go any deeper)
- Eats stratum corneal keratinocytes
- Make ‘tunnels’ to burrow by eating and there they will mate on the host’s skin
- Fertilized female mite will burrow in stratum corneum 1 mm deeper
- Salivary secretions contain proteolytic enzymes (strong enough to digest
keratinocytes)

Epidemiology
 Highly prevalent in children (50%)
 Adults (25%)
 In tropical remote communities

Transmission
- Spread through closed physical contact

Presentation
 Itchiness (exacerbated during night time and during hot showers)
 Excoriated (teared skin due to scratching) rash on trunk (associated with scaly
burrows on fingers and wrists)
 Often with vesicles and pustules on palms and soles and sometimes on the scalp

Clinical Feature
 Chronic itch with symmetrical rash
 Presence of burrows

Clinical Diagnosis
 Skin scraping (looking for scabies mites)
- Intact larvae with adults
- Unhatched or hatched eggs
 - Molted skin of mites
- Fragments of molted skins
- Mite feces

Treatment
 Topical Permethrin
 Oral Ivermectin (beneficial)
Environmental Measures
 Proper Sanitation of Materials
- Mites can contaminate beds, chairs, floors, and even walls
- Usually only a problem with crusted scabies
- Wash then exposure to sun
- Vacuum
- Surface Insecticide

Community Prevention
 Simultaneous Effective Treatment
- Treat all close contacts (especially in indigenous communities)
- Treat again for 7 days

B. PEDICULOSIS
- Lice/ Kuto
- Can affect different areas of the body

3 TYPES OF PEDICULOSIS
1. HEAD LICE/ PEDICULUS HUMANUS CAPITIS
Epidemiology
  Common in primary school children in the tropics
 Higher prevalence in aboriginal (being the first or earliest known of its kind
present in a region) children

Diagnosis
 Use conditioner
 Use a fine-tooth comb
 Wipe the comb in a white tissue paper

2. BODY LICE/ PEDICULUS HUMANUS CORPORIS

- Live on clothes
- Come to the body to feed
- Not frequently taking a bath

3. PUBIC LICE/ PHTHIRUS PUBIS

- Sexually transmitted
- Blood feeders
- Can infect any body hair (pubic, trunk, legs, axilla, beard) but rarely the head

Life Cycle
- Eggs (Nits) laid in hair
- Eggs  larva  adult  sucks blood

Transmission
 Head-to-head contact

Presentation
 Scalp and neck itchy
 Nits noticeable in hair
Diagnosis
 Conditioner and comb technique
- Very practical
- Cost effective
- High/hydro sensitivity
- Conditioner ‘stuns’ the lice by suffocating them and prevent them from moving

Management/ Treatment
 Conditioner and Nit Comb
 Physical removal
 Cut the hair
 Topical insecticidal cream
 Wash pillows and hats (hot wash preferred)
 Treat all body hair (for pubic lice)

VIRAL INFECTIONS
I. WARTS
- Benign tumors of skin
- Infectious (spread by direct contact)
Appearance
- Verrucous surface (keratotic exophytic surface) or thick keratin surface
- Rough lumps on skin (can be confused with kaylo)
- Marker: a tiny black dot in the middle (due to a thrombosed capillary blood
vessel)

Etiology
- Caused by:
 Human Papilloma Viruses (HPV)

Presentation
 Common on the back the fingers, toes, and knees (common warts)
 Cervix, vulva, penis (genital warts)
 Cervical papilloma = can cause cervical cancer
 Laryngeal papilloma (controversial)
Treatment
- No reliable treatment
- 50% of childhood warts disappear within 6 months
- 90% are gone in 2 years
- Many do not bother for treatment
 Surgical incision/ treatment
 Chemical treatment (salicylic acid)
 Cryotherapy
 Electrosurgery (cauterize) or burning of warts
 Vaccines
- Gardasil: blocks HPV 6, 11, 16, and 18 (HPV viruses that cause genital and
continuous warts)
- Cervarix: blocks HPV 16 and 18 (viruses that cause cervical cancer)
- Gardasil Nano: blocks HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58

II. HERPES SIMPLEX

- Form of cold sore or genital lesion
- Common mucosal infection that presents with localized blistering
- Can reside in a latent stage

2 TYPES OF HERPES
1. TYPE 1
- Facial or oral infections
- Cold sores or fever blisters
Epidemiology
 Mainly in infants
 Young kids

2. TYPE 2
- Mainly genital
- Often sexually transmitted
Epidemiology
 Occur after puberty

Presentation
 - Similar to both types
Stages:
a. Prodromal stage vesicle or blister stage
-
b. Ulcerate stage
c. Crust stage

Pathophysiology
- Virus grows down the nerves and out into the skin  localized blistering
- Can experience:
 Neuralgia
 Lymphadenopathy (inflammation of lymph nodes)
 High fever

Reoccurrences
- Can be triggered by:
 Minor trauma/ other infections
 UV radiation
 Hormonal factors
 Stress (most common)
 Operations and procedures on the face

Treatment
 No treatment (for mild cases)
 Sun protection (prevention)
 Oral treatment (anti-viral drugs) to stop the virus from multiplying

Complications
 Encephalopathy (brain diseases)
 Trigeminal Neuralgia (neurogenic pain)
- Affects the trigeminal nerve (facial nerve)
- Will continuously cause pain
- Virus stay there
- Sharp pain in the face from time to time
 III. CHICKEN POX
- Highly contagious disease
- From person-to-person transmission
- Typical childhood disease
Etiology
- Caused by:
 Varicella zoster virus (HHV3 or Human alpha herpesvirus 3)
- Also known as: chicken pox virus, varicella, zoster

Signs and Symptoms

 Itchy rash or red papules
 Begins on the trunk and will progress on the face and extremities
 May cover the entire body
 High fever/headache/cold-like symptoms /vomiting /diarrhea.

Diagnosis
 Clinical Diagnosis
- simple medical history will do
- starts in the face = varicella
- physical manifestations (vesicular papules that can burst fluid)

 Test for Elevated VZV-Specific Antibodies

- IgM - Primary Infection
- IgG - Second Infection

Treatment
 Symptomatic
- Treats the symptoms
 - There is an old nation that chicken pox can resolve on its own but is now not the
case

 Anti-viral drugs

Complications
 Varicella during pregnancy  Congenital Varicella Syndrome
- Congenital Varicella Syndrome may result to spontaneous abortion (3-8% in 1 st
trimester or intrauterine growth restrictions/ IUGR)
- 30% severe mortality rate

 Skin
- Cutaneous defects
- Hypopigmentation

 Neuro
- Intrauterine encephalitis
- Brain damage
- Seizure
- Developmental delay

 Eye
- Chorioretinitis
- Cataracts
- Anisocoria

 Musculoskeletal
- Limb hypoplasia

 Systemic
- Cerebral cortical atrophy

 Renal
- Hydronephrosis
- Hydroureter

 Gastrointestinal
- GORD

 Cardiovascular System
- Congenital heart defects
BACTERIAL INFECTIONS
I. IMPETIGO
- School Sores
- Superficial bacterial skin infection
- Most common in school kids
- Very contagious (spread by close contact & poor hygiene)
- Usually resolves slowly

Etiology
- Caused by:
 Staphylococcus Aureus (most common)

 Streptococcus Pyogenes
- Some are caused by these bacteria
- Can lead to Glomerulonephritis or Rheumatic Fever if it is not controlled
- Can also hurt kidney and the heart

Presentations:
 Occur most commonly on the face
 Fragile vesicles rupture & crust
 Can be confused with HSV (HSV lesions are smaller and only located on the
mouth)

Two Types of Impetigo

i. Nonbullous/ Crusted Impetigo
-
- Most common
- Yellow crusts and erosions
- Itchy/Irritating
- not painful

ii. Bullous Impetigo

- Always due to S. Aureus
- Mildly irritating blisters that erode rapidly leaving a brown crust
Treatment
 Cover affected area
 Refrain going to school
 Drink topical antibiotics (penicillin, amoxicillin, oxacillin)

II. FOLLICULTITIS AND FURUNCULOSIS (BOILS)

FOLLICULTITIS
- Acute pustular infection of a hair follicle
- Commonly after waxing/Shaving

FURNUCULOSIS
- A deeper form of folliculitis

Etiology
- Caused by:
 Staphylococcus Aureus

Presentation
Folliculitis
 An erythematous pustule centered on a hair follicle
Boils
 Tender, red nodule which enlarges & may later discharge pus (painful and
deeper)

Treatment
 Treated aggressively with antibiotics
 Along with drainage
 III. ABSCESSES
- Begin as superficial infections of hair follicles (folliculitis)
- Organisms travel down Hair Follicles following Disruption (Eg. After Shaving)
- Development of boils (furuncles)
- Number of boils cluster together = abscess
Etiology
- Usually by:
 Staphylococcus Aureus

IV. CELLULITIS
- Bacterial infection of the dermis and sub-cutaneous tissue

Etiology
- Caused by:
 Staphylococcus aureus/ GAS
- 90% of adults

 H. influenzae B
- Children

 Pasteurella Multocida
- Associated with dog/cat bites
Presentation
 Painful, raised and Edematous Erythema (most common on lower leg)
 Possible blistering
 Lymphadenopathy
 Malaise
 Fever

Distribution
 Children
- Periorbital area

 Adults
- Lower leg

There’s usually an underlying cause:

 Lymphoedema
 Tinea, Herpes simplex infection,
 Chronic sinus infection
 Chronic dermatitis
 Poor lower leg circulation
 Untreated wounds

Treatment
 Antibiotics

V. NECROTIZING FASCIITIS
- Medical emergency
- Often needs radical debridement/ removal of necrotic tissue

Etiology
 - Caused by:
- Both GA and S. Aureus cause severe, systemic toxicity

 Group A Strep (GAS)

 Staph. Aureus
 Others (Vibrio, Clostridium, Bacteroides)

Pathogenesis
- The Necrosis is toxin-mediated
- Cannot be treated by antibiotics
- Not due to a flesh-eating bacteria (bacteria produce toxin that cause tissue
necrosis)

Types of Necrotizing Fasciitis

i. Type I
- Polymicrobial infection

ii. Type II
- Monomicrobial infection

VI. GAS GANGRENE

Etiology
- Caused by:
 Clostridium perfringens

Pathogenesis:
- Generally, occurs at site of trauma or recent surgical wound
 - Usually only occurs with poor blood supply (Eg. Diabetic foot)
- Anaerobic conditions
- Toxins are produced  cause the tissue death and associated symptoms

Presentation:
 Inflammation at the Site of Infection
 Brownish-red and extremely painful tissue swelling
 Gas may be felt in the tissue when the swollen area is pressed
 Margins of the infected area expand rapidly (Within a few minutes)

Prognosis
 The involved tissue is completely destroyed (Toxin-Mediated Destruction)

VII. MYOBACTERIAL INFECTIONS

A. LEPROSY
Etiology
- Caused by:
 Mycobacterium leprae

Presentation
 Tuberculoid and lepromatous forms
 Mainly affects skin and nerves

B. TUBERCULOSIS
- Infects the lungs in a form of tuberculosis
Etiology
- Caused by:
 Mycobacterium tuberculosis

SKIN MANIFESTATION OF METABOLIC DISEASES

I. JAUNDICE
- Yellowing of the skin due to high levels of bilirubin
Bilirubin
- Yellow breakdown product of normal heme catabolism
- Responsible for the yellow color of bruises and the brown color of feces