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Patho- skin > Patho- Skin > Flashcards

Patho- Skin Flashcards

1
Q

macule

A

small (<10mm)
brown, tan
circumscribed/flat

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2
Q

patch

A

large macule

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3
Q

papule

A

small (<10mm)
varying shapes (flat top/dome)
not fluid filled

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4
Q

nodule

A

large papule

dome/round

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5
Q

plaque

A

large papule

flat top

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6
Q

blister

A

fluid filled (either vesicle or bulla)

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7
Q

vesicle

A

small, fluid filled

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8
Q

bulla

A

large, fluid filled

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9
Q

pustule

A

pus filled vesicle (raised lesion)
pus –> PMN, dead cells, bacteria
can lyse and get huge

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10
Q

wheal

A

transient (rapid, within minutes)
elevated: d/t edema
erythema
blanching

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11
Q

scales

A 
tiny elevations (horn like) 
d/t excessive cornification
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12
Q

lichenification

A

thickened skin d/t rubbing (prominent skin markings)

usually no problem

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13
Q

excoriation

A

linear lesion

bad b/c break epidermis (skin is not sterile), b/c holds out bacteria

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14
Q

hyperkeratosis

A

abnormal thinking of S. corneum

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15
Q

keratin

A

structural protein
retards water loss
problem with burn patients

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16
Q

parakeratosis

A

abnormal retention of nuclei in S. corneum

normal in mucous membranes

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17
Q

hypergranulosis

A

abnormal growth of S. granulosum
load up on keratin at expense of other organelles
d/t rubbing: irritation–>phys contact of cells–>stimulates mechano receptors–>mitosis

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18
Q

aconthosis

A

diffuse epidermal hyperplasia

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19
Q

papillomatosis

A

enlargement or hyperplasia of dermal papilla

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20
Q

dyskeratosis

A

accumulation of granulation too deep in the skin
(norm= S. granulosum, not S. spinosum)
similar to MD, looks normal but doesn’t function well

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21
Q

spongiosus

A

intercellular edema of the epidermis

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22
Q

ballooning

A

intracellular edema of keratinocyte (skin cell)

osmotic pressure problem

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23
Q

exocytosis

A

blood cells in the epidermis (any blood cell)
aka infiltration of inflammatory cells
don’t want because epidermis= dead

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24
Q

erosion

A

partial loss of epidermis
usu d/t trauma
not problematic

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25
Q

ulceration

A

complete loss of epidermis

reveal dermis/SQ

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26
Q

vaculoization

A

formation of large vacuoles within or outside of cells

normal in plants

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27
Q

lentiginous growth

A

linear pattern of melanocyte proliferation within the epidermal basal cell layer
may be problem- Dx. melanoma

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28
Q

vitiligo

appearance, location, symptoms, cause, diagnosis

A

appearance: smooth, white on skin
location: cm on feet/hands
symptoms: asymptomatic, only cosmetic
cause: autoimmune/ neurohormonal (but hormones= usu systemic) nn –>detrimental to melanocytes
Dx. verify loss of melanocytes/w immunoassay

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29
Q

difference between abino and vitiligo

A

abino= systemic & melanocytes present, but not functioning well

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30
Q

freckles

ocurrence, location, color, patho

A

common in young
small & universal in location
sensitive to light (fade in winter vs lentigo)
color: brown/tan NOT red/blue/black
patho: localized increase in melanin production

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31
Q

melasma

A 
"mask like" pigmentation of face
patho: hormones, common during pregnancy/ OC
excessive hormones-->stim melanocytes
steroids-->stim growth of melanocytes
(when remove hor stim, goes away)

Cause (dx. black light): epidermal (increase melanin deposition) –>tx. bleach

dermal: MO pago melanin from epidermis and acc in dermis (can’t bleach)

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32
Q

melanocytic nevus color, size, appearance/location, patho

A

diverse group of lesions
color: brown or tan
size: papule (raised), @interface b/w epidermis & dermis
patho: increase activity of melanocytes –>grow in aggregates–>uniform intense color
(cells differentiate approp)

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33
Q

dysplastic nevus location, color, size, appearance

A

aka: BK moles
location: could have hundreds, may/not be in sunexposed areas, could–>melanoma
color: striking variability in color (red/blue/tan), likely to change
size: >6mm
appearance: macule/plaque/bull’s eye

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34
Q

why skin is more prone to cancer than other areas of body

A

high rate of mitosis

inevidally exposed to carcinogens

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35
Q

malgnant melanoma, risk fac, symp, size, appearance, growth

A

cancerous neoplasm from cells that make melanin (exponentially increasing in US)
Risk factors: UV rad & light skin
Symp: usu asymp, maybe pruritis
Size: >1cm at diagnosis (unique to this)
Appearance: irregular borders, change size, shape, color
Growth: Radial–>cells spread longitudinally within a layer of the skin (sometime basement mem = good barrier for metas)
deep/vertical growth: cells spread into dermis/epidermis
+correlation/w metas

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36
Q

Seborrheic keratosis

A

seborrheic- may/not have to d/w etiology
common on trunk of older people (can be on limbs)
round, waxy plaque, can peel off w/o pain/bleeding b/c coin like/w layers of skin

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37
Q

acanthosis nigricans

appearance, patho, prog

A

Appearance: hyperpigmentation in skin folds (ex. pits/groin)
velvet like
unique linear component

Patho: hyperplasia of S. spinosum (lager-han/dendritic cells can facilitate adhesion)

Prog: ben–> 3/4 and usu in young adults
mal–>when man in adulthood

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38
Q

fibroepithelial polyps

A

aka acrocordons
CT/collagen skin, grape like
can pick off if annoying

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39
Q

epithelial cyst

A 
aka wen
tumor contains keratin/sebum/fat
could be dermis/SQ
maleable (can palpate and not fixed) 
not problem, just annoying
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40
Q

“adnexal” tumor

A

appendages of skin (sweat gland/ follicles)

highly dependent on which appendage is involved

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41
Q

keratoacanthoma

A 
fast growing fumor
especially in old white men >50 yo
> or equal to 1cm
usu on sun exposed area
flesh colored & dome shaped, but cells are differentiated
mimics SCC
usu cures itself
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42
Q

actinic keratosis

A

“cutaneous horn”
get huge keratin growth
usu SCC

43
Q

SCC,

patho, appearance, prog, tx

A

patho: UV light–>mutations–>DNA repair mech
“in situ” carcinoma: in it’s normal location, contained in jxn b/w dermis & epidermis, basement mem = barrier

Appearance: sharply defined, red, scaling plaques–>nodules–>ulcerates (cells/w nuclei, enlarged & hyperchromatic)

Prog: usu caught in US
<5% metas

Tx. excision

44
Q

BCC,

where, associated with, appearance, prog

A

most invasive cancer in US (NK cells can kill tumors)
Where: different layer than SCC, in basal cell layer
Assoc: sun exposure, light skin, immunosuppression
Appearance: papule/w prominent surface
subepideral vessels thru it
ulcerates
+/- pigmentation
org look norm–>multifocal growths (epidermis) OR nodules (dermis) (surrounded by: fibroblasts make collagen & elastin; WBC recogn prob)
Prog: rarely metas, but may bone, ex. skull sinuses

45
Q

urticaria

age, cause, patho, prog

A

usu 20-40 yo
Patho: degran of mast cells–>hist release–>increase perm of vessels–>wheals (can –>papule/plaque)
Cause: detergent/IgE sensitive to antigen
Prog: very acute, dissipate within hrs
can get again w/o re-exposure

46
Q

Eczema

greek word, appearance, classifications (multifac), patho

A

“boiling over” (fluid acc & boils over)
Appearance: red papulovesicular –>ooze & crust–>become raised, scaly plaques
Classification: Primary irritant, allergy related, photo induced, drug related, atrophic dermatitis
Patho: Ant presentation (dendritic cells)–>CD4 Tcells in lymph node–>mem cells–>inflam at exposure site

47
Q

Seborrheic dermatosis

appearance, location, cause

A

Appearance: dandruff & greasy skin
+/- macules & papules
Location: areas/w large # of sebac glands: scalp/glabella
Cause: yeast?

48
Q

Acne Vulgaris

age, patho, subtypes

A

Age: universal in teens (M>F)
Patho: hor & abrupt changes in follicular dev

49
Q

inflammatory acne vulgaris

A

“white heads”
pustule formation of follicle
does not have keratin plug

50
Q

non-inflammatory acne vulgaris

A

“black head”/ open comedomes

follicular plug of keratin–>oxidized melanin (hor increase melanin locally)

51
Q

Psoriasis

ocurrence, appearance, location, patho, associated with

A

1-2% pop (usu mild)
cm assoc/w arthritis, 1/3 have nail issues (yellow/brown)
Appearance: pink, scaly plaque–>while over time
Location: diff from eczema, target extensor: elbows, knees, glands, penis, lower back
Patho: decrease function of S. granulosum–>decrease water retention
Assoc: inflam & angiogenesis

52
Q

what type of scale seen in psorasis

A

parakeratotic scale (because decrease function of S. granulosum)

53
Q

Verruca vulgaris

location, cause, spread, prog

A

Location: usu on hand
Cause: papilloma (150+ types of DNA viruses)
Spread: contact
Prog: 6 mo–>2 yrs spontaneously disappear

54
Q

Cerebral edema

types

A

(brain parenchymal edema)
vasogenic edema
cytotoxic edema

55
Q

cause of cerebral edema

A

secondary to a lot of causes, consequence of starling forces

56
Q

vasogenic edema

cause

A

type of cerebral edema
disruption of BBB & increase perm of cap in CNS
loc (inflam/tumor) or gen

57
Q

cytotoxic edema

cause, appearance, prog

A

Cause: secondary to neural, glial, endothelial cell membrance injury (d/t hypoxia/ metab dam)
Appearance: widened gyri, narrow sulci
prog: could–>herniation

58
Q

Hydrocephalus

cause, presentation, types, tx

A

acc of excessive CSF within the ventricular sys
Cause: drainage prob (rarely tumor –> increases CSF prod)
in neonatals–>alien head, if after sutures close, DEAD.
types: non-communicating: a portion of ventricular sys enlarged, ex d/t tumor
communicating: enlargment of entire ventricular sys
Tx: Sx to restore dam

59
Q

CSF pressure that will cause problems
what prob?
types

A

> 20 cmH20 in recumbent patient
hernia thru falx cerebri/ten cerebelli
localized vs. generalized

60
Q

types of cerebral hernias

A

subfalcine
transtentorial
tonsillar

61
Q

subfalcine hernia

cause, effect

A

d/t expansion of a cerebral hemisphere displaces cingulate gyrus pushing against falx cerebri (may compress Ant cerebral a. )

62
Q

transtentorial hernia

cause, effect

A

Cause: medial aspects of temp lob push against tent. cerebelli
Effect: usu bigger prob than subfalcine hernia b/c vasc on surface of pans (basilar/circle of Willis)

63
Q

tonsillar hernia

cause, effect

A

Cause: bulge of cerebellum into f. magnum
Effect: very prob b/c interfere/w medulla & pons –>CV/respir control

64
Q

norm amount of CSF made QD

A

2-3 L QD

65
Q

BBB anatomic mech?

A

yes

66
Q

BBB made up of?

A

endothelial cells

astrocytes= fence

67
Q

brain good at draining?

A

no

68
Q

why increase in perm of BBB bad?

A

neurotransmitters can cause uncontrolled stim of brain

69
Q

neural tube defects

A

most cm CNS malformation

70
Q

when does the neural tube close?

A

1 mo. (28 d gestation)

aka 1st trimester

71
Q

composition of neural tube

A

CNS=
ANT–>brain
POST–>SC
(encased in bone)

72
Q

consequences of neural tube not closing

A

miscarriage or

change in fxn after birth

73
Q

neural tube re-opening?

A

yes, less cm

74
Q

anencephalos

ocurrence, cause, appearance

A

fairly rare: 1-5/1,000 births (F>M)
no brain or may get rest of CNS ok, but forebrain= smaller than cerebellum
gross changes in calvaria (skull cap, what immediate covers forebrain)
Cause: forebrain doesn’t dev d/t defect in ANT neural tube- maybe d/t hor/genetics? (multifac)
Appearance: poorly differentiated mass of neurons/glial cells

75
Q

spina bifida

ocurrence, mech, appearance, cause, prog

A

most cm type of neural tube defect in POST end
Mech: no closure of neural tube during dev
Appearance: teratogenic (monster)
outgrowths of tissue from vertical canal, vert gap, mylomeningeocele
Cause: not well known; genetic/environ or folate levels–>correlation, NOT cause/effect
Prog: can be asymp
usu big deal- usu lumbar/sacral regions (parasymp –>groin (bladder, bowel), & LE s/m of pelvic appendages)

76
Q

myelomeningocele

A

only meningeal extrusion b/w vertebrae

77
Q

vertebral gap

A

shooting bodies b/w adjacent vertebrae

78
Q

Contusion of brain

A

lesion assoc/ w direct parenchymal injury thru transmission of kinetic energy

79
Q

laceration of brain

A

lesion assoc /w penetration/ tearing of tissue

laceration can cause contusion

80
Q

mechanism of contusion of brain

A

associated with anatomic morphology
ex. gyri most suseptible b/c where direct force is the greatest
frontal lobe along orbital lobe/temporal lobe b/c overly rough surface of skull
not usu occ lobe/brainstem

81
Q

coup injury

A

injury at site of impact

82
Q

contrecoup injury

A

injury opposite site of impact

83
Q

do neurons regenerate?

A

no except hippocmapl/olfactory

84
Q

shape of contusions

A

wedge shaped, with broad base lying along the surface

85
Q

trauma of CNS

cause, appearance, considerations, severity

A 
Cause: blunt force
Appearance: wedged shaped & brown/yellow
Considerations: 
\+/- penetrating/blunt
\+/- open/closed

+/- skull frac
parenchymal tissue
vasc (sever vv)
movement of head at time of injury (stationary = worse)
Severity: small lesions: mm3-cm3 (cortex may be silent)
(brainstem lethal) (SC severe impairment of s/m)

86
Q

Concussion

cause, mech, symp

A 
Cause: 
usu force to skull (can be force to body) 
Mech: 1)change RMP (dep) d/t release of excitatory AA
2)mit decrease ATP prod
3)increase vasc perm
Symp: transient alternation in LOC
amnesia of event
temporary respir arrest
decrease reflexes
87
Q

Contusion of brain

process

A 
hemorr & edema in area/inflam/w WBC
usu 1 d dam to soma of neuron
increase eosinophils
axonal swelling
PMN, then MO invade
88
Q

Contusion of brain

Patho

A

blood clot>fibroblasts invade>sec collagen/prot fibers>scaffolding networks around clot (may need to remove if lasts for a while)

89
Q

epidural hematoma

cause, patho, tx.

A

pocket of blood in space b/w dura mater (2 layers) &periosteum
Cause: menin. a. leak
Patho: increase space b/w skull&brain (normally fused)
Tx. if sever>Sx.

90
Q

periosteum

A

sheet of fibrous CT that covers bone

91
Q

subdural hematoma

mech, Tx

A

bleeding in the arachnoid space (norm CSF collects here)
Mech: arach not very malleable, bridge vv fixed in this space b/c venous sinuses are fixed- brain shifts and tears vv
Tx. high rate of recurrence +/- Sx

92
Q

path of bridging vv

A

travel from cerebral hemisphere>subarach sapce>subdural space>sup sagittal sinus

93
Q

2 most cm hematomas

A

epidural & subdural

94
Q

are hematomas always obvious?

A

no, b/c could have internal bleeding

95
Q

Cerebrovasc dz.

ocurrence

A 
any neurologic dz. caused by vasc pathology
#3 killer in US (heart dz, than ca)
96
Q

Cerebrovasc dz.

cause

A

Cause: thrombosis (clot)
hemorr
emobolism (clot/fat/tumor/air- iatrogenic)
all 3 = stroke

> > > can be global (carotid/circle of willis) or focal (sm region of brain)

97
Q

Cerebrovasc dz.

mech

A

Mech: hypoxia (brain norm gets 15% of CO), if lg area>DEAD

isch: decrease Q to area>decrease metab>decrease cell fxn (global-cardiac arrest, shock, hypoten/focal-thrombus, embolus, vasculitis)
infarct: spec area of dam, usu not repairable

98
Q

cells most affected by isch/infarct

fxn of oligodendrocytes & astrocytes

A

neurons > glial cells

(oligodendrocytes >prod myelin & astrocytes> around vessle & neurons, reg Q & brain fxn)> also sensitive

99
Q

hypoxia

A

decrease in partial press of O2

100
Q

isch

A

decrease in a tissue’s use of O2 d/t occlu of Q

101
Q

Meningitis- bact

cause, appearance, symp, CSF, prog

A

aka pyogenic
inflam of the meninges (not brain)
Cause: E. Coli, S. Pneumo, others
Appearance: pocket of pus on brainstem floor
Symp: photophobia, increase irritability, stiff neck, neuro impairments (reflexes)
CSF: increase prot, decrease glc, no change WBC
prog: acute & life threatening

102
Q

Meningitis- viral

cause, symp, CSF, tx, prog

A

aka aseptic
Cause: may be bact that can’t find, usu d/t enterovirus, ex. echovirus
symp: slower onset
CSF: slight increase prot, no change glc, increase WBC
Tx. symp, b/c IS fights virus

103
Q

Cerebral Palsy

cause, symp, Dx

A

non-progressive motor deficit condition/w strong neurologic component
Cause: exogenous insult during prenatal/perinatal period (ex. brain hemorr)
Symp: ataxia, dystonia (mm partially & constantly contracting), partial paralysis (momentary mm weakness)
Dx. may not be dx right away, but will recogn soon b/c have prob during dev

Patho- skin (2 decks)

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