Pathophysiology > Dermatology > Flashcards
Dermatology Flashcards
Beau’s lines
Onycholyis
paronychias
ingown toenail
Digital mucous cyst
primary lesion
secondary lesions
anatomy of the nail
papule
patch
plaque
wheel
nodule
vesicle
bulla
pustule
cyst
crust
erosion
ulcer
comedone
milia
telangiectasia
scale
lichenification
fissure
petechia
purpura
burrow
acute inflammation
chronic inflammation
3 phase of wound healing
structure of bacteria
classif of bacteria
aerobic bacteria
anerobioc bacteria
cocci
bacilli
spirochytes
gram stain
mycoses
dermatophytes
pathological bacterial infections of skin
pathological fungal infections of skin
pathogenic fungal organisms & disorders
acne rosacea
acne vulgaris
allergic dermatitis
irritant contact dermatitis
atopic dermatitis
bowen’s disease
candidiasis
cellulitis
condylomata accuminata
dermatophytes
Tinea unguem
dermatophytes
Tinea pedis
dermatophytes
Tinea cruris
dermatophytes
Tinea Corporis
Tinea Capitus
dermatophytes
erythema multiform
folliculitis
furuncle
carbuncle
herpes simplex
herpes zoster
impetigp
lichen planus
molluscum contagiosum
onychomycosis
pediculosis
pemphigus
pityriasis rosea
psoriasis
psoriasis
plaque
psoriasis
guttate
psoriasis
inverse
seborrheic dermatitis
acute urticaria
chronic urticaria
vitiligo
verruca vulgaris
keratocanthoma
basal cell carcinoma
squaumous celll carcinoma
melanoma
high risk nevi
(melanoma)
alopecia androgenica
alopecia areta
tinea to groin
macule
primary skin lesions
Primary skin lesions: Lesions that DEVELOP as a direct result of the disease process + present at the onset of disease. Ex: macule, papule, plaque, pustule, vesicle, wheal, bulla, cyst, nodule
secondary skin lesions
Secondary skin lesions: Lesions that EVOLVE from primary lesions overtime caused by disease progression, manipulation (scratching, picking, rubbing), or treatment. Characteristically brought about by modification of the primary lesion either by the individual or natural evolution of the lesion in the environment. Ex: Crust, excoriation, lichenification, scale
ulcer
Ulcer: Concave lesion varying in size depending on degree of trauma. Loss of epidermis and dermis tissue. E.g. Pressure ulcer or stasis ulcer.
comodone
Comedone: A plug of sebaceous and keratinous material lodged in a hair follicle. An open comedone with a dilated orifice is commonly called a blackhead. A closed comedone with a closed orifice is commonly called a whitehead. Comedones are a clinical characteristic of acne vulgaris.
milia
Milia: Small (approx. 1mm) numerous white cysts that are not related to acne vulgaris or acne rosacea. Commonly termed “milk spots” and characteristic of neonatal milia where multiple milia are found on or around the nose of infants.
telangiestasia
Telangiectasia: fine (0.5-1mm) irregular red lines produced by capillary dilation. Associated with acne rosacea, venous hypertension, systemic sclerosis, and developmental abnormalities. Commonly called “spider veins”, characteristic of rosacea.
scale
Scale: heaped up keratinized cells. Irregular raised areas of flaky skin. Can vary in size and can be oily or dry. Commonly seen in skin with seborrheic dermatitis or generally dry skin.
lichenification
Lichenification: Rough, thickened epidermis following persistent rubbing or itching. Common secondary lesion to pruritic conditions or skin irritations and often expressed on flexor surface of extremity such as the elbow or wrist. E.g. chronic dermatitis
fissure
Fissure: A linear crack or break through the epidermis and dermis. May be moist or dry. Commonly seen at the corners of the mouth with vitamin deficiencies, in infected dermatitis, or Athlete’s foot (Tinea Pedis).
Petechia:
Petechia: circumscribed (def’n: confined or limited to a specific area) of blood/burst capillaries in an area of less than 2mm in size.
purpura
Purpura: circumscribed area of blood in an area of greater than 2mm in size. A rash of larger purple spots caused by bleeding.
burrow
Burrow: Characteristic of parasitic infection. A narrow, raised, irregular channel caused by the burrowing of a parasite.
patch
Patch: flat skin lesion >10 mm diameter (macule is flat skin lesion < 10 mm)
plaque
Plaque: raised skin lesion > 10 mm diameter & Papule: raised skin lesion <10 mm diameter
nodule
Nodule: raised, solid-filled, deeper in dermis than a papule
vesicle
Vesicle: raised, liquid-filled, <10 mm diameter
Bulla
Bulla: raised, liquid-filled, >10 mm diameter
Pustule
Pustule: raised, pus-filled
cyst
Cyst: raised, filled with liquid or semisolid material in dermis
wheal
Wheal: raised, irregular shape, cutaneous edema (ex. Urticaria)
crust
Crust: dried out exudate/sebum on skin
erosion
Erosion: loss of part of epidermis, depressed, moist, glistening
acute inflam
Acute inflammation
Self-limiting (ends when the threat to the host is eliminated)
Approximately 8-10 days from time of infection until healing has occurred.
If acute response is inadequate a chronic inflammation may develop – persists for weeks to months. (see characteristics below)
Etiology & Manifestations of Acute Inflammation
Localized/acute:
Swelling: increased vascular permeability
Pain: stimulation of nerve endings
Heat: Vasodilation
redness (erythema): Vasodilation
Exudate types:
Exudate in early stages is watery/serous
In more severe of advanced inflammation exudate may be thick and clotted (fibrinous) containing plasma proteins.
If large number of leukocytes accumulate the exudate is pus like or purulent.
If bleeding occurs exudate is hemorrhagic exudate
Systemic Manifestations of Acute Inflammation
Systemic Manifestations of Acute Inflammation
Fever
Induced by specific cytokines, known as endogenous pyrogens, released from neutrophils and macrophages
Pyrogens act directly on the hypothalamus which controls the body’s temperature.
Some microorganisms are sensitive to temperature and an increase = death. Others can thrive in a warmer temperature = gram-negative bacterial infections.
Leukocytosis
Increase in the number of circulating white blood cells
Left shift seen in the ratio of immature to mature neutrophils
Plasma Protein Synthesis
Increase in synthesis of proinflammatory and anti-inflammatory plasma proteins by the liver. These are called acute-phase reactants
Acute-phase reactants reach maximal circulating levels within 10-40 hours after the start of inflammation
Common lab tests that measure acute phase reactants include:
Erythrocyte Sedimentation Rate (ESR): fibrinogen increases = increased binding of erythrocytes and increased sedimentation rate.
C-reactive protein also produced by the liver increases in response to acute inflammation
chronic inflammation
Chronic Inflammation
Lasts 2 weeks or longer regardless of the cause
Sometimes predicated by acute inflammation: e.g., a sliver in a wound with persistent pus and incomplete wound healing
Can also occur without previous acute inflammation:
Microorganisms that are insensitive to breakdown by phagocytes
Microorganisms that can survive within macrophages and avoid removal by acute inflammation (e.g., syphilis & leprosy)
Microorganism may release toxins that can damage tissue even after the organism is killed.
Chemical matter, particulate and physical irritants (inhaled dust, suture material) can cause a prolonged inflammatory response
causes of chronic inflammation
tiology
Presents clinically with dense infiltration of leukocytes and macrophages.
If the macrophages are unable to protect the host from tissue damage, the body attempts to wall off and isolate the infected area.
Inflammation may progress to granulomatous response = designed to contain and “wall off” the cause of tissue damage so it no longer poses any harm. E.g., tuberculosis granuloma in the lungs. TB can live in latent form in these spores and divide when host immune is low.
Macrophages differentiate into large epithelioid cells, which specialize in taking up debris and other small particles. Others fuse into multinucleated giant cells, which are active phagocytes that can very large particles. These 2 cells for the center of the granuloma which is walled off by lymphocytes. The granuloma is further encapsulated by fibrous deposits of collagen.
Impetego
Highly contagious (Direct or indirect contact), superficial skin infection produced by Staphylococcus aureus (80% of cases), Streptococcus pyogenes, or a combination of both
lichen planus
Benign autoimmune inflammatory disorder of the skin and mucous membranes
verrica vulgaris
common wart
HPV replicates in the epidermal cells, causing irregular thickening of the stratum corneum in the infected areas.
Vitiligo
Vitiligo
Chronic (long-lasting) autoimmune disorder that causes patches of skin to lose pigment or color
Keratoacanthoma
Keratoacanthoma
Rapidly growing crateriform (dome shaped/volcano shaped) nodule regarded as a low-grade squamous cell carcinoma
Molluscum Contagiosum Virus (MCV)
Poxvirus that is member of the poxvirus family
-4 major genotypes, MCV1 & MCV2 most common
-Causes a chronic, localized infection with small papules on the skin
-Only known host for MCV is humans
-Spread by direct skin to skin contact, autoinoculation
Onychomycosis
Chronic fungal infection of the toenails or fingernails
-Causative fungi include: dermatophytes, yeasts, and nondermatophyte molds
-Acquired through direct contact of the nail with the causative fungi or through spread of fungal infection from affected skin
-Fungal production of proteases that degrade keratin may facilitate invasion
-Factors that can compromise barriers to infection such as nail injury or disease may inc. risk for fungal invasion
-Formation of fungal biofilms is a proposed contributor to persistent infection
Basal Cell Carcinoma
Basal layer keratinocytes of the epidermis.
-Keratinocytes are susceptible to DNA damage. DNA damage leads to mutations in cell genes, which leads an activation of oncogenes, inactivation of tumour-suppressor genes, and inactivation of apoptosis controlling genes, then there is unregulated cell growth and differentiation.
-TP53 & PTCH1 commonly mutated.
Squamous Cell Carcinoma
-Originate in epidermis.
-Keratinocytes are susceptible to DNA damage. DNA damage leads to mutations in cell genes, which leads an activation of oncogenes, inactivation of tumour-suppressor genes, and inactivation of apoptosis controlling genes, then there is unregulated cell growth and differentiation.
-TP53 and NOTCH commonly mutated.
-May originate from actinic keratoses
melanoma
-malignant tumour of the skin originating from melanocytes
- Can also arise in the uvea of the eye and on mucous membranes
- result of malignant degeneration of melanocytes located either along the basal layer of the epidermis or in a benign melanocytic nevus
Psoriasis (Plaque, Guttate, Inverse)
Bowen’s disease
Very early form of skin cancer or Squamous Cell Carcinoma in situ. Rarely invade or metastasize
Irritant Contact Dermatitis
A nonspecific inflammatory dermatitis caused by activation of the innate immune system by pro inflammatory properties of chemicals.
Atopic dermatitis
Filaggrin gene mutations also are associated with increased risk for asthma in AD and ichthyosis vulgaris (dry, scaly skin).
There is an altered skin microbiome
with formation of biofilm by S. aureus that may act as superantigens causing exacerbations of eczema.
Candidiasis
(Moniliasis)
-
infection of the skin and mucous membranes by candida
Cellulitis
:
bacterial infection of deep dermis and subcutaneous tissue
Condylomata Accuminata
(Singular: Condyloma Acuminatum):-
Infection of genital or perianal skin by the Human Papillomavirus (HPV) leads to manifestation of condylomata accuminata (CA)
- typically caused by HPV subsets 6 or 11
Dermatophytoses
Fungi are relatively large eukaryotic microorganisms with thick walls that have 2 basic structures: single cell yeasts (spheres) or multicellular moulds (filaments or hyphae).
Tinea Unguem
oenail fungus (onychomycosis), can be fingernails
Tinea Cruris
Jock itch – infection of the groin, proximal inner thighs, or buttocks
Common cause: T. rubrum
Tinea Corporis
Ringworm.
Infection of body surfaces other than the feet, groin, face, scalp or beard hair.
Superficial dermatophyte infection.
Tinea Capitus
Fungal infection of the scalp (scalp ringworm)
Primary microorganism responsible: Microsporum canis
Often from contact with young kittens/puppie
Pityriasis Rosea
Common rash (cause thought to be viral but unconfirmed).
-Characterized by oval pink to red papules and plaques with a distinctive collarette of scale.
Scabies
-Contagious disease caused by itch mite Sarcoptes scabiei which can colonize epidermis. -Infestation initiated by female mite that tunnels into stratum corneum, deposits eggs, and creates a burrow up to 1cm long.
-Eggs mature into adult mites over several weeks.
Seborrheic dermatitis
Seborrheic dermatitis
SD and dandruff are a continuous spectrum of same disease that affects the seborrheic areas (areas rich in sebaceous gland) of the body. Dandruff is restricted to scalp*
Urticaria (Acute)
(urticaria = hives)
Mast cell activation with histamine release.
Induced by allergens or triggers (e.g. medication, lotion, foods, or airborne allergens)
bacteria
Bacteria are prokaryotic cells with cholesterol-free cell membranes. The cytoplasm is contained by a plasma membrane, cell wall, and capsule(collective called the cell envelope). The outermost layer may have pili or fimbriae which facilitate adherence to targets, and they may have flagella
Classification of bacteria
Classification of bacteria is based on shape, Gram-stain, and oxygen requirements.
shape of bacteria
Shape (there are additional variations but these are the 3 main shapes)
Cocci - sphere shaped
Bacilli - rod shaped
Spirochetes - spiral shaped
bacteria
Gram-stain (positive or negative) see figure 8.1, p.179
Refers to how the bacteria stains and appears under the microscope. Can guide treatment based on known resistance to antimicrobials.
Gram positive bacteria have a thick layer of peptidoglycan within the cell wall that stains
Gram negative bacteria also have a layer of peptidoglycan + outer membrane forming the cell wall; doesn’t stain and tend to be more resistant to antibiotic treatment
bacteria
Oxygen requirements
Aerobic: requires oxygenated environment to live and proliferate
Anaerobic: requires oxygen free environment to live and proliferate
Facultative: can live + grow with or without oxygen
Mycoses:
Diseases caused by fungi.
They can be described as superficial, cutaneous, subcutaneous, and systemic (opportunistic fungi) based on their degree of invasiveness.
Superficial and cutaneous mycoses occur on the skin, hair, and nails. No inflammation noted, skin redness and localized itching.
Subcutaneous mycoses are localized infections of the skin and underlying tissue.
Systemic mycoses affect internal organs (lungs, brain, GI tract). Usually harmless for healthy individuals unless a person is immune compromised.
Mycoses can be caused by dermatophytes, candida genus and rarely Aspergillus (mold).
Candida:
Candida:
Candida naturally presents on the skin and is harmless when low.
When overgrowth appears, it can damage skin and nearby tissue causing infections such as vaginitis or oropharyngeal infection (thrush).
A weakened immune system often results in overgrowth and as a result candidiasis forms.
It typically affects individuals who are immune compromised (diabetics, HIV, Cancer patients) and are at risk for systemic infections caused by opportunistic fungi.
Signs and symptoms of a deep disseminated candidiasis: abscesses in the kidney, brain, liver, or heart and is characterized by a persistent or recurrent fever, hypotension, tachycardia, and disseminated intravascular coagulation (DIC).
Aspergillus:
Aspergillus:
A cutaneous mycosis caused by an infection by a non-dermatophyte fungus.
Aspergillus is a family of molds consisting of many varied species that causes a condition called aspergillosis.
It is a rare locally invasive disease that spreads to the skin from somewhere else in the body, e.g., Lungs.
Skin infections are less common but can occur through trauma, burns, or surgery.
Presents with distinctive skin wounds (eschar) in affected areas.
Dermatophytes:
Spread occurs through direct skin contact, rarely, through contact with an infected animal or soil.
Most cutaneous mycoses are caused by dermatophytes that invade the skin, hair, or nails.
Dermatophytes are a group of filamentous fungi that colonize and infect keratinized tissues. Most common dermatophyte infections are caused by a fungus called Trichophyton, Microsporum and Epidermophyton genera.
Dermatophytes that produce skin lesions are called tineas (aka. ringworm: ring like appearance)
On the scalp it is referred to tinea capitis.
On the feet it is referred to as tinea pedis (athlete’s foot).
In the groin area it is referred to as tinea cruris (jock itch).
It presents as an itchy rash that has a central clearing surrounded b
Alopecia Androgenica
physiologic reaction induced in men by androgens in those genetically predisposed
- for women, occurs with or without high androgen levels
-probable polygenic pattern of inheritance
-occurs as a result of an increased production of the hormone dihydrotestosterone which is produced from the circulating male hormone testosterone, and which acts on the hairs that are genetically predestined to fall out
-(Unknown why dihydrotestosterone is produced in excess in areas that are balding, while at the same time, in other areas of the same individual, including permanently hair-bearing areas of the scalp, the hormone is being produced at normal levels)
-terminal hair follicles are transformed into vellus-like follicles
-terminal hair is replaced by fine light vellus hair (shorter & reduced diameter)
-over time further atrophy occurs ->scalp=shiny & smooth (follicles
Alopecia Areata
-immunologic phenomenon;
-hair follicle danger signals attract specific T cells, result in immunologic damage
-trigger cause unknown
-hair shaft poorly formed; breaks when reaching the surface
benign skin tumours
Seborrheic Keratosis
Keloid scars
keratoacanthoma
Basal Cell Carcinoma
basal layer of epidermis
rarely metasticize
pink/white
spider veins
papule/nodules
bleed and ulcerate
Actinic keratosis
may lead to SCC
sun exposed/elderly
sandpaper like skin
Squamous cell carcinoma
skin and mucosal
face ,head,neck hands old people
EARSpin/red dome shaped nodule.
bleeds/ulcers
BOWEN’s disease-SCC insitu .full thickness involvement. skin/mucosal -looks like eczema or psoriasis
moles/nevi melancytes cells
