Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology 205 > bones > Flashcards

bones Flashcards

1
Q

COMPONENTS of the Bone

A 
CELLS
Osteoblasts
Lay down osteoid
PTH, Vit C, Vit D
Osteocytes
PTH, Vit D, Calcitonin
Osteoclasts
Howship’s lacunae (microscopic bone concavities due to bone resoprtion)
PTH, Vit D, Calcitonin, PG2, etc.
MATRIX!!! (first thing)
Collagen
Glycoproteins
Mineral
Calcium hydroxyapatite
Non-mineralized matrix may be called “osteoid”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 areas of the bone

A

epiphysis (end),
metaphisis (inbetween)
diaphysis (middle part of bone (longest part/ shaft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epiphysis

A

covered by cartlidge- form joint with other bone joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

diaphysis

A

lenthg and strenghs- center in mostly hollow and bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

metaphysis

A

blood supply comes in and gives it to other areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

epiphyseal growth plate

A

the way the long bones growth- lay down the cartiledge (first) that gets converted to the bone
endocontral osification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

first step

A

lay down collagen (osteoite)and sprinkle calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

osteoid

A

first step in bone formation where it is just collagen before calcium has been sprinkled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what lays down ca

A

osteoblast make osteoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

mature osteoblasts

A

osteocytes (function depends on hormones and vit c, d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

osteoclasts

A

remodeling bone- eat away part of the bone so that osteoblaste replace it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

is bone fixed

A

no-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Achondroplasia

A

Defect of endochondral ossification
Causes dwarfism
Growth of the long bones is retarded: Short legs, short arms but normal trunk
Autosomal dominant
lack of endocartiocarcitofication- short bones are made by different process so are ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Osteogenesis Imperfecta(defective bone formation)

A

Basic problem: Mutations in gene encoding collagen I (which is the principal component of osteoid).
Autosomal recessive or dominant

Age of presentation depends upon the extent of gene defects
Some born with multiple fractures, others develop symptoms in childhood , puberty or later.

Other defects
Blue sclerae (eye whites)
Think skin
Thin dental enamel

weak bones- not enough collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Osteopetrosis

A

don’t need to know

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Osteomyelitis

A

Bacterial infection of bone
Causes
Pyogenic cocci: Staph aureus.
Mixed flora ( drug addicts)
TB
Usually presents as acute infection which may progress to chronic
Starts with hematogenous deposit of Staph in metaphysis
PMN’s attracted, forming pus
Pus spreads into epiphysis, and through compact bone under periosteum
Sequestra: devitalized bone fragments cut off from blood supply
Involucrum: reactive bone formed to wall off infection
can go to diaphysis area (mostly hollow) can take over it
becomes necrotic- sequestral

17
Q

Osteoporosis(thin bones)

A

enough calcium and collagen just less so prone to breaks
Bone is normal but thinned out (less than normal tissue density)
Absolute reduction of total bone mass
1/3 of women > 65 years are affected
Causes
Primary – disease of elderly
Secondary
Hormonal problems ( thyroid,  cortisol,  estrogen)
Dietary (calcium, vitamin C)
Immobilization
Drugs (anticonvulsants, heparin)
Pathogenesis
Loss of bone matrix !!!and mineral
After age 30y, bone loss exceeds formation
After menopause in women, bone loss accelerates 5-fold ( due to loss of estrogen)

18
Q

Osteoporosis(thin bones)- pathlogy

A 
Pathology
Thin, brittle, prone to fracture
Type I (postmenopause)
Trabecular bone 			(vertebrae, wrist)
Type 2 (old age)
Cortical & trabecular bone of long bones (e.g., neck of femur)
19
Q

Osteoporosis(thin bones)

A 
Clinical Features
Vertebral fractures (crush Injury)
Back pain,  kyphosis
Fracture of neck of femur
Incapacitation
> 1 Million/year in USA
20
Q

Osteomalacia soft bones

A

Bone is abnormal (i.e., normal tissue present but not calcified)
Inadequate mineralization of organic matrix
Caused by disturbance of vit. D or PO4 metabolism
Called “rickets”!!!! (word in kids) in young people
Causes
Vitamin D deficiency
Inadequate intake
Inadequate exposure to sunlight
Intestinal malabsorption
Hypophosphatemia
Malabsorption
Excess loss of PO4

enough collagen but not of anything else
enough osteoites
not enough calcium -no sprinkling

21
Q

Osteomalacia and Rickets

A

lowAbsorption of calcium + PO4 in intestines leads to increase in Urinary PO4 loss leads to increase Bone resorption
Loss of minerals  leads bone softening
 compensatory new bone formation (without mineralization) called osteoid

Children: New bone formation is affected in children
Growth retardation
Including delayed dentition
Deformities
Bow legs
Pigeon breast
Rachitic rosary (enlarged costochondral junction – excess osteoid)
Adults and Children
Fractures
Muscle spasms (tetany)
22
Q

Fractures

A

Disruption of bony continuity from mechanical stress
Simple – one fracture line; bone not exposed to environment
Compound – one fracture line; bone exposed to environment
Comminuted – several fragments
Complete – Cortex to cortex
Incomplete – part way through bone (also called “greenstick”)
CLOSED fractures are when skin is not broken

23
Q

simple

A

one fracture line; bone not exposed to environment

24
Q

compound

A

– one fracture line; bone exposed to environment

25
Q

Comminuted

A

several fragments

26
Q

Complete

A

Cortex to cortex

27
Q

Incomplete

A

– part way through bone (also called “greenstick”)

28
Q

Cause of fracture?

A

Traumatic – obvious physical cause

Pathologic – Fracture through pre-existing disease in bone (e.g., tumour, osteoporosis)- don’t need a lot of force to break

29
Q

Fracture Healing

A

Hematoma fills and surrounds injured area
Clotted blood seals off farcture site
Clot organizes to soft tissue pro-callus
Conversion to new formed fibrocartilaginous callus by one week)
Replacement by bony provisional callus – this creates spindle-shaped splint maximum at 2-3 weeks
Callus strengthened by widening of bone spicuels
Remodeling (final stage)with osteoclastic and osteoblastic activity

get a callus- healy of the fracture

30
Q

fracture treatment

A 
Treatment
Immobilization of Fracture
Reconstruction of any gap
Debridement 			 (removal of necrotic tissue)
Immobilization (pins +/or plates)
Factors that delay healing
Nutrition
Vitamins C & D, Calcium, PO4
Infection
Foreign Bodies
Failure of immobilization   leads to Fibrous non-union leads to	  Pseudoarthrosis (false joint)
31
Q

Bone Tumors

A

know osteosarcoma

seen in younger men and not good tumor

32
Q

osteosarcoma

A 
Most Common
Metaphysis of long bones of extremities (50% in Knee)
Young persons (rare in adults)
Rx: surgery & chemotherapy
5 year survival: 30%
33
Q

Osteoarthritis

A 
Degenerative joint disease
Wear and tear of the articular cartilage
Cartilage shows 
Softening 
Surface defects 
Irregular thinning -> fibrillation & vertical clefts
Denuded bone ->  eburnation (polished bone)
Bone degeneration ->		      bone cysts
Spicules of new bone (osteophytes)

affects the joint

without the cartilidge there is rubbing which may lead to broken down bones
try to regrown = sclerotic bone

34
Q

3 main

A

thinkening of the bone
thinned cartelidge
bone defect
broken down fragments of cartiledge

35
Q

osteophytes

A

new bones forming

36
Q

Clinical Features

osteoarthristis

A

Clinical Features
Weight-bearing (hip, knees, spine) and small joints of hands are affected
Pain & stiffness (in morning especially) (lasting 15 - 20 min)
 Mobility & deformity
Crepitus (grating on movement can hear about it)
Swelling & warmth (2º Inflammation)
Heberden’s nodes: osteophytes ( bony spicules)- bumpy on hands

ULNAR DRIFT IS NOT SEEN

37
Q

Heberden’s nodes

A

osteoarthritis

38
Q

Rheumatoid Arthritis

A

Chronic systemic disease of unknown etiology
Systemic autoimmune disease affecting synovial joints
Chronic symmetric inflammation
Affects women more (M:F::1:4)
Affects 1% of population

Synovitis – exudation of fluid & inflammatory cells into joint
Ingrowth of vessels & synovial cells->  granulation tissue (pannus)
Pannus secretes lytic enzymes & inflammatory mediators -> destruction of cartilage & erosion of bone
Joints immobilized
Intra-articular space obliterated ->  ankylosis

Insidious onset
Systemic disease with fever, malaise, anemia etc.
Symmetrical involvement of small joints
Hand: PIP, MP
Wrist
Elbow & ankle also common
May be juvenile or adult
10% of adults   severe disability
50% of children  severe disability
Complications
Joint deformities
Contractures
E.g., ULNAR DRIFT
Subcutaneous nodules
Fibrinoid necrosis surrounded by macrophages and lymphocytes
Lungs 					      Interstitial & pleural fibrosis
Eyes, heart, vasculature

Pathology 205 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions