Pa Exam I

Front 1

what kind of result do tests have?

Back 1

quantitative result

Front 2

what is the most impt thing to know about any patient?

Back 2

history

Front 3

what is the purpose of screening test?

Back 3

looking for something w/o any predetermination (ex: Health fair screenings)

Front 4

Typically what is the purpose of the first test? second test?

Back 4

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

Front 5

What are the 4 tests?

Back 5

1. screening: no hypothesis
2. case finding
3. confirming test
4. monitering test (when you know they have disease and want to monitor it)

Front 6

what are some examples of physical exams used as a test?

Back 6

score reflexes
BP- yes or no (binary)
pulse (quantitative)

Front 7

which tests tend to be the best test?

Back 7

physiologic tests

Front 8

which tests are high specificity?

Back 8

anatomic pathology b/c they confirm diagnosis, very definitive via biopsies

Front 9

in general, what does analytical characteristics of medical tests mean?

Back 9

what actually happens to get a valid test: Doing the test (if you dont do EKG right, you won't get valid result)

Front 10

What is the reference range?

Back 10

anything that falls outside of normal range is abnormal (disease) however, some can be outside of range and are NOT abnormal

Front 11

what is the reference range dependent on

Back 11

geographic location, instrument, age, lab

Front 12

what is always specific for each laboratory and each test?

Back 12

reference range

Front 13

what type of curve is assumed for reference range?

Back 13

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

Front 14

what is multiphasic testing?

Back 14

detect common diseases before becoming clinical manifest

Front 15

what happens with the more tests that you perform?

Back 15

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

Front 16

what are the 3 sources of error that are analytical characteristics?

Back 16

pre-analytical
analytical
post-analytical

Front 17

what are some factort to be aware of that could result in preanalytical errors?

Back 17

specimen requirements (testing correct specimen)
patient factors (time of day, standing or supine, tourniquet time)
amt. of specimen
biological variability

Front 18

when does biological variability matter in the case of pre-anayltical errors?

Back 18

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

Front 19

what percent of lab error is preanalytical?

Back 19

99% therefore it is better to get no result than a bad result

Front 20

in terms of analytical errors, what is the problem?

Back 20

labs are very PRECISE, but not always accurate thefore they need something w/ absolute accuracy/truth to measure against
ex: cholesterol

Front 21

what are we aiming for during the measurment?

Back 21

excellent precision, excellent accuracy, but usually get excelling precision, low accuracy

Front 22

how can post-analytical errors occur?

Back 22

-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 result..do not do this unless it fits w/ what you are thinking ex: to diagnose hypercholesteremia need 2 consecutive measurments in 2 wk period

Front 23

what are the 5 fxns of skin? Primary fxn?

Back 23

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

Front 24

where are apocrine secretions generally?

Back 24

axillary and groin regions (proteinaceous therefore good mileu for bacteria)

Front 25

skin differences results from differences in what?

Back 25

four basic layers
distribution of adnexal structures

Front 26

what are the 4 basic layers of skin?

Back 26

epidermis
papillary dermis
reticular dermis
subcutaneous tissue (hypodermis)

Front 27

what are the 3 major adnexal structures?

Back 27

1. pilar (hair) units w/ pilosebaceous unites, arrector pili mm
2. eccrine units (eccrine gland and ducts)
3. apocrine units (apocrine glands and ducts)

Front 28

what cells are found in the epidermis? explain proli

Back 28

keratinocytes that proliferate at the basal layer. each makes 2 cells; 1 descends upward while the other fills with keratin very rapidly

Front 29

what is the site of edema?

Back 29

papillary dermis b/c it is expansile

Front 30

compare the collagen fibers in papillary dermis vs. reticular

Back 30

papillary: very fine collagen fibers
reticular: rigid fibers

Front 31

what happens to keratinocyts as they move up in epidermis?

Back 31

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

Front 32

what are the 5 layers of the epidermis?

Back 32

stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale

Corn Lover's Grow Several Bales

Front 33

what is the horny layer?

Back 33

the stratum corneum: outermost layer of epidermis composed of dead cells that lack nuclei "basket weave apperance"

Front 34

explain the appearence of stratum granulosum

Back 34

compact kertain layers of cells with keratohyalin granules underneath the glue keratin fibers together

Front 35

besides keratin, what else do keratinocytes contain?

Back 35

melanin from melanocytes for protection

Front 36

where do you find melanocytes? what does it look like?

Back 36

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

Front 37

what acts as a "glue" w/n the stratum granulosum?

Back 37

keratin hyalin granules

Front 38

what are recognized as spinous processes?

Back 38

desmosomes (intercellular bridges) that hold squamous keratinocytes together

Front 39

what do melanocytes make?

Back 39

melanosomes that catalyze dopa to melanin *fxn of melanin: inert polymer that absorbs UV radiation

Front 40

difference in skin color b/n individuals is due to what?

Back 40

level of melanocyte activity
tan= increase melanin to protect from UV

Front 41

what cells are present in stratum basale? How many layers?

Back 41

melanocytes and Merkel cells
single layer of columnar or cuboidal keratinocyte stem cells, which are mitotically active

Front 42

how is melanin transferred?

Back 42

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.

Front 43

where will you see more melanin?

Back 43

near stratum basale b/c ratio of melanin:keratin is high

Front 44

job of Merkel cell?

Back 44

fxn unknown
found in stratum basale
precursor for Merkel cell carcinoma

Front 45

job of langerhans cell? whre located?

Back 45

antigen recognition cell
dendritic
upper spinous layer

Front 46

interrelatinships b/n epidermis and dermis?

Back 46

epidermis influences the dermis and vice versa

Front 47

which layer of dermis is most impt?

Back 47

papillary dermis

Front 48

where isthe superficial vascular plexus located?

Back 48

papillary dermis *very expansile

Front 49

what are rete pegs

Back 49

invag of epi into dermis
act as track shoes for stabilization

Front 50

what are dermal papillae?

Back 50

highly vascular
extensions of the dermis into epidermis
*cause you to blush
*not as deep in older ppl

Front 51

fxn of Meissner's corpuscle?

Back 51

a specialized structured nerve ending
-touch receptor

Front 52

where do you find meisnner's corpuscles w/n skin? on body?

Back 52

dermal papillae
most numerous on hands and feet

Front 53

fxn of reticular dermis?

Back 53

serves as cushion and stable platform for the epidermis and papillary dermis

Front 54

where are adnexal structures located?

Back 54

reticular dermis

Front 55

where is reticular dermis thickest?

Back 55

in areas subject to pressure such as back, butt
-not on fingertips b/c you need flexibility

Front 56

which dermis layer is movable/stretchable ?

Back 56

papillary dermis

Front 57

where are pacinian corpuscles located?

Back 57

deep reticular dermis or hypodermis

Front 58

fxn of pacinian corpuscle?

Back 58

encapsulated nerve ending to detect pain and temp
pressure R

Front 59

what does subcutaneous tissue contain?

Back 59

loose and dense CT consiting of adipocytes and fibroconnective tissue

Front 60

what does subuctaneous tissue connect?

Back 60

reticular dermis with fascia of underlying tissue (muscle, bone, tendon)

Front 61

is subcutaneous tissue vascularized?

Back 61

yes, with deep vascular plexus

Front 62

fxn of subcutaneous tissue?

Back 62

body temp regulation
depot for fat storage (large energy reserve)

Front 63

which layer of skin is aging most evident?

Back 63

subcutaneous tissue; with aging there is a progressive loss of subcutaneous tissue particularly in extremities (hands and feet)

Front 64

location of adnexa?

Back 64

reticular dermis and exit via epidermal surface

Front 65

why do you lose hair after chemo treatment?

Back 65

b/c the agent kills rapidly dividing cells such as those involved in hair growth (epithelial cells and melanocytes)

Front 66

what is attached to the hair follicle?

Back 66

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

Front 67

what are eccrine glands?

Back 67

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

Front 68

where are eccrine sweat glands located?

Back 68

mid-to lower reticular dermis

Front 69

what are apocrine glands? where located?

Back 69

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)

Front 70

what are the 9 primary lesions?

Back 70

1. macule
2. patch
3. papule
4. nodule
5. plaque
6. wheal
7. vesicle
8. bulla
9. pustule

Front 71

what is a macule?

Back 71

flat area of color change less than 1 cm in diameter (freckle)

Front 72

what is a patch?

Back 72

larger flat (non-palpable) lesion greater than 1 cm (cafe au lait spots)

Front 73

what is a papule?

Back 73

discrete solid RAISED lesion less than 1 cm in diameter (nevus)

Front 74

what is a nodule?

Back 74

larger discrete, rounded, RAISED solid lesion (rheumatoid nodule)

Front 75

what is a plaque?

Back 75

raised, flat topped lesion greater than 1 cm in diameter (think mesa with flat top)

Front 76

what is wheal?

Back 76

transient edematous erythematou plaque (hive or mosquito bite) itchy

Front 77

what is a vesicle?

Back 77

fluid filled lesion with clear top less than 0.5cm in diameter (herpes simplex infxn)

Front 78

what is a bulla?

Back 78

larger fluid filled lesion in papillary dermis that raises epidermis (friction blister)

Front 79

what is a pustule?

Back 79

vesicle like lesion filled with purulent exudate (folliculitis or acne)

Front 80

what are the 8 secondary lesion?

Back 80

1. erosion
2. ulcer
3. fissure
4. scale
5. crust
6. lichenification
7. atrophy
8. verrucous

Front 81

what are secondary lesions related to?

Back 81

secondary factors such as rubbing, scratching, superimposed infxn or tissue loss

Front 82

what is an erosion?

Back 82

2nday lesion
partial or complete loss of the epidermis

Front 83

what is an ulcer?

Back 83

loss of epidermis and part of dermis (goes through the epidermis)
2ndary lesion

Front 84

what is a fissure?

Back 84

thin, linear erosion or ulceration (cracked lips)

Front 85

what is a scale?

Back 85

2nday lesion
hyperkeratosis (dry skin)-almost always the result of rubbing

Front 86

what is crust?

Back 86

2nday lesion
dried serous and serosanguinous exudate (impetigo: crust with infxn at surface)

Front 87

what is lichenification?

Back 87

2ndary lesion
accentuation skin markings with thickening of the skin
subject to a lot of friction

Front 88

what is atrophy?

Back 88

2dary lesion
decrease in amt of epidermis, dermis or subcutaneous tissue

Front 89

waht is verrucous?

Back 89

2ndary lesion
wart like surface

Front 90

what changes occur in skin with aging?

Back 90

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

Front 91

what type of damage is due to sun? whre most vulnerable?

Back 91

actinic damage with fine wrinkling and white spots most commonly on forehead, face, dorsum of hands

Front 92

what is lentigo senilis or solar lentigo?

Back 92

benign, discrete hyperpigmented macule occuring on chronicaly exposed skin in adults especially on the back of the hands and forehead

Front 93

what is the cause of Lentigo Senilis?

Back 93

increased melanin pigment only in keratinocytes-there is NO increase in # of melanocytes

Front 94

is there an increase in melanocytes in Lengtigo Senilis?

Back 94

no, ony due to increased syn of melanin even though the term lentigo means a prolif of melanocytes

Front 95

what are some common names for Solar Lentigo?

Back 95

age spot
liver spots

Front 96

are the areas of hyperpigmentation seen in solar lentigo macular or papular?

Back 96

always macular

Front 97

do African Americans have more melanocytes?

Back 97

no, more effective at production of melanosomes but same amt of melanocytes

Front 98

vitigo is due to what?

Back 98

disorder of de-pigmentation in which there is a depletion of melanocytes due to sloughing or congenital absence of melanocytes (albinism)

Front 99

def of melasma?

Back 99

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

Front 100

are melasma due to an increase in melanocytes?

Back 100

no! hypermelanosis: increased production of melanin by estrogen or progesterone

Front 101

other names for melasma?

Back 101

chloasma or mask of pregnancy

Front 102

in which population do you see most melasma?

Back 102

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)

Front 103

cause of freckles?

Back 103

increaed production of melanin in focal area (ppl with freckles will get darker freckles in sun)

Front 104

what is acanthosis nigricans? where is is generally?

Back 104

hyperpigmentation in flexural regions (axillae, skin folds of neck, groin, and anogenital regions)

Front 105

what percent of Acanthosis nigricans benign? malignant?

Back 105

benign 80%
malig 20%

Front 106

benign Acanthosis Nigricans mainly occurs in? inheritance? associated with?

Back 106

during childhood or during puberty
AD
associtatd with obesity or endocrine abnormalities

Front 107

malignant Acanthosis Nigricans mainly occurs in what pop? associated with?

Back 107

arises in middle aged and older individuals
-occurs in association with underlying adenocarcinoma

Front 108

describe the evolution and localization of a tatoo

Back 108

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

Front 109

where do Nevocelluar Nevi occur? in what population?

Back 109

face and neck
childran and young adults (at 30-40 they go away)

Front 110

3 types of Nevi

Back 110

jxnl
compound
intradermal

Front 111

appearance of jxnl nevi on skin

Back 111

macular
called beauty spot or mole

Front 112

where is jxnl nevus located?

Back 112

as a proliferation of melanocytes at dermal/epidermal jxn. as they migrate into dermis they are called nevus cells

Front 113

appearance of compound nevus on skin?

Back 113

more raised and dome shaped
red b/c they stimulate their own blood supply
located in papillary dermis therefore raised

Front 114

appearance of intradermal Nevus on skin?

Back 114

older
no prolif at dermal/epi jxn
everything migrataed into dermis
brown, not red b/c not recruiting blood supply

Front 115

are Nevi associated with incresaed risk of melanoma?

Back 115

no, 80-90% of melanomas arise de novo and are not associated with benign neoplasmas

Front 116

how do you biopsy a nevus?

Back 116

shaved biopsy: parallel to skin surface

Front 117

which form of nevi are associated with increased risk of melanoma?

Back 117

congenital nevus: very large found in deep dermal. present at birth

Front 118

def of malignant melanoma. where occur?

Back 118

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

Front 119

in which pop do malignant melanoms primarily occur? how do they originate

Back 119

adults
originate de novo as an isolated lesion (80-90%) or adjacent to a melanocytic nevus

Front 120

what is Melanoma in situ?

Back 120

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).

Front 121

compare the distribution of malignant melanoma is males vs females

Back 121

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

Front 122

in which population are malignant melanomas greatest?

Back 122

white male then white females bc decreased pigmentation

Front 123

what is prevalence?

Back 123

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.

Front 124

what is incidence? incidence rate?

Back 124

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.

Front 125

what is typically the age of onset of malignant melanoma?

Back 125

see it increase with age and peak in older ppl (see at 20yrs then progressivly increse)
*disease of older ppl

Front 126

what are the 4 criteria for Malignant Melanoma?

Back 126

1. asymmetrical
2. irregular, vague borders
3. maculopapular "chaos"
4. variation in pigment hues/colors

Front 127

how do you biopsy melanomas?

Back 127

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)

Front 128

where would you find a melanoma in a biopsy?

Back 128

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

Front 129

what is the Pagetoid spread "Buckshot Pattern"?

Back 129

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.

Front 130

what type of spread to you see in melanoma?

Back 130

hemoatogenous spread therfore will kll you

Front 131

Melanoma survival is dependnet on what?

Back 131

stage: melanoma metastatic to any lymph node represents advanced disease (stage III)

Front 132

what is the percent of 5year surival with Stage I melanoma? 10year survival?

Back 132

98% : 5
95%: 10

Front 133

waht is the percent of 5year survival with Stage IV melanoma? 10year?

Back 133

15% : 5
5% :10

Front 134

how does the Breslow level determine Melanoma Mortality?

Back 134

a Breslow level b/n 0.76 mm and 1.00 mm is associated with an 80% 5 yr survival
*less thickness=more survival

Front 135

Fibroepithelial Polyps (FEP) are also known as (4 names)

Back 135

skin tags
acrochrodon
fibroma molle
squamous papilloma

Front 136

where do fibroepithelial polyps occur? associated with?

Back 136

on neck and groin in older individuals
associated with areas of rubbing by clothing

Front 137

what is typical of the core of fibroepithelial polyps (FEP)?

Back 137

fibrovascular core thefore if cut them at the base they will bleed

Front 138

Epithelial Inclusion Cysts (EIC) occur where? caused by what? filled with?

Back 138

occur around face and upper trunk *extremely common
caused by obstruction of hair follicle
filled w/ keratinous debris and sebum

Front 139

what happens in EICs are ruptured?

Back 139

provoke a chronic inflammatory rxn and even granuloma to the keratin

Front 140

all EICs have what?

Back 140

have epithelium lining which grows and lining becomes progressively attenuated

Front 141

color of hemangiomas? xanthomas?

Back 141

hemangiomas: red
xanthomas: yellow

Front 142

in which pop do you see hemangiomas mostly?

Back 142

children

Front 143

what are hemanogiomas? capillary?

Back 143

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

Front 144

where are benign fibrous Histiocytomas (Dermatofibroma) normally seen? what pop?

Back 144

benign soft tissue neoplasm
seen in adults
on legs of young-middle aged adults

Front 145

what do Benign Fibrous Histiocytomas (dermatofibroma) look like?

Back 145

tan brown papules which are usually small and may be tender

Front 146

more common name for Benign Fibrous Histiocytomas?

Back 146

dermatofibroma

Front 147

are Dermatofibromas true neoplasmas?

Back 147

no, but an exaggerated fibroblastic response to trauma

Front 148

what is Dermatofibrosarcoma protuberans (DFSP) ?

Back 148

rare malignant superficial variant of Dermatofibroma that is locally aggressive, but rarely metastasizes

Front 149

how can you tell if a dermatofibroma is young?

Back 149

red= recruiting vssls to support growing tissues

Front 150

describe the histological features of dermoatofibromas

Back 150

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

Front 151

most benign fibrous histiocytomas occur how?

Back 151

Some physicians and researchers believe dermatofibromas form as a reaction to previous injuries such as insect bites or thorn pricks *often occur after trauma

Front 152

Seborrheic Keratosis is what?common in what pop?

Back 152

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)

Front 153

appearance of Seborrheic Keratosis?

Back 153

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

Front 154

where on body are Seborrheic Keratosis normally found?

Back 154

trunk, proximal extremities, face and neck (not in sun exposed areas)
if pull/scratch called irritated seborrheic keratosis

Front 155

how can you tell that Seborrheic Keratosis is not melanoma?

Back 155

b/c has sharp borders and reasonably symmetrical

Front 156

adnexal tumors begin where?

Back 156

in adnexa: gland, hair follicle, ducts

Front 157

what do adnexal tumors look like? where most likely found?

Back 157

shiny, firm
run in families
multiple cylindromas
see in face and hair bearing areas b/c occur in adnexa

Front 158

why are adnexal tumors called cylindroma?

Back 158

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)

Front 159

multiple trichoepitheliomas are found where?

Back 159

hair bearing areas (adnexa) b/c tricho = hair

Front 160

what percent of adnexal tumors are benign?

Back 160

99%

Front 161

characteristics of benign adnexal tumors vs malignant

Back 161

benign: symmetrical, small, superficial, vertical in orientation (bc grow along plane of adnexal structure)
malignant: asymmetrical, large, deep, wide

Front 162

what is the most common malignant adnexal tumor?

Back 162

sebaceous carcinoma

Front 163

is actinic keratosis a pre-malignant condition?

Back 163

yes, presents on sun exposed areas

Front 164

why do actinic keratosis appear white and flaky?

Back 164

bc of keratin generation

Front 165

what conditions place an individual at risk for actinic keratosis?

Back 165

fair complex (less melanin protection)
old scars
organ trasplant (immunocompromised)
albinism
XP

Front 166

how will actinic keratosis appear histologically?

Back 166

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

Front 167

what is solar elastosis? where do you see it?

Back 167

solar elastosis is the actinic degeneration of the dermal collagen that is irreversible
*see in Actinic Keratosis

Front 168

where and what population does actinic keratosis occur?

Back 168

on sun exposed areas of the body (face, forehead, neck, dorsum of hands) in middle aged (45-64) and elderly individuals

Front 169

how does actinic keratosis look?

Back 169

erythematous (b/c rapidly gowing cells tend to recruit blood suppply)
reddish brown MACULES or minimally elevated PAPULES with SCALES due to increased keratin

Front 170

how is Actinic Keratosis different thant Bowen Disease?

Back 170

bown disesae = SCC in situ
Actinic Keratosis is incompletely developed or nascent SCC

Front 171

how can you diff Seborrheic Keratosis from Actinic Keratosis?

Back 171

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

Front 172

difference b/n solar lentigo and actinic keratosis?

Back 172

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!

Front 173

Order of progresson from Actinic Keratosis?

Back 173

Actinic Keratosis
SCC
invasion SCC

Front 174

what is SCC?

Back 174

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)

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what are some other causes of SCC (synergistic with sunlight)?

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Human papillomavirus
Arsenic*
extensive X-ray exposure
Genetic syndromems: XP

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incidence of SCC increases with what?

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age! male predominance

*organ transplant recipients are prone to SCC bc immunosuppressed
*2nd most common cutaneos malignancy

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what does early invasive SCC look like?

What do older SCC look like?

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early: small, firm, skin-colored may be granular and bleed easy
Older: larger, invasive an rarely involve the underlying soft tissue. center is ulcerated

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why do you see ulcerated centers in late SCC?

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b/c rapidly growing cells
all around periphery are blood vssls
**reddish tan b/c of blood vssls

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what is characteristic histologically of SCC?

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invasive: epithelium infiltration into dermis..passes BM into dermis (pushing down therefore see ulcer)

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is SCC lethal?

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not very, equivalent to 1 death in 2500 individuals each with 40 years of sun exposure

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when you think Keratocanthoma, think what?

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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

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what is Keratocanthoma?

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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)

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histologically, SCC is now termed what?

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SCC, keratoacanthoma type

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is BCC malignant?

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yes but it seldom metastasizes but has the potential for local invasion and destruction (should be called Basal Cell Epithelioma)

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what makes you prone to BCC?

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incresaed sunlight exposure in childhood and adolescence and chronic exposure during childhood

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what is the most common cutaneous neoplasm?

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BCC/epithelioma
*98% occur after age 40
same freq in males and females
after age 50, 1% of pop develops BCC each year

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major clinical characterisitcs of BCC?

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95% occur after age 40
85% occur on head/neck
rest on trunk/limbs
**predilection for hair-bearing skin on sun exposed areas

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the clinical appearance of what cancer is related to major histiologic type? what are the types?

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BCC
Nodular
Scerlosing or morpheaform
Pigmented BCC
Superficial BCC

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clinical appearance of Nodular BCC?

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dome shaped papule
*telangiectasia
flesh-colored
crusty
*shiny and sticking up
**on histo: clefts seperate nests of basaloid cells w/n dermis

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clinical appearance of Sclerosing or morpheaform BCC?

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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

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what are pigmented BCC often confused with?

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malignant melanoma b/c of dark irregular pigmentation

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where do superficial BCC occur? what do they look like?

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occur on NON-SUN exposed locations as on proximal limbs or trunk
appear as erythematous, scaly plaque with slightly elevated rolled edges
**never metastasizes

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Tumors of "Cellular Immigrants" to the skin?

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Histiocytosis X (LC Histiocytosis)
Mycosis Fungoides
Mastocytosis

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characteristic cell of Langerhans Cell Histiocytosis?

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LC which on EM has "Birbeck" granules in the cytoplasm

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what is Mycosis Fungoides?

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subtype of cutaenous peripheral T cell lymphoma that arises in dermis of skin *fatal skin disease that arises in lymphocyts in skin

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what are the 2 types of Mycosis fungoides?

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Mycosis fungoides: chronic, proliferative occuring over years
Mycosis fungoides d'emblee: more rapid variant

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what are the malignant T cells of Mycosis fungoides called?

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Sczary cells the result in diffuse erythema and scaling of the entire body surface (Sczary syndrome)-blood born component

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in which population does Mycosis Fungoides occur in? where on body?

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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

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what are the 3 phases of Mycosis Fungoides?

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Chronic Dermatitis
Patch Stage
Plaque Stage

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chronic dermatitis stage of Mycosis fungoides?

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growing in dermis causing elevation but initially difficult to discern

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patch stage of Mycosis fungoides? plaque stage?

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Patch: starts to elevate
red
field effect- spreads to speicific area
Plaque: ulceration
huge increase in T cells
pushing up and down
malignant cells in blood stream (Scarzy cells)

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what is a histological marker for Mycosis fungoides?

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Epidermaltropism: lymphocytes start to invade the epidermis

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what is Mastocytosis? in what pop does it occur?

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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)

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S&S of Mastocytosis? due to effects of what?

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flushing rxn in response to foods or alcohol
Pruritis (itches)
Nosebleeds if heparin part of degran release
**S&S effects of histamine

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What are Ichthyosis?

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genetic disorders resulting in skin changes characterized by hyperkeratosis giving "fishy" or "fish scale" appearance to skin
AD, AR or X linked

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what is the characteristic appearance of Ichthyosis?

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fishlike scales bc of hyperkeratosis: see compacted keratin with artifacts, no basketweave

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What is Urticaria?

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Hives: actue allergic rxn-Medical Emergency
Tx: subcut Epi and injection corticosteroids
think bee sting or penicillin rxn

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clinical apearance of Urticaria?

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erythematous, edematous, circular plaques covered by normal epidermal surface
**wheal that when scratched itches

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what is a characteristic of Urticaria when apply direct pressure?

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blanching with direct pressure
look red b/c dilated vssl due to histamine release

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What is the charasterstic description of Acute Eczematous Dermatitis?

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"Eczema": acute onset of red, papulovesicular (raised with clear area) lesions-boiling over appearance which may ooze or crust

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Eczema evolves into what?

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raised, scaling plaques that you treat with corticosteroids

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Eczema most commonly occurs in what populations?

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kids: pediatric age groups

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Atopic, idiopathic, and primary all mean what?

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we don't know what caused it

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Desribe the stages of eczema

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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

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there are many different types of eczematous dermatitis such as?

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contact dermatitis (laundry detergent ex)
atopic dermatitis
drug related dermatitis (penicillin)
insect bite

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where is the edema occuring in eczematous dermatitis cases?

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w/n the epidermis eventually resulting in small, fluid-filled inraepidermal vesicles

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what is Erythema Multiforme?

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skin condition of unknown etiology that usually follows an antecedent infection or drug exposure, malignancy and collagen vascular diseases

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what is the severe, systemic febrile form of Erythema Muliforme?

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Stevens-Johnson syndrome

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what is the characteristic appearance of Erythema Multiforme?

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target-like lesions with central blister or zone of epidermal necrosis surrounded by macular erythema

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Histologically, what does Erythema muliforme look like?

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dilated papillary dermis b/c site of edema
lymphocytes collecting along dermal/epidermal jxn

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what are the 3 chronic inflammatory dermatoses?

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psoriasis
lichen planus
discoid lupus erythematosus

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what isthe most freq clinical association with Psoriasis/

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arthritis which may vary from mild to severe and resembles Rheumatoid Arthritis

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Wht does Psoriasis look like? where does it occur?

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well-demarcated PINK (P for Psoriasis) to salmon plaque
affects elbows, knees, scalp, lumbosacral area, intergluteal cleft and glans penis

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chronic lesions that demonstrate erythema surmounted by characteristic silver-white scale is typical of what disease?

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Psoriasis: silver b/c increased turnover of keratinocytes

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Histologically how does Psoriasis appear?

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epidermal hyperplasia seen through accentuated rete pegs
large vssls therefor red
thick contact keratin giving scale appearance

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what are the 5 P's of Lichen Planus (to describe it)?

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5 P's": well-defined pruritic, planar, purple, polygonal papules

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what is Lichen planus?

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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

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The histological appearance of Lichen Planus?

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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

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waht is discoid lupus erythematous (DLE)?

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presentation of SLE with only skin symptoms and no systemic signs

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characteristic of discoid lupus?

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butterfly malar erythema across bridge of nose
Discoid lesions: central hypopigmentation surrounded by peripheral hyperpigmentation

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microscopic appearance of discoid lupus?

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infiltrate of lymphocytes w/n superficial and deep dermis
thinning of epidermis
loss of rete pegs
hyperkeratosisw

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what is the positive band test in lupus erythematous?

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granular deposits of Ig (IgG) and complement at dermal epidermal jxn

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what are the 3 blistering (bullous) disease autoimmune types?

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pemphigus
bullous pemphigoid
dermatitis herpetiformis

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what is a subcorneal blister?

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the stratum corneum forms the roof of the bulla
*occurs in impetigo or pemphigus foliaceus

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what is a suprabasal blister? associated with what disease?

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blister with edema just above basal layer of epidermis
blister=space
*pempigus vulgaris

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what is a subepithelial blister? associated with what disease?

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the entire epidermis separates from the dermis
site of friction blister
*most common form of blister
seen in bullous pempighoid

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what are Pemphigus diseases?

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autoimmune diseases with antibody directed against the desmosomes of the squamous epthelial cells preventing cells from holding tightly together

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while there are 4 types of Pemphigus, what is the most common ?

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Pemphigus vulgaris (80%) involves mucosa and scalp, face, axilla, groin and other pressure pts; classic bullous disease**

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how do you tell the difference b/n blisters of Pemphigus vulgaris and Bullous Pemphigoid?

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pemphigus vulgaris are larger >2cm
bullous pemphigoid are smaller than 2cm and more resistant to rupture b/c epidermis still intact

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loss of cell-cell adhesion in Pemphigus vulgaris is called what?

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acantholysis

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what type of blister forms in bullous pempighoid?

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friction blister: subepidermal
friction blisters with clear fluid and are generally smaller (<2cm) and more resistant to rupture

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who does Bullous Pemphigoid primarilly affect?

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older individuals on sites with less involvement of mucosa than pemphigus

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cause of Bullous Pemphigoid?

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IgG antibodies to skin basement membrane

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How does Bullous Pemphigoid appear microscopically?

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subepidermal cleft
normal epidermis
lymphocytes and PMNs associated initimately with basal cell layer destruction

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a "ribbon candy" linear deposition of complement along the dermoepidermal jxn is characteristic of what disease?

Back 245

bullous pemphigoid

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which skin infxn is majorly associated with Celiac Disease anti-gliadin antibodies?

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Dermatitis Herpitiformis: rare disorder that affects more males with onset in 3rd and 4th decades (age 20-30 and 30-40)

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the anti-gliadin antibodies of Dermatitis Herpitiformis may cross-react with regions of what?

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dermal papillae

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where does Dermatitis Herpetiformis occur?

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intensely pruritic plaques (itchy) located on extensor surfaces, elbows, knees, upper back and buttocks (contact points)

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the abscesses of Dermatitis Herpetiformis are rich in what Ab?

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IgA and fibrin deposits
affect dermal papillae

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hyperplasia?
hypertrophy?
atrophy?

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hyperplasia: increase # cells
hypertrophy: increase cell size
atrophy: decrease size and fxn of cells

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what happens when cells exceed the ability to adapt?

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they undergo cell injury which can be reverisble only up to a certain point. if stimulus persits get irreverisble cell injury causing cell death

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are necrosis and apotosis always pathologic/

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necrosis ALWAYS pathologic
apoptosis occurs in certain pathologic situations, but mostly in embryo, involution of hormone-responsive tissues upon withdrawal of hormone

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how do cells respond to increased damand and external stimulation?

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by hyperplasia or hypertrophy

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how do cells respond to decreased supply of nutrients and GF?

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atrophy

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how do cells respond to chronic irritation?

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metaplasia

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compare hyperplasia nd hypertrophy in both dividing and non-dividing cells

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dividing cells: both hyperplasia and hypertrophy
non-dividing cells: only hypertrophy ex: myocardial

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what adaptation takes place if cellular populations are capable of syn DNA, thus permitting mitotic division?

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hyperplasia
hypertrophy involves cell enlargment w/o cell division

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how is hyperplasia physiologic?

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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)

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mxn of hyperplasia?

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increase local production of GF, increase levels GF R's all act to produce TF's and turn on genes

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ex of pathological hyperplasia?

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excessive hormonal stimulation or GF acting on target cells ex: endometrial hyperplasia

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are new cells being made when hypertrophy occurs?

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no, only larger cells
increase cell size due to syn of more structural components

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physiologic hypertrophy?

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increase workload as in bodybuilders

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pathologic hypertrophy?

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hypertension leads to hemodynamic overload

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mxns of hypertrophy?

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indxn of #genes which stim TF
turn on contractile proteins of fetal origin
turn on genes that are normally on exprssed during development

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why do cells hypertrophy?

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when they want to increase mm activity and decrease workload

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what type of adaptation is this: decrease in the size of the cell by loss of cell substance?

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atrophy

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physiologic atrophy?

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early development such as when notocord and thyroglossal duct undergo atrophy
uterus after paturtition

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pathologic atrophy?

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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)
aging
pressure (tissue compression by tumor)

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why do cells become smaller as a result of atrophy?

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in attempt to survive and maintain homeostasis
although they have dimished in size nd fxn, they are NOT dead

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mxns of atrophy?

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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)

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waht are lipofuschin granules the result of?

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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)

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is metaplasia reverisable?

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yes!

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what is metaplasia?

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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

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most common form of metaplasia? ex?

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columnar to squamous
resp tract of smokers in which normal ciliated columnar cells of trachea and bronchi are replaced with strat squamous

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why is metaplasia considered double edged sword?

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+: rugged strat squamous can survive under circumstances in which fragile columnar would have failed
-: impt protection mxn of mucus secretion is lost

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Barrett esophagus is an example of what type of metaplasia?

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squamous to columnar
esophageal squamous replaced by intestinal like columnar cells b/c of refluxed gastric acid

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mxn of metaplasia: how does it occur?

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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

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agenesis?
aplasia?
atresia?

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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

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is atrophy reverisble? metaplasia?

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yes both are

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hypoplasia?

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incomplete development or underdevelopment of an organ w/ decrease in number of cells

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dysplasia?

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abnormal organization of cells

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problem in Chediak-Higashi syndrome?

Back 282

defect in phagolysosome fxn
neutropenia
defective degranulation
delayed microbial killing
alld due to decrease in transfer of lysosomeal enzymes to phagocytic vacuoles in phagocytes

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problem in Hashimoto Thryroiditis?

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cuase of hypothyroidism
autoimmune destrxn of thyroid gland
*progressive depletion of thyroid epi cells which are replaced by mononuclear cell infiltration and fibrosis