Name Pathogenesis Risk Factors

abnormal contact of femoral

Developmental Dyplasia of the head w/ acetabulum (constant female sex, breech position,
Hip hip flexion) genetics and swaddling

Greenstick Fractures

Torus/Buckle Fracture
Bowing deformity
Physis Injuries - Straight

Physis Injuries - Above

Physis Injuries - Lower (BeLow)

Physis Injuries - Two (Through)

Physis Injuries - Erasure

Inferior and posterior slippage

Slipped Capital Femoral of femoral epiphysis - Salter
Epiphysis Harris type 1

Epiphysis Injury - not sure how but separation of

Osteochondritis Dissecans articular cartilege and
(OCD) subchondral bone

idiopathic avascular necrosis of

Legg-Calve-Perthe Disease femoral epiphysis

overuse injury -
separation/fragmentation of
Apophysitis apophysis
Symptoms
femur grows bigger than
acetabulum
periostum on one side is still
intact
longitudinal pressure -->
compression
physis
physis and metaphysis
physis and epiphysis
meta/epi and physis
crush injury
dull, nonradiating
groin/thigh/knee pain -
worse wtith activity, limited
rotation
localized pain beginning to
develop over several
months - pain is worse after
activity (get swelling) and
everything is tender
persistant hip/knee pain,
limping (limping may be
the only symptom)
pain is localized to apophysis,
worse with muscle movement
(swelling) - NO LOSE OF
MOTION
Treatment Notes
position the acetabulum with
the femoral head
rarely causes bone growth
arrest
emergent surgery often
required - fragment MUST be POSSIBLE BONE GROWTH
returned to anatomical position ARREST
emergent surgery often
required - fragment MUST be POSSIBLE BONE GROWTH
returned to anatomical position ARREST
Most dangerous kind - happens
with a loading pressure, BONE
GROWth ARREST (diagnosis is
made AFTER arrest)
screw femoral head and common in adolesence; chronic
acetabulum into place (>3 weeks) is more common
mostly the knee (lateral part of
medial condyle)
these pts tend to get early
osteoarthritis…between 4-8
yoa
self-limiting (ossification of
apophysis) rest, ice, "little leage "little leage elbow" = medial
elbow" has the highest chance epicondyle; "osgood-schlatter"
of fragmentation = tibial tubercle
Name Epidemiology

women and elderly are at a higher

Osteoporosis risk (postmenopausal and >50yoa)

Osteomalacia/Ricketts

men, older than 55, NOT seen in

Paget's Disease Scandinavian, Africna and Asian

Osteogenic Osteomalacia

Hypophosphatasia
Formation/Resorption Pathogenesis

increase resorption b/c

age/hormones…altered quantity
low/HIGH and quality of bone

decreased mineralization of
collagen matrix caused by vit
D/calcium, phosphorous and
alkaline phosphate (mineralizing
LOW/normal agent)

LOCAL over acivation of

osteoclasts…genetic +
high/HIGH environmental
Caused by benign tumors (in soft
tissue/bone) that make FGF 23

autosomal disease that decreases

alkaline phosphate levels
(pyrophosphate is deposited
instead)
Risk Factors Symptoms

low body weight, prior

glucocorticoid, low vitamin asymptomatic until a fragility
D/calcium fracture

extremely low vitamin D, fat

malabsorption, advanced liver
disease, antiepileptics and chronic
kidney disease and autosomal most have bone and muscle
recessive disease weakness and bone tenderness

asymptomatic elevation of alkaline

phosphate or a random boney
AT risk FOR OSTEOSARCOMA lesion (most likely in the pelvis)

low phosphorous and osteomalacia

Treatment Notes

can have a secondary underlying

cause; osteopenia is between 1 and
2.5…diagnose if DXA <2.5 or
fragility fracture

osteomalacia - cortical bone;

rickett's - cortical bone, growth
plates and cartilage…most common
cause is going to be FGF23 (renal
treat with calcitrol phosphate wasting)

Bisphosphonates, Calcitron and creates a well-defined area in the

then maybe surgery bone

remove tumor

enzyme replacement therapy and

sometimes bone marrow
transplant
Name Class Agent

Aledronate
Ibandronate
Risedronate
Zoledronic Acid Bisphosphanate Antiresorptive agent

Denosumab Antiresorptive agent…potent

Selective Estrogen Receptor
Raloxifene Modulators Antiresorptive agent

Teriparatide Anabolic agent

Estrogen Replacement for
Osteoporosis
MOA Fracture Prevention SE

vert and nonvert hypocalcemia, upper GI side

VERT effects, one.joint pain, flu-like
symptoms, acute kidney injury…
osteoclast don't adhere to and vert and nonvert occular, atypical femur and
dissolve bone vert and nonvert osteonecrosis of the jaw

hypocalcemia and maybe

monoclonal antibody that binds osteonecrosis…don't really see
to RANK and inhibits osteoclasts vert and nonvert cellulitis
binds to estrogen receptor to
prevent bone resorption vertebral, NOT HIP venous thrombosis, hot flashes

hypercalcemia, gout and

amazing effect in the spine; no osteosarcoma (only see this in
PTH receptor on osteoblast atypical fractures rats)
venous thrombosis and hip
fractures
Notes

can also reduce bone formation;

reduce hip fractures significantly
and clinical fractures; take on an
empty stomach and wait for a
while before wating and take a atypical femur fracture aka
drug holiday and monitor DXA subtrochanteric fracture =
every 2 yrs thigh/groin pain

USE in RENAL DYSfunction and

give SQ injection every 6 months INTOLERANT to other therapies
Reduces risk for invasive breast
cancer

Daily SQ injection; intermittant

exposure to PTH = increased
osteoclast and osteoblast continous exposure to PTH =
recruitment…affects spine more osteoclast activation --> bone loss…
tha hip/forearm can't use after a resorptive agent
DO NOT use in posmenopausal
women
Name Epidemiology Cause

Growth, radiation, genetic

Osteosarcoma young adults (2nd decade) syndromes (RB, RecQL4, TP53)
LESS common in African descent;
diagnosed within the first 3
Eweing Sarcoma decades of life genetic translocation (t(11,22))

malignant bone tumor in collagen

Chondrosarcoma middle-aged - older matrix; mutation in IDH1 or IDH2

Osteochondroma

Enchondroma younger patients

Giant Cell Tumor of Bone between 20 and 40

small lesions made of osteoid and
Osteoid Osteoma males under 40 woven bone

Aneurysmal Bone Cysts blood-filled cystic lesions

Symptoms
progressive pain at the tumor
site….Just don't get better!
longer duration and other
symptoms (i.e. fever)
pain
non-painful bony mass
PAIN that gets worse at night
Location Diagnose
metaphysis of long bones - distal
femur and proximal tibia (causes
knee issues) tissue confirmation is required
normally the diaphysis and from
anywhere…see onion skin/moth
eaten appearance
Can arise in normal bone or
benign tumor (malignant
transformation) - pelvis and
proximal femur…see bright spot
in bone
femur or tibia - occurs in
metaphysis or diametaphysis Don't biopsy
hands and feet
epiphysis of long bones -
especially by the knee
cortex of tibia or fibula, can occur
in long bones
see this in long bones in
metaphysis
Pathology Notes
Treat by removing the tumor
malignant osteoid ; lytic sclerotic completely…get the negative
on imaging margins…NEED SURGERY + CT
metastatic spread to lungs, bone
see small round blue cells; and BONE MARROW…can treat
onion/moth skin on imaging locally w/ radiation

chondroid matrix; arcs and rings

on imaging Surgical, not as much CT

don't need to rmeove unless it's

muchroom outgrowth on imaging causing pain

see stippled calcification,

endosteal scalloping, ossification
na dexpansion of cortex on need to differentiate this from
imaging osteochondroma

locally aggressive but CAN

see multinucleated giant cell in METASTASIZE; treat w/ surgery or
stroma; dark spot in imaging denosumab
new bone with central
radiolucent nidus treat w/ NSAIDs
soap bubble appearance in
imaging
Name Inheritence Defective Gene

Marfan AD FBN1 - fibrillin

EDS, classic AD COL5A1 or COL5A2

EDS, vascular AD COL3A1

EDS, hypermobile/ BJHS AD unkown

Osteogenesis Imperfecta AD but some types can be AR COL1A1 and COL1A2

Historical Findings
family history
complications of joint
hypermobility - bruises, surgical
complications
chronic pain, easy bruising, family POTS, high/narrow palate,
history, bowel disorder
fractures w/out trauma,
family history and post-
pubertal hearing loss
Clinical Findings
smooth velvety skin, molluscoid
pseudotumors, subcutaneous
spheroids (subcutaenous
fat in elbows)
thin, translucent skin,
characteristic facial appearance
(large eyes, long narrow nose,
amsll chin and bo ear lobes),
acrogeria
dental crowding
short stature, lordosis, blue/gray
sclera
Diagnosis
Family history OR aortic
dissection/etopic lentis
skin hyperextendability,
widened atrophic scars
(thin and easy to tear) and
joint hypermobility
dissection, rupture, family history
joint hypermobility, soft skin with
normal/slightly increased
extensibilty, ANSENCE of skin
fragility
Treatment Notes

Beta-Blockers

Vitamin C - minimize bruising

Beta-Blockers

hypermobility physical therapy

bisphosphanates
Name Inheritence

X-linked (females have muscle

Duchenne Muscular Dystrophy weakness and cardiomyopathy)

Becker Muscular Dystrophy x-linked

AD…number of repeats increases

from one generation to the next
Myotonic Dystrophy (genetic anticipation)
Gene Age of Onset

deletion in DMD --> truncated,

shifte reading frame --> unstable
protein; recommend genetic
counseling
DMD mutation --> shorter
dystrophin but FUNCTIONAL
see it present at 3-5 - weakenes
limb/girdle muscels
5-15 but can occur in 30s

repeats in DMPK and ANF9 (two

types) adulthood
Clinical Findings Progression

progressive wasting of skeletal 8-12:contracture of calf muscles,

muscles…screen w/ creatine kinase ordosis; 20s-30s: cardiac/respiratory
(peaks b/c of muscle wasting) impairement --> death
similar but milder and slower…no
muscle biopsy if needed contractures/scoliosis

myotonia, perpheral neuropathy,

frontal baldness, catarats,slow
progressive muscle weakness,
cardiac conduction defects, pain,
temporal wasting and endocrine
issues
Treatment Notes

manage with corticosteroids

(prednisone) - watch out for side
efects; neuromuscular w/ live
vaccines; PT mst common form; legs before arms

live to normal adulthood

mst common in ADULTS; hard to

relax once they contract
Name Adult/Peds Location

cutaneous ir mucocutaneous…
Herpes Simplex Virus adults AND peds most likely on FACE

starts on trunk/scalp and spreads

out…LESIONS ARE AT DIFF
Varicella peds STAGES OF DEVELOPMENT

unilateral dermatome
distribution - normally thoracic
Herpes Zoster adults and 1-3 dermatome layers

extremeties, back, buttocks and

Dermatitis Herpetiforms peds scalp

Hand, Foot and Mouth Disease peds PALMS, SOLES and oral

where the allergen touches -

Allergic Contact Dermatitis adults AND peds normally on hands

Pemphigus vulgaris oropharyngeal are common

NON-mucosal -- trunk, limbs nad

Bullous Phemigod ELDERLY flexural surfaces
Etiology CM - Skin CM

primary infection is normally

asymptomatic but it can have
fever, lymphadeopathy and latent
1-2 mm vesicle on erythamtous infection is going to have a
base….painful and pruiriti prodrome

clear vesicle on erythamatous

base…becomes pustules and have low grade fever and maybe
then crusts over…pruiritis malaise

GROUPED vesicles on an
erythamtous base…becomes
pustules and then crust…
prodrome of pain, paresthesia malaise and mild fever with the
stays in the DRG and pruiritis rash

grouped erythematous
Have celiac disease papulovesicles
Caused by Coxsackievirus; late vesicle on erythamtous base…
summer and early fall painful…INDIVIDUAL prodrome of fever/malaise

there's a range…vesicles/blisters
-- scaling/litchenification…
activation of T cells --> immune INTENSE pruritis and atopic
response dermaitis see a linear progression

autoantibodies against
desmosomes -- >detachment
of adhesions between epithelial flaccid blisters on non-inflammed
cells on skin and mucous skin w/ weeping and denuded
membranes areas… PAIN

antibodies against basement

membrane zone - specifically can have preceding
hemidesmosomes Vesiculobollous RUPTURE pruiritis/hives
Dx Treatment Notes

PCR > HSV culture > acyclovir - prevents viral DNA

Antibody/Tzank Smear (the last polymerase from making new There is type 1 and 2, 1 is going
one is fast though) virla DNA to be more by the face

clinical diagnsis can take acyclovir… Winter and Spring

treat very early w/ antivrial

skin biopsy - neutrophil rich
supepidermal blister and
depositoin of IgA Diaminodiphenyl sulfone Require Skin Biopsy

Make sure they drink water

glucocorticoids

IgG on keratinocytes glucocorticoids Require Skin Biopsy

neutrophilic infiltration in dermal

layer; IgG and C3 bound to cotricosteroids
dermal and epidermal layer (immunosuppressant) Require Skin Biopsy
Name Epidemiology Cause
premature conversion of anagen
Telogen Effluvium women to telogen
autoreactive CD8 T cells that
Alopecia Areata men and women …younger attack hair follicles

nonscarring that can transform to

Traction Alopecia gradual hair loss due to traction scarring if traction is prolonged

Trichotillomania women pt has compulsion to pull out hair

Onychomycosis fungal infection of the nail

inflammation of lateral and

proximal nail folds…can be
Paronychia caused by staph/strep/eikinella

purulent infection/abscess
involving the fleshy part of the
finger (most common thumb and
Felon index) …. Caused by staph or HSV
CM - appearance
Hair that is shed has a whilte bulb
attached to it
well demarcated bald spot that
has black dots left on the scalp
asymmetric hair loss…hair is
short and bristly
white to yellow/brown
opafication of distal nail bed
can have an abscess and
erythema of nail folds
erythemia and swelling
CM - others Risk Factors
Many…can be associated with
thyroid/iron defeciency
notice exclamation points on the
side, and have nail pitting
trauma, immunosuppression,
can lead to subungla diabetes or peripheral vascular
hyperkeratosis insufficiency
nail biting, manicures, thumb
sucking, diabetes, chronically wet
acute pain hands and ingrown nails
pain
Treatment Notes

treat underlying cause

intralesional steroids OR topical
steroids

telogen comes out easier than

alogen..causes uneven
appearance

Terbinafine - inhibits an ezyme

needed for fungal cell wall

w/out abscess - antibiotics and

warm compress; abcess - cut and
drain

acyclovir if caused by HSV or can

treat w/ Augmentin
Name What Caused By
Folliculitis infection of hair follicle Staph aureus (+ diplococci)

staph aureus (+) and strep

Cellulitis pyogens (+ cocci in chains)

strep pyogens (+) - erythrogenic

Erysipelas toxins

collection of pus in dermis nd

Skin Abscess deeper skin tissue Staph aureus (+ diplococci)

colonization of lesion with

bacteria; starts off as vesicular
lesion and evolves into honey
Nonbollous Impetigo colored crusts staph/strep (+)

strep enters body through wound

and secretes enzyme that
Necrotizing Fasciitis destroys tissue strep pyogens (+)

gram +, encapsulated, spore

forming anaerobe…alpha toxin
(lecithinase-phospholipase
Clostridium Perfringes C) - breaks down lecithin
gram -, motile aerobic rod;
exotoxin A - inactivates EF-
Pseudmonas aeruginosa 2

skin lesion following septic

Ecthyma gangrenosum infeciton w/ pseudomonas

gram -, bacillus, aerobe…lipid A

Bartanella henselae cat scratch endotoxin = inflammation
 gram -, bacillus, aerobe…lipid A
Cutaneous lesions cat scratch - ONLY HIV endotoxin = inflammation

gram -, bacillus, aerobe…lipid A

Bacillary angiomatosis cat scratch - ONLY HIV endotoxin = inflammation

gram -, bi polar staining and

dog scratch OR cat (cats are facultative…lipid A endotoxin =
pasturella multicoda worse) inflammation

Eikinella corrodens human bite gram -, facultative rod

Scabies mite - direct or indirect

Pediculosis capitis head lice

dimorphic soil saprophyte (yeast

Sporothrix schenckii rose gardener's disease in body)
How Deep CM - other things CM - skin issues
red, pus filled raised, pus filled

any part of skin, fever, redness,

pain, swelling and if it gets into
the lympahtics you have
deeper dermis and subcutaneous streaking w/ non-distinct
fat margins NOT RAISED
release cytokines -->
upper dermis and superficial fever/rash/shock…infection
lymphatics --> raised above spreads to lymph nodes
skin and clear demarcation (painful) RAISED, distinct margins

painful, tender, fluctuant and fluctuant, erythematous

erythamatous nodule frequently nodule with a pustule on top
surrounded by a pustule and of it and it's surrounded by
epidermis/dermis surrounded by a ring of swelling erythematous swelling

small flattened red patched on

face/limbs, develop into oozing
pus filled vesicles on a red
base --> break and form honey
colored crusts that are itchy veiscular lesions --> honey
epidermis/dermis and attached firmly to skin colored crusts

surface is hot and VERY

PAINFUL, fever, nausea and
Fascia - not a great amount of lower BP as infection goes
blood vessels deeper…can get sepsis or SIRS skin is hot and painful

muscle - normally found in GI can cause myonecrosis --> gas in

though subcutaneous tissue = crepitus

oppertunisitc pathogen - see it in

burns, wounds and CF
red macules --> slightly elevated
--> hemorrhagic and
centrally necrotic …black macules --> papules -->black
eschars eschars

papule/lesion at site for 1-3

weeks, followed by fever,
headache, malaise and
lymphadenopathy
smart out small red lesions -> papular, nodular, pendunculated
expand and become more friable or verrucous forms
Also has fever, chills, malaise,
headache, anorexia w/ or w/out
headache vascular lesions involving the skin

papule/lesion at site for 1-3

weeks, followed by fever,
headache, malaise and
lymphadenopathy

generalized and intense

itching that worsens at night…
SPARES HEAD AND FACE…see
eosinophils since it's an allergic
reaction

pruritis b/c of allergic reaction to

saliva …increase the numebr of
eosinophils

painless pink/purple/black
papule --> enalrges and ulcerates
--> ulcerated nodules develop
along lymphatic channels that papule --> ulcerated nodules that
drain into the lesion follows lymphatic drainage
Treatment Notes

clindamycin (affect ribosome 50S -

no elongation in translation) or
dicloxacillin (non-purulent)
(inhibits linkage in peptidoglycan)

erythrogenic toxins in bacteria

clindamycin or dicloxacillin (non- stimulate macrophages to release
purulent) cytokines -->fever/rash/shock

out patient - clindo/bactrim; in

patient - vanco (inhibit cell wall assume this is MRSA until proven
synthesis) otherwise

mupirocin for single lesion,

dicloxacillin for multiple lesions

remove the necrotic tissue, then see moderate gas production in

clindo/bactrum skin if it's a mixed infection

Needs to necrotize tissue or have

other growth factors to grow…
need to have SEVERE TRAUMA -->
tissue necrosis or excess nutrients
green fruity smeeling colony; can
grow where there aren't many
nutrients

lesions are at sites distal from

wound = sepsis
 can have VASCULAR
PROLIFERATION of lesions

clenched fist injuries (punch

someone in the face)

finger webs, flexor surfaces of

wrists, elbows, axillae, buttocks,
genetalia and breasts; need to
Permethrin ID mites or eggs

permethrin

itraconazole - inhibits ergosterol

 oppertunisitc
pathogen - see it in
Pseudmonas gram -, motile burns, wounds and green fruity smeeling
aeruginosa aerobic rod CF colony
exotoxin A -
inactivates EF-2
Name Epidemiology Cause

Not enough Vitamin C intake to

elderly, alcoholics, food faddists make collagen --> decreased and
Scurvy and cancer pts abnormal collagen

sun and age damage dermis -->

>50 yoa, steroid, anticoagulant fragile blood vessels -->
Senile purpura use and chronic sun exposure superficial blood vessels rupture

Caused by Ricketsii in the spring

Rocky Mountain Spotted Fever and early summer

organ dysfunction caused by

dyregulated host response (local
inflammatory response -->
Sepsis systemic symptoms)

Get gram - bacteria (endotoxin)

DIC -- > endothelial damage (DIC)

Neisseria Meningitidis (gram -

diplococci)…blood stream
infection that damages blood
vessels --> bleeds into
Meningiococcemia children +young adults skin/organs

inflammation of blood vessel

Vasculitis that is immune system mediates
Location CM - skin CM - others

intramuscular/periosteal
hemorrhage, kerototic plugging
perifollicular purpura, large of hair follicles and hemorrhagic
ecchymoses on leg gingivitis

benign recurrent ecchymoses on

extensor surfaces of forearm

blanching erythamtous macules

--> petechia. Ankles + Feet -->
trunk; PALMS AND SOLES AT THE fever, headache, nausea, malaisa
END and myalgia/arthralgia

tachycardia, fever, hypothermia,

tachypnea, etc.

widespread clotting (tissue

Stellate non-palpable purpura - factor is released and activate
central area is necrotic (look common clotting cascade) -->
gray)..shape is classic for bleeding (excess thrombin -->
thrombosis/infarction fibrin clots --> use up platelets)

purpura fulminans (DIC w/ fever, headache, stiff neck, N/V

purpura and necrotic plaques) and photophobia

Palpable Purpura (w/ small

vessels)…big vessels have constitutional symptoms, pain
nodules and ulcers…normally on and presence of other organ
lower extremeties involvement
Treatment Notes

Vitamin C!!! pirates

NO COLOR CHANGE OVER TIME

SUPER ILL

Ceftriaxone and supportive FATAL in hours; Dx w/ blood

therapy culture and CSF

Get a stkin biopsy

Name Epidemiology Location

Mild Acne

Moderate Acne teens and sometimes young

Severe Acne adults face, chest and back

Rosacea men and women >30 yoa nose, chin and cheek

Perioral Dermatitis women around the mouth

beard, pubic area, axillae and

Folliculitis thighs

Pityriasis Versicolor adolescents/adults…NOT PEDS trunk, extremities and neck

Post-Inflammatory
Hypo/Hyperpigmented

areas prone to trauma (knees

and elbows); generalized form
starts symmetrically; segmental
Vitiligo form has a dermatomal pattern
obesity and insulin resistant
Acanthosis Nigracans syndromes neck, axillae and groin

Melasma RARELY occurs before pubery symmetric on sun-exposed areas

 face or dorsal surface of your
Solar Lentigo >40 yoa hands
Cause CM - skin CM - others

Comedones (caused by
obstruction of follicle opening
and keratin build up can make it
seem balck), papules and
pustules

androgen increaes --> stimulants

increase --> sebum production +
follicular growth --> pore gets
obsructed --> P. acnes grows and ^ + NODULES + few scars
becomes inflammed ^ + SCARING

innate immune system activates

to some trigger --> vascular
hyperactivity and altered vessel
permeability so inflammatory erythemia, telangiectasia and
cells stay around longer papules and/or pustules

small papules, pustules with

often after using topical/inhaled arythematous base, NO
corticosteroids COMEDONES

hair follicle is affected…Staph

aureus pustule centered on hair follicle

common fungal infection -
thrives in hot and humic
climates
inflammatory melanocyte
damage
small hypo/hyperpigmented
round macules. Well defined
and can coalesce…can have
pruritis
loss or gain of pigment (NO
absolute loss though)

autoimmune melanocyte well defined patches/macules

destruction with COMPLETE depigmentation
epidermal proliferarion w/ very velvet thickening of skin, brown
little melanin increase to gray in color
genetic and hormonal influence brown macules wit hirregular
w/ UV rays borders
 Round/oval/irregular shaped
UV exposure --> proliferation of circumscribed patch that is
melanocytes brown/black/tan
Treatment Notes

topical retinoid (normalizes

desquammation of follicular
epithelium + anti-inflammatory
properties) 1/4 of the face is involved

topical retinoid, benzoyl

peroxide (free radicals that
oxidizez protein in cell wall) and
+/- topical antibiotic
(Clinda/Erithro - decrease
protein synthesis) 1/2 of the face
^ + oral antibiotic 3/4 of the face

topical antibiotic avoid alcohol, spicy food, hot

(metronidazole) beverages and sunlight

topical antibiotic
(metronidazole)

topical antibiotics (mupirocin

and clinda) OR oral
(bactrum/clinda)

topical azoles, widespread use KOH prep would reveal short

lotion, and for recurrent use oral hyphae and spores (spaghetti
fluconazole and meatball)

manage underlying skin issues

refer out

hydroquinone and tretinoin are

skin-lightening agents
sun protection and cryotherapy