Skin

Question 1

Folliculitis

Answer 1

Inflammation of the hair follicle
Superficial: Development of pustule but should not scar.
Deep: Whole follicle is affected (base is in vascular dermis) so this may produce scarring.

Bacterial: Usually Staphylococcus Aureus
Atopic: non-pustular bumps on back of arms and buttocks - non-infectious form but may lead to infectious form if scratched.

Question 2

Pseudofolliculitis Barbae

Answer 2

Known as shaving bumps; occurs due to irritation of the follicle. Common in African American men.

Sequelae: pustules/abscess may occur d/t secondary infection.
Postinflammatory pigmentation and keloids are possible.

Question 3

Acne Vulgaris

Answer 3

Form of folliculitis that affects pilosebaceous glands
Etiology: adolescence and women
Open Comedomes: non inflammatory with black keratin plug
Closed Comedomes: inflammatory, trapped keratin plug
Relation to androgens –> pilosebaceous glands have androgen receptors and they cause increase production of sebum and upregulate production of keratin.
Insulin has similar effects

Question 4

Furuncle

Answer 4

Abscess/boil that is the progression of folliculitis
Typically involves only one follicle
Common in post-pubescent people and those who are immunocomprimised
Causative Factors: trauma to follicle, occlusion, diabetes, HIV, obesity, poor circulation.

Question 5

Carbuncle

Answer 5

Similar to furuncle but multiple follicles will be involved. Much larger.
Abscess - walled off collection of pus, paiful firm mass, systemic symptoms are possible.
Tissue destruction d/t ATP depletion, free radical damage, membrane disruption.

Question 6

Cellulitis

Answer 6

Progression of carbuncle - fingers of granulation tissue extend subcutaneously. 
Dermis + Subcutaneous Involvement 
Medical EMERGENCY
Causes: 
2dary to Tissue Trauma
Broup A Strep or Staph Aureus (adults)
Haemophilus Influenza B (children)

Sx’s - d/t neutrophilic infiltrate of tissues
Systemic - fever, chills, malaise
Erythema with ill defined, non-palpable borders
Extreme pain, warmth and inflammation
Possible lymphangitis and lymphadenopathy

Question 7

Dermatophyte Infections

Answer 7

Typical Presentation: 
Scaling d/t necrosis of epithelial cells (usually the stratum corneum involved)
Erythema
Central clearing of lesion is common
May be vesicular
Itching

Tinea Capitus: Ringworm - hair is broken in lesions on scalp, scaling, lymphadenopathy (triad of sx) - also itching present
Tinea Corporus: anywhere on the body
Tinea Cruris: Jock Itch - present in crural folds (ddx with candidiasis - cruris will not affect scrotum and will not be the ‘beefy red’ like candidiasis.
Tinea Manuum - hands
Tinea Pedis - Athletes Foot - painful
Tineas Unguuim - Onychomycosis (nails)

Diagnostics: Woods Light, KOH skin scraping.

Question 8

Onychomycosis

Answer 8

Tinea Unguium - affects toenails more than fingernails.
Distal Sunungal most common - distal nail plate + nail bed (trichophyton rubrum - causative agent)
Proximal Sunungal - least common

Infection of nail bed –> hyperkeratotic debris –> separation of nail from nail bed; may see crumbling of nail itself.
Ddx - psoriasis; must use KOH to be sure.

Question 9

Candidiasis

Answer 9

Ubiquitous, opportunistic.
Mucus Membranes: oral thrush, vulvovaginitis etc.
Epithelium: usually intertriginous areas
SX
erythematous maculopapular lesion, well demarcated, ocassionally satellite lesions; maceration in moist areas.
Mild to intense pruritis.

Question 10

Herpes Simplex Virus

Answer 10

HSV-1 and HSV-2 (both can affect oral/genital mucosa)
4-10 day incubation
30-100% carrier rate; 20-40%recurrence
Go dormant in nerve ganglion; this is why the prodrome is tingling/itch before recurrence - the virus is travelling along the nerve.

Sx:
Vesicles that are single or grouped with erythematous base, later form crusts that are well demarcated.
Soreness + Pain

Question 11

Human Papilloma Virus

Answer 11

Affects nuclei of BASAL epithelial cells causing verrucous hyperplasia and epidermal masses.
2-6 month incubation
HPV 6, 11 - non oncogenic, cause genital warts
HPV 16, 18 oncogenic

Will NOT go beneath basement membrane; black dots in the wart are blood vessels that have undergone thrombosis.

Question 12

Varicella Zoster Virus

Answer 12

Causes Chicken Pox and Shingles (Herpes Zoster)

Virus infect mucosal membranes, epithelium and neurons.
Evades immune response by latency in sensory ganglia (dorsal root).
Transmission: respiratory droplets

Chicken Pox: 
URTI 2 weeks prior to rah
Rash presents on torso and moves outward
Dew drop on a rose petal lesion
Fever + Malaise
No scarring unless secondary lesions. 
Self-limiting -- though secondary impetigo may result

Shingles:
Travels back along sensory ganglion and affects certain dermatomes.
Infection of keratinocytes.
Intense pain and burning is typical prodrome.
Lesions are similar to chicken pox but in a distinctly dermatomal pattern.

Question 13

Impetigo

Answer 13

Very CONTAGIOUS
Bacterial infx with Staph or Strep
Bacterial toxin causes breakdown of keratinocyte adhesion molecules (desmosomes) and causes the pustules.

Sx
superficial pustular, bullous or non-bullous eruption, followed by honey coloured crusts.
Typically the face is affected but may appear anywhere there is excoriation.

Diagnostic - bacterial culture

Question 14

Allergic Dermatitis

Answer 14

Type 4 Hypersensitivity; mediated by sensitized T cells.
Common in teens/adults
NON-SYMMETRICAL

Primary Exposure: activation of niave CD4+ T cells in LN’s
Secondary Exposure = REACTION
Memory T cells –> cytokine release –> activation of endothelial cells + inflammatory infiltrate into dermis/epidermis –> fluid separates keratinocytes –> dermal edema + vesicle formation –> Hyperkeratosis (thickened stratum corneum) and Acanthosis (thickened malpighian layer) –> possible lichenification + excoriation.

Note the mechanism of vesicle formation - it is physical stress d/t infiltrate NOT destruction of cellular components (i.e. desmosomes, hemidesmosomes) as in some viral, bacterial or autoimmune condx.

Question 15

Atopic Dermatitis

Answer 15

Typ I Hypersensitivity; Ig E mediated.
Risk Factors: 
Not breastfed
Urban Environment
Diet
Tendency to Histamine Release
Emotional/Stress

Sx:
Eryhtematous macules, papules and vesicles that occasional weep and or crust. Skin may become hyperkeratotoic and lichenified.
SYMMETRICAL

Major Diagnostic Criteria: 
Pruritis
Flexor surfaces
Spongiosum
Lichenification
Family Hx
Minor Diagnostic Criteria:
Xerosis - dry skin
Pityriasis Alba - hypogigmented macules
Keratosis Pilaris - keratotic papules with follicular base
Ichthyosis Vulgaris - sclay extensor surfaces
Occular Finding - allergic shiners, lichenification of eyelids.

Question 16

Psoriasis

Answer 16

Autoimmune Condition that enhances the turnover time of epidermal cells.
HOW?
T cell infiltrate –> Cytokines TNF-alpha and NF-kB increase the cGMP:cAMP ratio –> increased keratinocyte replication and thinning stratum granulosum occurs –> Acanthosis + Hyperkeratosis ensue – Pt may experience Auspitz sign; pinpoint bleeding.

cGMP is the proliferative molecule
cAMP is the maturation molecule
This means that in psoriasis you have more proliferation and not enough maturation; leads to the typical scaling and itch.

Sx
erythematous plaques, patches, papules with typical silvery scales.
Extensor surfaces, scalp and gluteal folds - also hands + nails.

CoMorbidities: Arthritis (25%), IBD, MS, Metabolic Syndrome, Depression –> related to the pro-inflammatory markers?

Question 17

Psoriatic Nails

Answer 17

Hyperkeratosis –> shedding –> punched out lesions –> pitting

Hyperplasia of nail bed –> debris –> lifts nail plate –> irregular nail separation

Oil Spot (typical) –> serum of nail bed looks oily under nail plate - bc psoriasis is affecting nail bed.

Ddx: Onychomycosis - Do KOH skin scraping.

Question 18

Urticaria

Answer 18

Type 1 Hypersensitivity; Histamine Mediated
ONLY in the epidermis - contrast to dermatitis which is also in dermis.
Wheals (last 24h) and Pruritis
Typically asymmetrical distribution

Ag sensitization IgE–> Mas Cell Degranulation –> Histamine –> Dermal Vascular Hyperpermeability

Question 19

Melanocytic Nevi

Answer 19

Benign tumours derived from melanocytes
ACTH and Estrogen both connected to increased melanocytes
Junctional Nevi: at dermoepidermal; macular at this stage
Compound Nevi: some migration into dermis - nests/cords of melanocytes
Dermal Nevi: midration of all nevus cells into dermis; some degeneration = maturation; will be quite elevated.

Question 20

Atypical Nevi

Answer 20

Tend to be compound with atypical growth + see an immune response: 
lymphocytic infiltrate
loss of melanin
phagocytosis of melanin by macrophages
linear fibrosis

Tend to have irregular borders and be large.

Question 21

Actinic Keratosis

Answer 21

Pre-malignant condition assx with chronic sun exposure and common in fair skinned people.

Processes:
Basal Cell Hyperplasia –> atypia and dyskeratosis (abnormal keratinization)
Fibroblast Damage –> Abnormal fibers synthesis and thickened dermis
Parakeratosis (retention of nuclei in cell sof stratum corneum – only normal in mucous membrane epithelium) —> thickened stratum corneum.

Usually removed bc of the potential to develop malignancy

Question 22

Squamous Cell Carcinoma

Answer 22

SECOND MOST COMMON
White Male +55 = higher risk
Epithelia Keratinocyte
Assx Chronic Skin damage – this is what Actinic Keratosis usually develops into.
LOW invasive potential though risk of metastisis increases with size of lesion + degree of dermal invasion.
Spreads laterally under skin - may get into mm and bone.
Related to SUN EXPOSURE + sun exposed areas
Metastasis: Lymph –> Blood –> lungs, liver, brain, skin, bone.

SX
indurated plaque, papule or nodule with thick scale that is eroded, crusted or ulcerated.
Lip/Mouth/Ears may be assx with regional lymphadenopathy.
95% cure rate if found early.
May be assx with HPV infection

Question 23

Basal Cell Carcinoma

Answer 23

MOST COMMON
White Male 40-80 = higher risk
SLOW growing and RARELY Metastisize
BUT - local destruction and invasion of tissue
ONLY found on epidermal or follicular epithelium NOT MUCOSA bc requires local stroma to support growth
Not typically following Sun Exposure patterns

SX
Flashy nodule with a waxy/pearly appearance and central lesion/depression. May have multiple telangiectasias.

Cure rate is 95% when properly treated.

Question 24

Malignant Melanoma

Answer 24

Not common but AGGRESSIVE
High mortality rate due to metestasis

Risk Factors
Sun exposure
Family Hx/genetics
Large or lots of Nevi ( Vertical Growth –> Metastasis

Carcinoma and Melanoma in biopsy:
Lots of mitotic Events (unlike nevi)
No Maturation (unlike nevi)
Cells Look Atypical (unlike nevi)

Question 25

Pemphigus Vulgaris

Answer 25

Pemphigus vulgaris is an uncommon, potentially fatal, autoimmune disorder characterized by intraepidermal blisters and extensive erosions on apparently healthy skin and mucous membranes. Diagnosis is by skin biopsy with direct immunofluorescence testing. Treatment is with corticosteroids sometimes along with other immunosuppressive therapies.
IgG mediated

SX
Painful NOT itchy
Flaccid blisters that rupture easily - d/t acantholysis of suprabasal cells 
Blisters present in MOUTH
Damage is due to desmosomal damage. 

Will Give Positive:
Nikolsky sign: Upper layers of epidermis move laterally with slight pressure or rubbing of skin adjacent to a bulla.
Asboe-Hansen sign: Gentle pressure on intact bullae causes fluid to spread away from the site of pressure and beneath the adjacent skin.

Question 26

Bullous Pemphigoid

Answer 26

Bullous pemphigoid is a chronic autoimmune skin disorder resulting in generalized, pruritic, bullous lesions in elderly patients. Diagnosis is by skin biopsy and immunofluorescence testing of skin and serum.

SX
Tense bullae on normal-appearing or erythematous skin
Itching NOT painful
RARE mucosal involvement
Nikolsky’s sign NEGATIVE
Basement membrane is attacked (hemidesmosomes).

Question 27

Vitiligo

Answer 27

Vitiligo is a loss of skin melanocytes that causes areas of skin depigmentation of varying sizes. Cause is unknown, but genetic and autoimmune factors are likely.
Sx
depigmented areas, usually sharply demarcated and often symmetric.

Question 28

Albinism

Answer 28

Oculocutaneous albinism (OCA) is a group of rare inherited disorders in which a normal number of melanocytes are present but melanin production is absent or greatly decreased. 
Sx
White skin
White/yellow hair
Decreased retinal pigmentation

Question 29

Pos Inflammatory Hypopigmentation

Answer 29

Loss of skin pigmentation post injur

Question 30

Melasma

Answer 30

Melasma consists of dark brown, sharply marginated, roughly symmetric patches of hyperpigmentation on the face (usually on the forehead, temples, cheeks, upper lip, or nose). It occurs primarily in pregnant women (melasma gravidarum, or the mask of pregnancy) and in women taking oral contraceptives. Overstimulation of melanocytes via female sex hormones.

Sun Exposure is a Risk Factor

Question 31

Molluscum Contagiosum

Answer 31

Molluscum contagiosum is clusters of pink, dome-shaped, smooth, waxy, or pearly and umbilicated papules 2 to 5 mm in diameter caused by molluscum contagiosum virus, a poxvirus.

Non pruritic, non-painful however may become inflamed as body tries to fight the virus.

Question 32

Erythema Nodosum

Answer 32

Erythema nodosum (EN) is characterized by tender, red or violet, palpable, subcutaneous nodules on the shins and occasionally other locations. It often occurs with an underlying systemic disease, notably streptococcal infections, sarcoidosis, inflammatory bowel disease, and TB.
Other Sx
Fever, malaise, and arthralgia.

Question 33

CBC Assessment

Answer 33

Hemoglobin (Hb) - amount of Hb = oxygen carrying

Hematocrit (Hct) - % of RBC in given volume of bld
RBC Mass; dehydration shows hematocrit as higher.

Mean Corpuscular Hb (MCH): – low in iron deficient anemia; B12 deficient anemia tends to be higher.

Mean Corpuscular Hc Concentration (MCHC): Value based on chromicity of the RBC – how red it is. If its pale we have a low concentration of hemoglobin

Mean Corpuscular Volume: Smaller RBC’s have less iron and reflected here as low MCV. Larger RBC’s reflect a B12/folic Acid deficient anemia.

Red Cell Distribution Width (RDW): Size variation of RBCs, Can be increased d/t rapid RBC production and release of immature reticulocytes

Red Blood Cell count (RBC)

White Blood Cell Count (WBC):absolute WBC count is basically useless - just tells us immune sx is ON

Platelet Count: clotting factors

Question 34

MRSA

Answer 34

Methicillin-resistant S. aureus (MRSA)

Resistant to beta-lactam antibiotics due to mutation; very difficult to treat

Nosocomial and community-acquired

Tend to be very aggressive and virulent

Research shows that tea and coffee consumption may reduce nasal carriage of MRSA :)

Question 35

Causes of Non-Lethal Genetic Damage?

Answer 35

Main sources: chemicals, infections, radiation
Also inherited (breast cancer, prostate cancer, colon cancer …)
Most act to promote free radical generation through inflammatory processes
Interact with DNA directly in attempt to gain stability through acquisition of electrons
Viruses and physical traumas to tissue also promote frequent mitoses (either because adapting to stressors, loss of cell cycle control, or promotion by viral genome, eg. HPV)

Question 36

Tumour Cell Generation

Answer 36

tumor cells that have no need of hormone support survive antihormone therapy.

Tumor cells that produce large amounts of angioneogenesis factor are more capable of growing their own blood supply and become more numerous.

Some tumor cells escape natural cell growth control mechanisms and also become more numerous. As a result, late stage tumors are composed of a varied (heterogeneous) mix of cells that have special characteristics and that outnumber cells of the unchanged original tumor line.