rangkuman week 1 (pbl) - fracture

7/23/2019 Rangkuman Week 1 (PBL) - Fracture

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Rangkuman Week 1 – Fracture

1. Bone Growth and Formation

a. Intramembranous Ossification

• Membentuk tulangtulang !i!ih

• "embentukan tulang tidak didahului !embentukan tulang rawan.

• #erda!at trabekel tulang.

"roses$

o "embentukan ossification center

o Calcification

o "embentukan trabekel

o "erkembangan !eriosteum



b. %ndochondral Ossification

• #ulang terbentuk dari tulang rawan h&aline

• 'da primary ossification center !ada fetus dan infants

• 'da secondary ossification center !ada anakanak( rema)a dan early adulthood .

• Membentuk ham!ir seluruh tulang !ada skeleton manusia *selain &ang dibentuk !ada

osifikasi desmal+.

"roses$

o "erkembangan model tulang rawan

o "ertumbuhan model tulang rawan

o "erkembangan primary ossification center

o "erkembangan medullary *marrow+ cavity

o "erkembangan secondary ossification center

o "embentukan articular cartilang dan eoiohyseal * growth+



c. Normal epiphyseal * growth+ plate

•Growth in the length of the metaphysis and diaphysis of a long bone.

•#er)adi interstitial growth sel tulang rawan( membuat epiphysis terletak lebih )auh dari

metaphysis

•#er)adi calcification, death and replacement dari tulang rawan !ada metaphysical surface

melalui osifikasi endokondral.

•'da , -ona !ada epiphyseal

plate$

o ona rehat$

ona terdekat dengan

e!i!h&sis.

#erdiri dari kondrosit

&ang kecil.

o ona !roliferasi

#erda!at &ang

kondrosit &ang sedikit

lebih besar. /ondrositn&a

mengalami

!ertumbuhan

interstitial.

o ona hi!ertrofi0maturasi

/ondrositn&a sudah

matang dan besar serta

tersusun dalam kolom

kolom.

o ona kalsifikasi

/ondrositn&a

keban&aka telah mati.

2. Bone types ( cortical,trabecular, woven) and histologic features ofeach.cortical bone /compact bone

- system havers(osteon) :untuk menyalurkan sirkulasi ke tulang, terdiridari lamel konsentrik yang mengikuti saluran havers.

- lamel interstisiales:lamel sisa osteon yang mengalami remodeling. - volkmann’s canal:saluran havers yang menembus lamel-lamel,berguna

untuk menyalurkan aliran darah,nerves. - canaliculi : menghubungkan antar lacuna dan central canal untuk

menyampaikan nutrisi. - osteosit :mature cell yang terletak didalam lacuna



woven bone / immature bone- pada skeleton embrio,yang matriksnya terusun dari proteogyclan dengan

sedikit cement tetapi belum memiliki lamel.- Umumnya woven bone akan hilang dan digantikan dengan cortical bone

pada usia !tahun,tapi dalam keadaan patologis woven bone tetap adapada orang dewasa

.

trabecular bone/cancellous bone

- less comple" in lamellae arrangement making it thin in its trabeculae andnourished by vessels in the marrow spaces

a. Basic structures of diaphysis, metaphysis bone and their bloodsupply#etaphysis$aerah perbatasan antara growth plate dan diaphysis,tersusun daritrabecular bone.$an terdapat epiphyseal plate yang merupakan lapisankartilago hyaline yang ber%ungsi dalam pertumbuhan meman&ang daridiaphysis.'ada usia !-! tahun epiphyseal plate pada metaphysis akandigantikan oleh tulang,sehingga men&adi epiphyseal line.

*liran arah pada metaphyseal berasal dari arteri yang mensupplysendi,anastomose dengan diaphyseal kapiler dan berakhir di corticalbone,trabecular bone.$iaphysis$iaphysis adalah bagian dari tulang pan&ang yang terletak diantarametaphysis yang terdiri dari compact cortical bone.'ada bagian tengahdiaphysis terdapat medullary canal yang berisi marro dan sedikit trabecularbone.*liran darah pada diaphysis disupply oleh diaphyseal nutrient artery yangmerupakan artery paling penting pada long bone,diaphyseal nutrient arteriesmelalui cortical bone secara obli+ue,artery ini dibedakan men&adi ascendantdan descendant dan mensupply / dari corte" dan medullary cavity.

b. Structure of periosteum



#erupakan &aringan double layer yang melapisi seluruh permukaan tulang

yang tidak dilapisi oleh articular cartilage.

'ada lapisan luar periosteum berhubungan langsung dengan pembuluh

darah

dan terdiri dari &aringan brosa,pada lapisan dalam terdiri dari lapisan

osteogenic dimana terdapat sel osteoprogenitor.'eriosteum berhubungan dengan tulang melalui serat kolagen yang kuat,

harpey’s bres.

ungsi periosteum:

-ebagai tempat menempelnya tendon dan ligament

-berperan penting dalam proses bone healing.

-memberi nutrisi pada sel-sel tulang melalui pembuluh darah yang terdapat

di periosteum

c. Major bone cells and their function0steoblast - #erupakan di%erensiasi dari sel mesenkim,ber%ungsi dalam proses osteogenisis atau osikasi. - 0steoblast mensintesis kolagen dan komponen organic lainnya yang

digunakan untuk membuat matri" e"tracellular agar dapat ter&adiproses

kalsikasi,&ika sudah tertutupi oleh matri" e"tracellular maka osteoblast berubah men&adi osteosit - el osteoblast yang belum mengalami kalsikasi disebut osteoid(prebone)

pada tahap ini tulang masih lunak. - 1idak mengalami mitosis dan tidak dikelilingi matri".0steosit - #ature bone cells dikelilingi matri" yang berasal dari osteoblast. - 2er%ungsi untuk mengatur metabolism tulang dalam pertukaran nutrisidan waste dengan aliran darah - 1idak mengalami mitosis.0steoclast

- 2er%ungsi sebagai bone resoption karna memiliki en"im lisosom dan acidyang berguna untuk melisis komponen protein dan mineral dalam

matri"e"tracellular tulang.

- 'eran penting dalam proses pertumbuhan,perkembangan dan bonerepair. - #engatur kadar kaslium dalam darah

- ecara mikrokopik berada diluar trabekel tulang dengan ukuran sel yang besar dan memiliki banyak inti.

0steoprogenitor bone stem cell yang berasal dari mesenkim dan mengalami

perkembanganmen&adi osteoblast. -terletak pada periosteum tulang.



d. !omponent of bone matri"2one matri" consist o%: - organic component - anorganic component-0rganic component(34)5

- osteoprogenitor cell - osteosit

- osteoblast - osteoclast - osteoid(sel osteoblast yang belum mengalami

kalsikasi)-6norganic component(734)5 - 8ydro"yapatite (mineral salts)

calcium phosphate 9a('0;) .(08) <(men&adikan tulang kuat)

-calcium carbonate, =uoride, magnesium.

e. !ommon type of collagenollagen ada &enis:collagen ! dan collagen .collagen type 6

- ma&or collagen pada kulit,tulang,brokartilago,meniskus- ber%ungsi untuk menguatkan tulang- ada &enis: 0>!*!

0>!*-collagen type ! terdiri dari rantai procollagen !?!men&adi 0>!*!

!rantai procollagen !?men&adi 0>!* &ika ter&adi mutasi pada kolagen type ! maka dapat menyebabkanosteogenesis imper%ect.collagen type

- banyak terdapat di kartilago,articular cartilage,vitreous(eyeball)- dalam &umlah kecil ditemukan pada &aringan skeleton pada awal masapertumbuhan.

- 2er%ungsi untuk menguatkan connective tissue pada otot,sendi. @ika ter&adi mutasi makan dapat menyebabkan chondrodisplasia(dwarsm)

f. #escribe the minerali$ation of bone 1he mineraliAation o% so%t callus begins about ! week later, a%ter the

%ormation o% new so%t callus. 1he increased o"ygen tension leads to the production o%osteoid(visible on

radiographs) 1he presences o% osteoid provides rigidity within the callus id

dependent on the relative stability o% the%racture site, the larger callus is prevent this motion.

been

gained across the %racture site,thepatient may resume limited activity.

callus may take anything %rom ; to !7weeks and is a +uicker process in children and spongy bones.



. Bone Remodelling.

a. 2ortical *2om!act+ bone

- 2haracteri-ed b& the concentric arrangement dari lamella dan com!le3 formation dari sistem

ha4ers atau osteon.

b. 2ancellous *trabecular+ bone

- #he arrangement dari lamelan&a lebih sederhana dibandingkan dengan cortical bone karena

trabekeln&a thin dan da!at dinutrisi oleh !embuluh darah disekitarn&a dan marrow spaces.

c. Wolff’s Law

•Bone Reaction

o 'da , basic wa&s of bone reaction to abnormalities$

Local death$ keadaan sebuah area !ada tulang telah completely deprived of its blood

supply.

An alteration of bone deposition$

Increased de!osition$ !eningkatan !embentukan matri3 dengan kalsifikasi normal

5ecreased de!osition$ !engurangan !embentukan matri3 atau hypocalcification

An alteration of bone resorption$ increased reso!rtion dan decreased resor!tion

!echanical failure or fracture

o Reaksireaksi tulang lainn&a terhada! disorders and in"uries$

#steoporosis * !arble $ones+

Acromegaly

#steoporosis *#steopenia+

%ickets in children( #steomalacia in adults.

&egenerative #steoarthritis

'ractures

(nfection

#steosclerotic Neoplasms %heumatoid Arthritis

#steolytic Neoplasms

•Bone 6ealing

o Formation of fracture hematoma$ Blood 4essels crossing the fracture line are broken. 's

blood leaks from the torn ends of the 4essels( a mass of blood *usuall& clotted+ forms

around the site of the fracture. #his mass of blood( called a fracture hematoma, usuall&

forms 7 to 8 hours after the in)ur&. 9welling and inflammation occur in res!onse to dead

bone cells( !roducing additional cellular debris. "hagoc&tes *neutro!hils and

macro!hages+ and osteoclasts begin to remo4e the dead or damaged tissue in and around

the fracture hematoma.

o 'ibrocartilaginous callus formation: Fibroblasts from the !eriosteum in4ade the fracture

site and !roduce collagen fibers. In addition( cells from the !eriosteum de4elo! into

chondroblasts and begin to !roduce fibrocartilage. #hese e4ents lead to the de4elo!ment

of a fibrocartilaginous )soft* callus, a mass of re!air tissue consisting of collagen fibers

and cartilage that bridges the broken ends of the bone. Formation of the fibrocartilagi

nous callus takes about weeks.

o $ony callus formation$ osteogenic cells de4elo! into osteoblasts( which begin to !roduce

s!ong& bone trabeculae. #he fibrocartilage is con4erted to s!ong& bone( and the callus is

then referred to as a bony )hard* callus. #he bon& callus lasts about to , months.

o $one remodeling $

#he final !hase of fracture re!air is bone remodeling of the callus.5ead !ortions of the original fragments of broken bone are graduall& resorbed b&

osteoclasts. 2om!act bone re!laces s!ong& bone around the !eri!her& of the fracture.



• &iaphyseal +ealing

o 9tage of 6ealing from 9oft #issue

#steogenic cells &ang ber!roliferasi dari la!isan dalam !eriosteum untuk membentuk

eternal callus dan to a lesser etent from endosteum untuk membentuk internal callus.

o 9tage of 2linical :nion

#em!orar& eternal and internal callus mengelilingi fracture site dan membentuk

;biological glue< &ang mem!erkeras saat cartilaginous components dari callus digantikan dengan tulang melalui osifikasi endokondral.

o 9tage of Radiogra!hic :nion

9eiring waktu ber)alan( the temporary callus digantikan oleh mature lamellar bone. "ada

saat tulang &ang belum matang telah digantikan oleh mature lamellar bone dan tulang

sudah kembali ke diameter &ang ham!ir normal( fraktur itu sudah bisa dikatakan

radiographic union.

• !etaphyseal +ealing

5iawali dengan !embentukan internal atau endosteal callus( walau!un eternal atau

periosteal callus &ang mengelilingi thin shell of corte )uga memegang !eran !enting.

/arena ban&akn&a su!lai darah !ada thin trabeculae dari cancellous bone sehingga ter)adisedikit necrosis tulang. #he #steogenic repair cells ber!roliferasi membentuk primary

woven bonedi internal fracture hematoma. 9aat telah ter)adi :nion( fraktur sudah clinically

united . =alu( woven bone digantikan oleh lamellar bone saat fraktur telah radiographic

united .

• Growth "late Reaction

o 'da basic wa&s$

Increased Growth$

Generali-ed$

Arachnodactyly * +yperchondroplasia+ * !arfan’s -yndrome+

ituitary /igantism

=ocali-ed$

Chronic (nflammation

&isplaced fracture of the shaft long bone

Congenital Arteriovenous !alformations

5ecreased Growth

Generali-ed$

Achndroplasia

ituitary &warfism * Lorain type+

%ickets

=ocali-ed$

&isuse retardation

0hermal (n"ury

(schemia

(nfection

#orsional Growth

=ocali-ed$ when a growing long bone and its e!i!h&seal !late are sub)ected to

either continual or intermittent twisting forces. %3$ /nock /nees

•Bone 5eformit&

o =oss of 'lignment$

#er)adi !ada long bone. Bisa karena twisted in its long ais *torsional deformity+ atau

karena crooked *angulatory deformity+.

o 'bnormal =ength



Bisa abnormally !endek atau meman)ang. /alau han&a ter)adi !ada salah stu kaki atau

salah satu tangan disebut limb length discrepancy.

o Bon& Outgrowth$ ' lesion( se!erti #steochondroma.

•Bone >eo!lasm

o >eo!lasmlike =esions of Bone

Osteogenic

Osteoma *i4or& e3ostosis+

9ingle Ostechondroma *osteocartilaginous e3ostosis+

Multi!le Osteochondroma *multi!le hereditar& Osteoma+

Osteoid Osteoma

Benign Osteoblastoma

2hondrogenic

%chondroma

Multi!le %chondromata *Ollier?s 5&schondro!lasia+

Fibrogenic

9ub!eriosteal cortical defect *meta!h&seal fibrous defect+

>onosteogenic fibroma *nonossif&ing fibroma+

Monostotic fibrous d&s!lasia

"ol&ostotic fibrous d&s!lasia

Osteofibrous d&s!lasia *2am!anacci s&ndrome+

;Brown tumor< *h&!er!arath&roidism+

'ngiogenic

'ngioma of bone *hemangioma and l&m!hangioma+

'neur&smal bone c&st *'B2+

:ncertain origin

9im!le bone c&st *:nicameral bone c&st *:B2++

o #rue "rimar& >eo!lasm of Bone

Osteogenic

Osteosarcoma *Osteogenic 9arcoma+

9urface osteosarcoma *!eriosteal sarcoma+

2hondrogenic

Benign chondroblastoma

2hondrom&3oid fibroma

2hondrosarcoma

Fibrogenic

Fibrosarcoma of Bone

Malignant fibrous histioc&toma of bone

'ngiogenic

'ngiosarcoma of bone

M&elogenic

M&eloma of bone *Multi!le m&eloma+

%wing?s sarcoma *%wing?s tumor+

6odgkin?s l&m!homa of bone

>on6odgkin?s l&m!homa *reticulum cell sarcoma+

9keletal reticuloses *=angerhan?s cell histioc&toses+

=eukemia

:ncertain origin

Giant cell tumor of bone *Osteoclastoma+



%. Muscle &hysiologya. #escribe the innervations of muscle and neuromuscular junction.

b. '"plain the physiology of muscle contraction



c. '"plain the mechanism of muscle growth (hypertrophy, atrophy,growth in length) and contracture.

i. #uscle 8ypertrophy- *erobic, short-duration, high intensity resistance training (weight li%ting)

results in muscle enlargement by increase in its diameter (hypertrophy)o% %ast, glycolytic bers during power%ul contractions.- #uscle enlargement by thickening o% myosin and actin lament,

allowing cross-bridge interaction and increase the muscle’s contractilestrength.

- $uring contraction, muscle ber triggers signaling proteins that turn ongenes to direct synthesis o% more o% these contractile proteins. 1hus, e"ercises with endurance compared to brie% periods are moreeBective.

ii. #uscle *trophy- Chen muscle is not in use, actin and myosin content decreases as its

bers becomes smaller and eventually atrophies and weaker.• $isuse *trophy

0ccurs when muscle is not in use %or a long time.D". when casting or brace is worn %or prolonged period.

• $enervation atrophy0ccurs a%ter nerve supply to a muscle is lost which can be treated bystimulation electricity, but this doesn’t %ully treat denervation. 1hus, muscle contraction is important as it activates *h %or nerves towork.



racture structural break in continuity.

*ypes of racture

$irection o% %racture

lines

1ransverse

0bli+ue

piral



omminuted

omminuted

(egmental)

omminuted (2utter=y)



6mpacted

*natomic location 'ro"imal#iddle$istal

*lignment ($egree o%

angulation o% distal

%ragment and pro"imal

%ragment)

Eood alignment

*ngulation

$isplacement 'artial apposition$isplaced$istracted

*ssociated so%t tissue

in&ury

losed (uncomplicated)

0pen (complicated)tability table

Unstable

S&'!+- '*'# /!*/'



!olles ractures results %rom %all on an outstretched hand, o%ten in osteoporotic

women. 1he de%ormed and pain%ul wrist looks like a Fdinner %orkG. 1he main lesion is a

dorsally displaced, dorsally angulated fracture of distal radius. 1reat with close

reduction and long arm cast.

Smith racture

mithHs %ractures are either e"tra or intraarticular. 1hese %ractures are essentially

inverted olleHs %racture since there is ape" dorsal angulation. 6% the %racture is

intraarticular, it is called a Barton's fracture.



Monteggia fracture result %rom direct blow to the ulna (such as on a raised

protective arm hit by a nightstick). 1here is diaphyseal fracture of the pro"imal

ulna, with anterior dislocation of the radial head.

0alea$$i fracture is the mirror image o% the previous one: the distal third of the

radius gets the direct blow and has the fracture, and there is dorsal

dislocation of the distal radioulnar joint. 6n both o% these, the broken bone o%ten

re+uires open reduction and internal "ation, whereasthe dislocated one is typically

handled with closed reduction.



I>*66I*6 0'DJ K*1UKD



Bone 6ealing "rocess



C*I1U 'DJLD#2U8*J

'erkins rules

• ractures o% cancellous (metaphyseal) bone (e.g. those around &oints) will take 7

weeks to unite.

• ractures o% cortical (diaphyseal) bone (e.g. sha%ts o% long bones) will take !

weeks to unite.

• ractures o% the tibia (because o% poor blood supply), will take ; weeks to

unite.

• 1ime to union %or children e+uals the age o% the child in years plus one, e.g.

tibial %racture in a -year-old child will unite in weeks. ommon sense needs to

be applied when applying the rule to %ractures o% cancellous bone in older

children.

$6*EJ06

M-ray (rule o% )

- views

- &oints

- limbs

- in&uries

- occasions

1KD*1#DJ1

!. >0D$ K*1UKD

a. Keduce

i. losed Keduction

ii. 0pen reduction

b. 8old Keduction

i. ontinuous traction

!. kin traction

. keletal traction

. i"ed traction (1homas plint)

;. 2alanced traction

3. ombined traction

ii. ast plintage

iii. unctional 2racing

iv. 6nternal i"ation

!. 6nter%ragmentary screw

. Cires (trans"ing, cerclage and tension band)



. 'lates dan screw

v. D"ternal i"ation

. 0'DJ K*1UKD

a. $ebridement

b. Cound closure

c. tabiliAation o% %racture

d. *%tercare

e. e+uels to open %racture

0#'>6*160J 0 K*1UKD

!. D*K>L 0#'>6*160J

a. Nisceral in&uryb. Nascular in&ury

c. Jerve in&ury

d. ompartment syndrome

e. 8emarthrosis

%. 6n%ection

g. Eas gangrene

h. racture blister

i. 'laster sores and pressure sores

. >*1D 0#'>6*160J

a. $elayed Union: %ailure o% union to occur in !.3 times the normal time %or

%racture union.

b. Jon-Union: %ailure o% union to occur within times the normal time to

%racture union. 8owever, e"pect open %ractures to normally take times

the normal 'erkins rule. Jon-union can be broadly divided into:

i. hypertrophic: normally due to e"cess mobility, i.e. good healing

potentialO

ii. atrophic: normally due to poor blood supply, i.e. poor healing

potential.

c. #al-Union

d. *vascular Jecrosis

e. Erowth $isturbances epiphyseal %racture in children

%. 2ed ores elderly/paralyAed patients

g. #yositis ossicans heterotopic ossication in the muscle

h. 1endon lesion

i. Jerve compression



&. #uscle contracture

k. @oint instability

l. @oint stiBness

m. *lgodysthropy (omple" regional pain syndrome)

0steoarthrytis

rangkuman week 1 (pbl) - fracture

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