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283 Cards in this Set

  • Front
  • Back
what kind of result do tests have?
quantitative result
what is the most impt thing to know about any patient?
what is the purpose of screening test?
looking for something w/o any predetermination (ex: Health fair screenings)
Typically what is the purpose of the first test? second test?
first test: check to see if disease could be present (Is it possible?)
second test: definitive test to determine what it is
*you always need more than 1 test
What are the 4 tests?
1. screening: no hypothesis
2. case finding
3. confirming test
4. monitering test (when you know they have disease and want to monitor it)
what are some examples of physical exams used as a test?
score reflexes
BP- yes or no (binary)
pulse (quantitative)
which tests tend to be the best test?
physiologic tests
which tests are high specificity?
anatomic pathology b/c they confirm diagnosis, very definitive via biopsies
in general, what does analytical characteristics of medical tests mean?
what actually happens to get a valid test: Doing the test (if you dont do EKG right, you won't get valid result)
What is the reference range?
anything that falls outside of normal range is abnormal (disease) however, some can be outside of range and are NOT abnormal
what is the reference range dependent on
geographic location, instrument, age, lab
what is always specific for each laboratory and each test?
reference range
what type of curve is assumed for reference range?
gaussian curve, 95% is normal
if way over reference range (2.5%) more likely to be abnormal while if jsut outside reference range, due to sampling
what is multiphasic testing?
detect common diseases before becoming clinical manifest
what happens with the more tests that you perform?
the more tests you do, the higher the chance of obtaining abnormal results that isn't abnormal
Ex: do 20 tests, 66% chance that there will be abnormal value that isn't abnormal
what are the 3 sources of error that are analytical characteristics?
what are some factort to be aware of that could result in preanalytical errors?
specimen requirements (testing correct specimen)
patient factors (time of day, standing or supine, tourniquet time)
amt. of specimen
biological variability
when does biological variability matter in the case of pre-anayltical errors?
inter-individual variability: we are all diff hts, wts
intra-individual variability
Ex: IgM variability: stable w/n each person, but b/n people they are all stable at different levels
what percent of lab error is preanalytical?
99% therefore it is better to get no result than a bad result
in terms of analytical errors, what is the problem?
labs are very PRECISE, but not always accurate thefore they need something w/ absolute accuracy/truth to measure against
ex: cholesterol
what are we aiming for during the measurment?
excellent precision, excellent accuracy, but usually get excelling precision, low accuracy
how can post-analytical errors occur?
-remembering wrong reference range and interpreting results incorrectly
-every lab value has a useful life span, so if not paying attn to life span (ex: urine) results could produce errors
- problems arise when acting on single not do this unless it fits w/ what you are thinking ex: to diagnose hypercholesteremia need 2 consecutive measurments in 2 wk period
what are the 5 fxns of skin? Primary fxn?
1. protective covering-protect internal environment (primary fxn)
2. tactile interaction w/ external world
3. body temp regulation
4. antigen recognition
5. sexual attractivness/apocrine secretions
where are apocrine secretions generally?
axillary and groin regions (proteinaceous therefore good mileu for bacteria)
skin differences results from differences in what?
four basic layers
distribution of adnexal structures
what are the 4 basic layers of skin?
papillary dermis
reticular dermis
subcutaneous tissue (hypodermis)
what are the 3 major adnexal structures?
1. pilar (hair) units w/ pilosebaceous unites, arrector pili mm
2. eccrine units (eccrine gland and ducts)
3. apocrine units (apocrine glands and ducts)
what cells are found in the epidermis? explain proli
keratinocytes that proliferate at the basal layer. each makes 2 cells; 1 descends upward while the other fills with keratin very rapidly
what is the site of edema?
papillary dermis b/c it is expansile
compare the collagen fibers in papillary dermis vs. reticular
papillary: very fine collagen fibers
reticular: rigid fibers
what happens to keratinocyts as they move up in epidermis?
they become bigger b/c they fill with keratin *highly specialized
nuclei are farther apart
cells are very adherent to one another to make strong barrier
what are the 5 layers of the epidermis?
stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale

Corn Lover's Grow Several Bales
what is the horny layer?
the stratum corneum: outermost layer of epidermis composed of dead cells that lack nuclei "basket weave apperance"
explain the appearence of stratum granulosum
compact kertain layers of cells with keratohyalin granules underneath the glue keratin fibers together
besides keratin, what else do keratinocytes contain?
melanin from melanocytes for protection
where do you find melanocytes? what does it look like?
stratum basale of epidermis
has halo around it b/c it lacks the cell-cell connection that keratinocytes have (desmosomes)
it stays at basal layer always
what acts as a "glue" w/n the stratum granulosum?
keratin hyalin granules
what are recognized as spinous processes?
desmosomes (intercellular bridges) that hold squamous keratinocytes together
what do melanocytes make?
melanosomes that catalyze dopa to melanin *fxn of melanin: inert polymer that absorbs UV radiation
difference in skin color b/n individuals is due to what?
level of melanocyte activity
tan= increase melanin to protect from UV
what cells are present in stratum basale? How many layers?
melanocytes and Merkel cells
single layer of columnar or cuboidal keratinocyte stem cells, which are mitotically active
how is melanin transferred?
Once made, melanin is moved along arm-like structures called dendrites in a special container called a melanosome which is shipped to the keratinocytes. Melanosomes are vesicles or packages of the chemical inside a plasma membrane.

When ultraviolet rays penetrate the skin and damage DNA; thymidine dinucleotide fragments from damaged DNA will trigger melanogenesis and cause the melanocyte to produce melanosomes, which are then transferred by dendrite to the top layer of keratinocytes.

The melanin is in organelles called "melanosomes", that are organized as a cap protecting the nucleus of the keratinocyte.
where will you see more melanin?
near stratum basale b/c ratio of melanin:keratin is high
job of Merkel cell?
fxn unknown
found in stratum basale
precursor for Merkel cell carcinoma
job of langerhans cell? whre located?
antigen recognition cell
upper spinous layer
interrelatinships b/n epidermis and dermis?
epidermis influences the dermis and vice versa
which layer of dermis is most impt?
papillary dermis
where isthe superficial vascular plexus located?
papillary dermis *very expansile
what are rete pegs
invag of epi into dermis
act as track shoes for stabilization
what are dermal papillae?
highly vascular
extensions of the dermis into epidermis
*cause you to blush
*not as deep in older ppl
fxn of Meissner's corpuscle?
a specialized structured nerve ending
-touch receptor
where do you find meisnner's corpuscles w/n skin? on body?
dermal papillae
most numerous on hands and feet
fxn of reticular dermis?
serves as cushion and stable platform for the epidermis and papillary dermis
where are adnexal structures located?
reticular dermis
where is reticular dermis thickest?
in areas subject to pressure such as back, butt
-not on fingertips b/c you need flexibility
which dermis layer is movable/stretchable ?
papillary dermis
where are pacinian corpuscles located?
deep reticular dermis or hypodermis
fxn of pacinian corpuscle?
encapsulated nerve ending to detect pain and temp
pressure R
what does subcutaneous tissue contain?
loose and dense CT consiting of adipocytes and fibroconnective tissue
what does subuctaneous tissue connect?
reticular dermis with fascia of underlying tissue (muscle, bone, tendon)
is subcutaneous tissue vascularized?
yes, with deep vascular plexus
fxn of subcutaneous tissue?
body temp regulation
depot for fat storage (large energy reserve)
which layer of skin is aging most evident?
subcutaneous tissue; with aging there is a progressive loss of subcutaneous tissue particularly in extremities (hands and feet)
location of adnexa?
reticular dermis and exit via epidermal surface
why do you lose hair after chemo treatment?
b/c the agent kills rapidly dividing cells such as those involved in hair growth (epithelial cells and melanocytes)
what is attached to the hair follicle?
Attached to the follicle is a sebaceous gland, a tiny sebum-producing gland found everywhere except on the palms, lips and soles of the feet. The thicker density of hair, the more sebaceous glands are found.
*need oil to lubricate hair shaft
what are eccrine glands?
Eccrine sweat glands are distributed over the entire body surface but are particularly abundant on the palms of hands, soles of feet, and on the forehead. These produce sweat that is composed chiefly of water with various salts. These glands are used for body temperature regulation.
*coiled tubular glands
where are eccrine sweat glands located?
mid-to lower reticular dermis
what are apocrine glands? where located?
These glands produce sweat that contains fatty materials. Mainly present in the armpits and around the genital area, their activity is the main cause of sweat odor, due to the bacteria that break down the organic compounds in the sweat.

*located in the deep dermis and often at jxn of reticular dermis and subcutaneous tissue (axilla, scalp, perineum)
what are the 9 primary lesions?
1. macule
2. patch
3. papule
4. nodule
5. plaque
6. wheal
7. vesicle
8. bulla
9. pustule
what is a macule?
flat area of color change less than 1 cm in diameter (freckle)
what is a patch?
larger flat (non-palpable) lesion greater than 1 cm (cafe au lait spots)
what is a papule?
discrete solid RAISED lesion less than 1 cm in diameter (nevus)
what is a nodule?
larger discrete, rounded, RAISED solid lesion (rheumatoid nodule)
what is a plaque?
raised, flat topped lesion greater than 1 cm in diameter (think mesa with flat top)
what is wheal?
transient edematous erythematou plaque (hive or mosquito bite) itchy
what is a vesicle?
fluid filled lesion with clear top less than 0.5cm in diameter (herpes simplex infxn)
what is a bulla?
larger fluid filled lesion in papillary dermis that raises epidermis (friction blister)
what is a pustule?
vesicle like lesion filled with purulent exudate (folliculitis or acne)
what are the 8 secondary lesion?
1. erosion
2. ulcer
3. fissure
4. scale
5. crust
6. lichenification
7. atrophy
8. verrucous
what are secondary lesions related to?
secondary factors such as rubbing, scratching, superimposed infxn or tissue loss
what is an erosion?
2nday lesion
partial or complete loss of the epidermis
what is an ulcer?
loss of epidermis and part of dermis (goes through the epidermis)
2ndary lesion
what is a fissure?
thin, linear erosion or ulceration (cracked lips)
what is a scale?
2nday lesion
hyperkeratosis (dry skin)-almost always the result of rubbing
what is crust?
2nday lesion
dried serous and serosanguinous exudate (impetigo: crust with infxn at surface)
what is lichenification?
2ndary lesion
accentuation skin markings with thickening of the skin
subject to a lot of friction
what is atrophy?
2dary lesion
decrease in amt of epidermis, dermis or subcutaneous tissue
waht is verrucous?
2ndary lesion
wart like surface
what changes occur in skin with aging?
flattening and loss of rete pegs at dermal-epidermal jxn
loss of subcutaneous tissue
loss 25-50% of cross sectional diameter of hair shaft
decrease in number of hair follicles therefore decrease in oil productin
change in distribution of hair
loss of subcutaneous fat pad
what type of damage is due to sun? whre most vulnerable?
actinic damage with fine wrinkling and white spots most commonly on forehead, face, dorsum of hands
what is lentigo senilis or solar lentigo?
benign, discrete hyperpigmented macule occuring on chronicaly exposed skin in adults especially on the back of the hands and forehead
what is the cause of Lentigo Senilis?
increased melanin pigment only in keratinocytes-there is NO increase in # of melanocytes
is there an increase in melanocytes in Lengtigo Senilis?
no, ony due to increased syn of melanin even though the term lentigo means a prolif of melanocytes
what are some common names for Solar Lentigo?
age spot
liver spots
are the areas of hyperpigmentation seen in solar lentigo macular or papular?
always macular
do African Americans have more melanocytes?
no, more effective at production of melanosomes but same amt of melanocytes
vitigo is due to what?
disorder of de-pigmentation in which there is a depletion of melanocytes due to sloughing or congenital absence of melanocytes (albinism)
def of melasma?
hypermelanosis characterized by development of sharply demarcated blotchy, brown macules in a symmetrical distribution over the cheeks and forehead and less freq on upper lip and neck
are melasma due to an increase in melanocytes?
no! hypermelanosis: increased production of melanin by estrogen or progesterone
other names for melasma?
chloasma or mask of pregnancy
in which population do you see most melasma?
Although it can affect anyone, melasma is particularly common in women, especially pregnant women and those who are taking oral contraceptives or hormone replacement therapy (HRT) medications (menopause)
cause of freckles?
increaed production of melanin in focal area (ppl with freckles will get darker freckles in sun)
what is acanthosis nigricans? where is is generally?
hyperpigmentation in flexural regions (axillae, skin folds of neck, groin, and anogenital regions)
what percent of Acanthosis nigricans benign? malignant?
benign 80%
malig 20%
benign Acanthosis Nigricans mainly occurs in? inheritance? associated with?
during childhood or during puberty
associtatd with obesity or endocrine abnormalities
malignant Acanthosis Nigricans mainly occurs in what pop? associated with?
arises in middle aged and older individuals
-occurs in association with underlying adenocarcinoma
describe the evolution and localization of a tatoo
particles put in papillary dermis bc if in epidermis, they will slough off. want the particles to be inert so they wont break down. When the enter the papillary dermis, histiocytes (mac) will eat the particles but they can't digest them so they concentrate them making tatoo look bright. when mac die, new mac eat particles diluting particles cuasing fade b/c they diffuse down into reticular dermis
where do Nevocelluar Nevi occur? in what population?
face and neck
childran and young adults (at 30-40 they go away)
3 types of Nevi
appearance of jxnl nevi on skin
called beauty spot or mole
where is jxnl nevus located?
as a proliferation of melanocytes at dermal/epidermal jxn. as they migrate into dermis they are called nevus cells
appearance of compound nevus on skin?
more raised and dome shaped
red b/c they stimulate their own blood supply
located in papillary dermis therefore raised
appearance of intradermal Nevus on skin?
no prolif at dermal/epi jxn
everything migrataed into dermis
brown, not red b/c not recruiting blood supply
are Nevi associated with incresaed risk of melanoma?
no, 80-90% of melanomas arise de novo and are not associated with benign neoplasmas
how do you biopsy a nevus?
shaved biopsy: parallel to skin surface
which form of nevi are associated with increased risk of melanoma?
congenital nevus: very large found in deep dermal. present at birth
def of malignant melanoma. where occur?
malignant neoplasm derived from cells capable of forming melanin
may occur in skin of any part of the body, in the eye, anus, oral cavity , etc
in which pop do malignant melanoms primarily occur? how do they originate
originate de novo as an isolated lesion (80-90%) or adjacent to a melanocytic nevus
what is Melanoma in situ?
Lentigo maligna is a melanoma in situ: it consists of malignant cells but does not show invasive growth. It can remain in this non-invasive form for years. It is normally found in the elderly (peak incidence in the 9th decade), on skin areas with high levels of sun exposure (for example, face and forearms).
compare the distribution of malignant melanoma is males vs females
males: mostly on trunk: 35%
females: mostly on legs: 56%
*do not predom occur on head or neck
*don't howver see too many on legs; mostly trunk
in which population are malignant melanomas greatest?
white male then white females bc decreased pigmentation
what is prevalence?
prevalence, which is a measure of the total number of cases of disease in a population, rather than the rate of occurrence of new cases. Thus, incidence conveys information about the risk of contracting the disease, whereas prevalence tells us how widespread the disease is.
what is incidence? incidence rate?
number of new cases of a disease during a given time interval, usually one year
INCIDENCE RATE is the incidence divided by the number of people at risk for the disease.
what is typically the age of onset of malignant melanoma?
see it increase with age and peak in older ppl (see at 20yrs then progressivly increse)
*disease of older ppl
what are the 4 criteria for Malignant Melanoma?
1. asymmetrical
2. irregular, vague borders
3. maculopapular "chaos"
4. variation in pigment hues/colors
how do you biopsy melanomas?
don't want to shave them like a nevuceullar nevus!! instead to excision biopsy
*do case finding test first (4 criteria) then confirmatory test (biopsy)
where would you find a melanoma in a biopsy?
if normal melanocytes: dermal/epi jxn
if in epidermis then it means it is proliferating and is melanoma. will also see lymphocyte infiltrate w/n dermis
what is the Pagetoid spread "Buckshot Pattern"?
Pagetoid is a term used in dermatology to refer to "upward spreading" of melanocytes into the epidermis. It is uncommon and a possible indication of a precancerous or cancerous condition. Cells display pagetoid growth when they invade the upper epidermis from below.
what type of spread to you see in melanoma?
hemoatogenous spread therfore will kll you
Melanoma survival is dependnet on what?
stage: melanoma metastatic to any lymph node represents advanced disease (stage III)
what is the percent of 5year surival with Stage I melanoma? 10year survival?
98% : 5
95%: 10
waht is the percent of 5year survival with Stage IV melanoma? 10year?
15% : 5
5% :10
how does the Breslow level determine Melanoma Mortality?
a Breslow level b/n 0.76 mm and 1.00 mm is associated with an 80% 5 yr survival
*less thickness=more survival
Fibroepithelial Polyps (FEP) are also known as (4 names)
skin tags
fibroma molle
squamous papilloma
where do fibroepithelial polyps occur? associated with?
on neck and groin in older individuals
associated with areas of rubbing by clothing
what is typical of the core of fibroepithelial polyps (FEP)?
fibrovascular core thefore if cut them at the base they will bleed
Epithelial Inclusion Cysts (EIC) occur where? caused by what? filled with?
occur around face and upper trunk *extremely common
caused by obstruction of hair follicle
filled w/ keratinous debris and sebum
what happens in EICs are ruptured?
provoke a chronic inflammatory rxn and even granuloma to the keratin
all EICs have what?
have epithelium lining which grows and lining becomes progressively attenuated
color of hemangiomas? xanthomas?
hemangiomas: red
xanthomas: yellow
in which pop do you see hemangiomas mostly?
what are hemanogiomas? capillary?
a congenital benign skin lesion consisting of dense, usually elevated masses of dilated blood vessels".
Hemangiomas can be vivid superficial lesions, known as capillary hemangiomas (often referred to as "Strawberry Marks" that are frequenlty reactive
where are benign fibrous Histiocytomas (Dermatofibroma) normally seen? what pop?
benign soft tissue neoplasm
seen in adults
on legs of young-middle aged adults
what do Benign Fibrous Histiocytomas (dermatofibroma) look like?
tan brown papules which are usually small and may be tender
more common name for Benign Fibrous Histiocytomas?
are Dermatofibromas true neoplasmas?
no, but an exaggerated fibroblastic response to trauma
what is Dermatofibrosarcoma protuberans (DFSP) ?
rare malignant superficial variant of Dermatofibroma that is locally aggressive, but rarely metastasizes
how can you tell if a dermatofibroma is young?
red= recruiting vssls to support growing tissues
describe the histological features of dermoatofibromas
They are composed of disordered collagen laid down by fibroblasts.
see proliferation of epi basal cells as they move down
prolif of benign appearing fibroblasts
**characteristic tendency of fibroblasts to surround individual collagen bundles
most benign fibrous histiocytomas occur how?
Some physicians and researchers believe dermatofibromas form as a reaction to previous injuries such as insect bites or thorn pricks *often occur after trauma
Seborrheic Keratosis is what?common in what pop?
benign prolif of keratinocytes
benign skin growth that is very common among people over 40 years of age. (45-64=middle age or 65-75 near old)
appearance of Seborrheic Keratosis?
round, flat but elevated (stick above surface level of skin b/c at epidermsis layer so when they prolif they grow up)
Because only the top layers of the epidermis are involved, seborrheic keratoses are often described as having a "pasted-on" appearance
where on body are Seborrheic Keratosis normally found?
trunk, proximal extremities, face and neck (not in sun exposed areas)
if pull/scratch called irritated seborrheic keratosis
how can you tell that Seborrheic Keratosis is not melanoma?
b/c has sharp borders and reasonably symmetrical
adnexal tumors begin where?
in adnexa: gland, hair follicle, ducts
what do adnexal tumors look like? where most likely found?
shiny, firm
run in families
multiple cylindromas
see in face and hair bearing areas b/c occur in adnexa
why are adnexal tumors called cylindroma?
b/c they are composed of islands of basaloid cells containing occasional ducts bc they try to mimic where they come from(if in hair follicle, will grow some hair)
multiple trichoepitheliomas are found where?
hair bearing areas (adnexa) b/c tricho = hair
what percent of adnexal tumors are benign?
characteristics of benign adnexal tumors vs malignant
benign: symmetrical, small, superficial, vertical in orientation (bc grow along plane of adnexal structure)
malignant: asymmetrical, large, deep, wide
what is the most common malignant adnexal tumor?
sebaceous carcinoma
is actinic keratosis a pre-malignant condition?
yes, presents on sun exposed areas
why do actinic keratosis appear white and flaky?
bc of keratin generation
what conditions place an individual at risk for actinic keratosis?
fair complex (less melanin protection)
old scars
organ trasplant (immunocompromised)
how will actinic keratosis appear histologically?
no basket weave appearnce of horny layer b/c has turned into compact keratin b/c keratosis
increased cellularity due to increased turn over of cells
many nuclei=neoplasm
thin papillary dermis
solar elastosis: degeneration of coarse reticular fibers b/c of UV damage
what is solar elastosis? where do you see it?
solar elastosis is the actinic degeneration of the dermal collagen that is irreversible
*see in Actinic Keratosis
where and what population does actinic keratosis occur?
on sun exposed areas of the body (face, forehead, neck, dorsum of hands) in middle aged (45-64) and elderly individuals
how does actinic keratosis look?
erythematous (b/c rapidly gowing cells tend to recruit blood suppply)
reddish brown MACULES or minimally elevated PAPULES with SCALES due to increased keratin
how is Actinic Keratosis different thant Bowen Disease?
bown disesae = SCC in situ
Actinic Keratosis is incompletely developed or nascent SCC
how can you diff Seborrheic Keratosis from Actinic Keratosis?
Seborrheic keratoses are other bumps that appear in groups like the actinic keratosis but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis.
*see if in sun exposed areas
difference b/n solar lentigo and actinic keratosis?
solar lentigo is NOT due to keratosis but results from hyperpigmentation of keratinocytes
*both appear in sun exposed areas
*solar lentigo is macular
*actinic keratosis can be papular and are scaly and erythematous..crusty!
Order of progresson from Actinic Keratosis?
Actinic Keratosis
invasion SCC
what is SCC?
malignant proliferation of epidermal keratinocytes which has the potential for metastasis to regional nodes or distant sites (doesn't happen very often. hardly ever malignant enough to kill you)
what are some other causes of SCC (synergistic with sunlight)?
Human papillomavirus
extensive X-ray exposure
Genetic syndromems: XP
incidence of SCC increases with what?
age! male predominance

*organ transplant recipients are prone to SCC bc immunosuppressed
*2nd most common cutaneos malignancy
what does early invasive SCC look like?

What do older SCC look like?
early: small, firm, skin-colored may be granular and bleed easy
Older: larger, invasive an rarely involve the underlying soft tissue. center is ulcerated
why do you see ulcerated centers in late SCC?
b/c rapidly growing cells
all around periphery are blood vssls
**reddish tan b/c of blood vssls
what is characteristic histologically of SCC?
invasive: epithelium infiltration into dermis..passes BM into dermis (pushing down therefore see ulcer)
is SCC lethal?
not very, equivalent to 1 death in 2500 individuals each with 40 years of sun exposure
when you think Keratocanthoma, think what?
of the histology slide that looks like a volcano: rapidly growing on sun exposed areas that involutes into crater like architecture: pushes up and pushes down createing crater in center b/c rapidly growing
what is Keratocanthoma?
rapidly growing (days-weeks) neoplasm; occurs in sun exposed areas (face, hands) or older adults
involutes and clears spontaneously.
central keratin-filled crater that is frequently filled with crust. The growth retains its smooth surface, unlike a squamous cell carcinoma.(also it is symmetrical)
histologically, SCC is now termed what?
SCC, keratoacanthoma type
is BCC malignant?
yes but it seldom metastasizes but has the potential for local invasion and destruction (should be called Basal Cell Epithelioma)
what makes you prone to BCC?
incresaed sunlight exposure in childhood and adolescence and chronic exposure during childhood
what is the most common cutaneous neoplasm?
*98% occur after age 40
same freq in males and females
after age 50, 1% of pop develops BCC each year
major clinical characterisitcs of BCC?
95% occur after age 40
85% occur on head/neck
rest on trunk/limbs
**predilection for hair-bearing skin on sun exposed areas
the clinical appearance of what cancer is related to major histiologic type? what are the types?
Scerlosing or morpheaform
Pigmented BCC
Superficial BCC
clinical appearance of Nodular BCC?
dome shaped papule
*shiny and sticking up
**on histo: clefts seperate nests of basaloid cells w/n dermis
clinical appearance of Sclerosing or morpheaform BCC?
yellowish-white or pearly white
indurated plaque with poorly defined margins

difficult to excise completely bc depressed:
***Rodent Ulcer:waxy,firm depressed lesion that is puckered,pulled in because infiltrated
what are pigmented BCC often confused with?
malignant melanoma b/c of dark irregular pigmentation
where do superficial BCC occur? what do they look like?
occur on NON-SUN exposed locations as on proximal limbs or trunk
appear as erythematous, scaly plaque with slightly elevated rolled edges
**never metastasizes
Tumors of "Cellular Immigrants" to the skin?
Histiocytosis X (LC Histiocytosis)
Mycosis Fungoides
characteristic cell of Langerhans Cell Histiocytosis?
LC which on EM has "Birbeck" granules in the cytoplasm
what is Mycosis Fungoides?
subtype of cutaenous peripheral T cell lymphoma that arises in dermis of skin *fatal skin disease that arises in lymphocyts in skin
what are the 2 types of Mycosis fungoides?
Mycosis fungoides: chronic, proliferative occuring over years
Mycosis fungoides d'emblee: more rapid variant
what are the malignant T cells of Mycosis fungoides called?
Sczary cells the result in diffuse erythema and scaling of the entire body surface (Sczary syndrome)-blood born component
in which population does Mycosis Fungoides occur in? where on body?
older ppl greater than 40
peak onset 60
**disease of elderly
twice as common in men
*affects trunk and extremities (NOTHING to do with sun exposed areas)
*slowly progressive but fatal
what are the 3 phases of Mycosis Fungoides?
Chronic Dermatitis
Patch Stage
Plaque Stage
chronic dermatitis stage of Mycosis fungoides?
growing in dermis causing elevation but initially difficult to discern
patch stage of Mycosis fungoides? plaque stage?
Patch: starts to elevate
field effect- spreads to speicific area
Plaque: ulceration
huge increase in T cells
pushing up and down
malignant cells in blood stream (Scarzy cells)
what is a histological marker for Mycosis fungoides?
Epidermaltropism: lymphocytes start to invade the epidermis
what is Mastocytosis? in what pop does it occur?
rare clonal neoplasm that affects predom children
mutliple, oval red brown scaling papules : Urticaria Pigmentosa (pigmented and when rub they itch b/c of histamine)
S&S of Mastocytosis? due to effects of what?
flushing rxn in response to foods or alcohol
Pruritis (itches)
Nosebleeds if heparin part of degran release
**S&S effects of histamine
What are Ichthyosis?
genetic disorders resulting in skin changes characterized by hyperkeratosis giving "fishy" or "fish scale" appearance to skin
AD, AR or X linked
what is the characteristic appearance of Ichthyosis?
fishlike scales bc of hyperkeratosis: see compacted keratin with artifacts, no basketweave
What is Urticaria?
Hives: actue allergic rxn-Medical Emergency
Tx: subcut Epi and injection corticosteroids
think bee sting or penicillin rxn
clinical apearance of Urticaria?
erythematous, edematous, circular plaques covered by normal epidermal surface
**wheal that when scratched itches
what is a characteristic of Urticaria when apply direct pressure?
blanching with direct pressure
look red b/c dilated vssl due to histamine release
What is the charasterstic description of Acute Eczematous Dermatitis?
"Eczema": acute onset of red, papulovesicular (raised with clear area) lesions-boiling over appearance which may ooze or crust
Eczema evolves into what?
raised, scaling plaques that you treat with corticosteroids
Eczema most commonly occurs in what populations?
kids: pediatric age groups
Atopic, idiopathic, and primary all mean what?
we don't know what caused it
Desribe the stages of eczema
at first see infiltration of inflammatory cells. 24-48 hrs see epidermal spongiosis and edema. Epidermis then starts thickening into scale (parakeratosis) and vssls increase
As lesion enters chronic stage see epidermal hyperplasis and hyperkeratosis
Incrse fibrosis over time
there are many different types of eczematous dermatitis such as?
contact dermatitis (laundry detergent ex)
atopic dermatitis
drug related dermatitis (penicillin)
insect bite
where is the edema occuring in eczematous dermatitis cases?
w/n the epidermis eventually resulting in small, fluid-filled inraepidermal vesicles
what is Erythema Multiforme?
skin condition of unknown etiology that usually follows an antecedent infection or drug exposure, malignancy and collagen vascular diseases
what is the severe, systemic febrile form of Erythema Muliforme?
Stevens-Johnson syndrome
what is the characteristic appearance of Erythema Multiforme?
target-like lesions with central blister or zone of epidermal necrosis surrounded by macular erythema
Histologically, what does Erythema muliforme look like?
dilated papillary dermis b/c site of edema
lymphocytes collecting along dermal/epidermal jxn
what are the 3 chronic inflammatory dermatoses?
lichen planus
discoid lupus erythematosus
what isthe most freq clinical association with Psoriasis/
arthritis which may vary from mild to severe and resembles Rheumatoid Arthritis
Wht does Psoriasis look like? where does it occur?
well-demarcated PINK (P for Psoriasis) to salmon plaque
affects elbows, knees, scalp, lumbosacral area, intergluteal cleft and glans penis
chronic lesions that demonstrate erythema surmounted by characteristic silver-white scale is typical of what disease?
Psoriasis: silver b/c increased turnover of keratinocytes
Histologically how does Psoriasis appear?
epidermal hyperplasia seen through accentuated rete pegs
large vssls therefor red
thick contact keratin giving scale appearance
what are the 5 P's of Lichen Planus (to describe it)?
5 P's": well-defined pruritic, planar, purple, polygonal papules
what is Lichen planus?
chronic inflammatory disease that occurs on skin and mucus membranes (oral cavity therefore better known by dentists)
consists of multiple plaques that occur on extremiteis: wrist, elbow
The histological appearance of Lichen Planus?
Hyperparakeratosis with thickening of the granular cell layer
Development of a "saw-tooth" appearance of the rete pegs
Degeneration of the basal cell layer
Infiltration of inflammatory cells into the subepithelial layer of connective tissue
waht is discoid lupus erythematous (DLE)?
presentation of SLE with only skin symptoms and no systemic signs
characteristic of discoid lupus?
butterfly malar erythema across bridge of nose
Discoid lesions: central hypopigmentation surrounded by peripheral hyperpigmentation
microscopic appearance of discoid lupus?
infiltrate of lymphocytes w/n superficial and deep dermis
thinning of epidermis
loss of rete pegs
what is the positive band test in lupus erythematous?
granular deposits of Ig (IgG) and complement at dermal epidermal jxn
what are the 3 blistering (bullous) disease autoimmune types?
bullous pemphigoid
dermatitis herpetiformis
what is a subcorneal blister?
the stratum corneum forms the roof of the bulla
*occurs in impetigo or pemphigus foliaceus
what is a suprabasal blister? associated with what disease?
blister with edema just above basal layer of epidermis
*pempigus vulgaris
what is a subepithelial blister? associated with what disease?
the entire epidermis separates from the dermis
site of friction blister
*most common form of blister
seen in bullous pempighoid
what are Pemphigus diseases?
autoimmune diseases with antibody directed against the desmosomes of the squamous epthelial cells preventing cells from holding tightly together
while there are 4 types of Pemphigus, what is the most common ?
Pemphigus vulgaris (80%) involves mucosa and scalp, face, axilla, groin and other pressure pts; classic bullous disease**
how do you tell the difference b/n blisters of Pemphigus vulgaris and Bullous Pemphigoid?
pemphigus vulgaris are larger >2cm
bullous pemphigoid are smaller than 2cm and more resistant to rupture b/c epidermis still intact
loss of cell-cell adhesion in Pemphigus vulgaris is called what?
what type of blister forms in bullous pempighoid?
friction blister: subepidermal
friction blisters with clear fluid and are generally smaller (<2cm) and more resistant to rupture
who does Bullous Pemphigoid primarilly affect?
older individuals on sites with less involvement of mucosa than pemphigus
cause of Bullous Pemphigoid?
IgG antibodies to skin basement membrane
How does Bullous Pemphigoid appear microscopically?
subepidermal cleft
normal epidermis
lymphocytes and PMNs associated initimately with basal cell layer destruction
a "ribbon candy" linear deposition of complement along the dermoepidermal jxn is characteristic of what disease?
bullous pemphigoid
which skin infxn is majorly associated with Celiac Disease anti-gliadin antibodies?
Dermatitis Herpitiformis: rare disorder that affects more males with onset in 3rd and 4th decades (age 20-30 and 30-40)
the anti-gliadin antibodies of Dermatitis Herpitiformis may cross-react with regions of what?
dermal papillae
where does Dermatitis Herpetiformis occur?
intensely pruritic plaques (itchy) located on extensor surfaces, elbows, knees, upper back and buttocks (contact points)
the abscesses of Dermatitis Herpetiformis are rich in what Ab?
IgA and fibrin deposits
affect dermal papillae
hyperplasia: increase # cells
hypertrophy: increase cell size
atrophy: decrease size and fxn of cells
what happens when cells exceed the ability to adapt?
they undergo cell injury which can be reverisble only up to a certain point. if stimulus persits get irreverisble cell injury causing cell death
are necrosis and apotosis always pathologic/
necrosis ALWAYS pathologic
apoptosis occurs in certain pathologic situations, but mostly in embryo, involution of hormone-responsive tissues upon withdrawal of hormone
how do cells respond to increased damand and external stimulation?
by hyperplasia or hypertrophy
how do cells respond to decreased supply of nutrients and GF?
how do cells respond to chronic irritation?
compare hyperplasia nd hypertrophy in both dividing and non-dividing cells
dividing cells: both hyperplasia and hypertrophy
non-dividing cells: only hypertrophy ex: myocardial
what adaptation takes place if cellular populations are capable of syn DNA, thus permitting mitotic division?
hypertrophy involves cell enlargment w/o cell division
how is hyperplasia physiologic?
hormonal hyperplasia: increase fxnl capacity of tissue (prolif of glandular epi of breast at puberty)
compensatory hyperplasia: increase tissue mass after injury (capacity of liver to regenerate)
mxn of hyperplasia?
increase local production of GF, increase levels GF R's all act to produce TF's and turn on genes
ex of pathological hyperplasia?
excessive hormonal stimulation or GF acting on target cells ex: endometrial hyperplasia
are new cells being made when hypertrophy occurs?
no, only larger cells
increase cell size due to syn of more structural components
physiologic hypertrophy?
increase workload as in bodybuilders
pathologic hypertrophy?
hypertension leads to hemodynamic overload
mxns of hypertrophy?
indxn of #genes which stim TF
turn on contractile proteins of fetal origin
turn on genes that are normally on exprssed during development
why do cells hypertrophy?
when they want to increase mm activity and decrease workload
what type of adaptation is this: decrease in the size of the cell by loss of cell substance?
physiologic atrophy?
early development such as when notocord and thyroglossal duct undergo atrophy
uterus after paturtition
pathologic atrophy?
decrease workload: atrophy of disuse (arm in cast)
loss of innervation
diminshed blood supply
inadquate nutrition: marasmus (use sk m as source of energy and develop cachexia (mm wasting))
loss of endocrine stimulation (loss of estrogen after menopause)
pressure (tissue compression by tumor)
why do cells become smaller as a result of atrophy?
in attempt to survive and maintain homeostasis
although they have dimished in size nd fxn, they are NOT dead
mxns of atrophy?
increase protein degradation via lysosomes eating cellular components and ubiquitin-protease pathway in which proteins to be degraded are tagged w/ ubiquitin
see increase in autophagic vacuoles (contain cell fragments destined for destruction-some persist and aren't degraded leaving behind residual bodies called liphfuschin granules)
waht are lipofuschin granules the result of?
in the case of atrophy, we have autophagic vacuoles that contain fragments of cell components that are destined for destruction. when some persist and are not destroyed they are residual bodies, lipofuschin granules, that in large amts give tissue brown discoloration (brown atrophy)
is metaplasia reverisable?
what is metaplasia?
1 adult cell type replaced by another adut cell type
represents an adaptive substitution of cells that are sensitive to stress by cell types that are better able to withstand the adverse environment
most common form of metaplasia? ex?
columnar to squamous
resp tract of smokers in which normal ciliated columnar cells of trachea and bronchi are replaced with strat squamous
why is metaplasia considered double edged sword?
+: rugged strat squamous can survive under circumstances in which fragile columnar would have failed
-: impt protection mxn of mucus secretion is lost
Barrett esophagus is an example of what type of metaplasia?
squamous to columnar
esophageal squamous replaced by intestinal like columnar cells b/c of refluxed gastric acid
mxn of metaplasia: how does it occur?
it does NOT result from a change in phenotype of different cell type. It is the result of re-programming of stem cells that are known to exist in normal tissues brought about by GF, cytokines that stimulate specific TFs that lead the cascade of phentype switch towards a fully diff cell
agenesis: failure of an organ to develop during normal embryo growth
aplasia: absence of all or part of an organ
atresia: absence of an opening
is atrophy reverisble? metaplasia?
yes both are
incomplete development or underdevelopment of an organ w/ decrease in number of cells
abnormal organization of cells
problem in Chediak-Higashi syndrome?
defect in phagolysosome fxn
defective degranulation
delayed microbial killing
alld due to decrease in transfer of lysosomeal enzymes to phagocytic vacuoles in phagocytes
problem in Hashimoto Thryroiditis?
cuase of hypothyroidism
autoimmune destrxn of thyroid gland
*progressive depletion of thyroid epi cells which are replaced by mononuclear cell infiltration and fibrosis