Brainscape's Knowledge GenomeTM

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


See full index

Year 5 Path Histopathology > Non-neoplastic Bone > Flashcards

Non-neoplastic Bone Flashcards

1
Q

What is the main function of osteoblasts?

A

Bulit + lay down of Bone

Osteo B lasts B uilt bone

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

What is the main function of osteoclasts?

A

Resorb bone

Multinucleate cells of macrophage family

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

In What categories can metabolic bone disease be classified (different aetiologies) ?

A
  1. non-endocrine (e..g age-related osteoporosis)
  2. Related to endocrine abnormality
  3. Disuse osteopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the usual aetiology of osteoporosis?

A

Age related (post-menopausal/ age)
or secondary to systemc diseases/ drugs (steroids!)

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

What is the pathophysgioloy of osteoporosis?

What test would you do and what do you expect?

A

Different processes leading to
↓bone mass

DEXA scan: T score > 2.5 SD below normal (1-2.5 = osteopaenia)

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

What are the typical clinicla features of osteoporosis?

A

Low impact fractures (#)
(hip - NOF, vertebrae; wrists - Colles’)

Pain (back) (vertebra # +/- nerve pain)

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

What are the expected x-ray changes in a patient with osteoporosis?

A

None

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

What does histology of osteoporosis show?

A

Loss of calcellous bone

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

What is osteomalacia/ rickets? (pathophysiology)

A

Overall calcium deficiency leading to
Reduced bone mineralisation

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

What are characteristic features of osteopenia on X-ray?

A

Looser’s zones
(pseudo-fractures)

Splaying of metaphysis

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

What are histological features of osteomalcia and rickets?

A

Excess of unmineralized bone (osteoids)

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

What are the biochemical findings of Osteomalacia/ Rickets?

A

Normal/ Low calcium
Low Po4
High ALP

Explanation:
Overall calcium is low –> activation of osteoclasts and increased bone resobtion to even out low calcium (can be corrected to normal biochemical levels and explains the high ALP due to high bone turnover)

Phosphate is low due to incereased renal excretion of phosphate due to higher PTH levels

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

What are the causes of primary hyperparathyroidism?

A

Parathyroid adenoma
Parathyroid hyperplasia
carcinoma
MEN

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

What are the symptoms of primary hyperparathyroidism?

A

Symptoms of Hypercalcaemia

Moans (abdominal pain), constipation
Stones: renal stones
Bone pains + fractures
Groans: psychological changes (depression, confusion)

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

What are common x-ray changes of Primary hyperparathyroidism?

A

Brown’s tumours
(collection of multinucleate giant cells)

Salt and pepper skull
Subperiosteal bone resorption in phalanges

Brow’s tumour

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

What is osteitis fibrosa cystica?

A

A rare skeletal disorder seen in advanced hyperparathyroidism characterized by replacement of calcified bone with fibrous tissue

(Most often seen in primary Hyperparathyroidism)

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

What are the biochemical findings in primary hyperparathyroidism?

A

High calcium
Low/Normal P04
High/normal ALP
High/ normal PTH (inappripriartely normal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the disease features of Paget’s disease of the bone?

A

Idiopathig high bone turnover

Seeing initally increased lysis (lytic lesions), then mixed (lytic + sclerotic) and sclerosis (sclorotic lesions)

18
Q

What are the symptoms of Paget’s disease?

A

Bone pain
Microfractures
Nerve compression (due to expansion of bone: sensorineural hearing loss, sciatica)

infreased head size
high output cardiac failure

19
Q

Whatare histological findings of Paget’s disease of the bone?

A

Huge osteoclasts
w > 100 nuclei Mosaic pattern of lamellar bone (like jigsaw puzzle)

20
Q

What are the biochemical findings of Paget’s disease of the bone?

A

Normal Calcium, Normal phosphate

High ALP

21
Q

What are the 4 stages of bone repair (after #)?

A
  1. Organisation of haematoma (pro-callus)
  2. Formation of fibrocartilaginous callous
  3. Mineralisation of fibrocartilaginous callous
  4. remodeling of bone among weight bearing lines
22
Q

What are the most common site of infection for osteomyelitis?

A

Vertebrae
Jaw (dental abscess)
toe (diabetic ulcers)
Long bones

23
Q

Whatare the expected X-ray changes in osteomyelitis?

A

Early: sub-periostel new bone formaion

Later (10 days) lytic destruction of bone

24
Q

What is the most common organism causing Osteomyelitis in adults?

A

S.aureus

25
Q

What is the most common organism causing osteomyelitis in children?
What bone are more commonly involved?

A

Haemophilus influenza
Group B strep

often affecting long bones

26
Q

Which orgnaisms cause osteomyelsitis in the following patient populations
1. SIckle cell patients
2. Immunocompromised
3. Congenital osteomyelitis

A
  1. Sickle cell - Salmonella
  2. Immunocompromised -TB
  3. Congenital - Syphilis
27
Q

What are the expected X-ray changes of Osteoarthritis?

A

LOSS

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

28
Q

What chagnes of the Hands can be seen in a patient with Osteoarthrits?

A

Hberden’s nodes (DIPJ)
Bouchard’s nodes (PIPJ)

29
Q

What are common x-ray changes see in Rheumatoid arthritis?

A

Early: juxta-articular osteopenia

Later: joint space narrowing, marginal erosions of cartilage and bone, osteopenia (generalized), subchondral cysts

30
Q

What would a hand-exmaination of a patient with RA show?

A

Overall DIPJ sparing

Radial deviation of wrist and ulnar deviation of fingers

  • “swan neck” and “Boutonniere” deformity of fingers
  • Swan neck = hyperextension of PIPJ & flexion of DIPJ
  • Boutonniere = flexion of PIPJ & hyperextension of DIPJ
    ● “Z” shaped thumb
    ● Synovial swelling
31
Q

What are histophatologicla findings of Rheumatoid Arthritis?

A

thickening of synovial membran
hyperplasia of surface synoviocytes
intense inflammatory cell infiltrate & fibrin deposition & necrosis

32
Q

What is the epidemiology in Gout compared to pseudo-gout?

A

Gout: middle aged-obese men
Pseudo-grout: Women >50

33
Q

What joints are most commonly affected in a patient with gout?

A

Acute monoarthritis

  • Classically 1st MTP (big toe)
  • Precipitated by
    trauma/infection

Although there is a chronic form that is polyarticular: Chronic tophaceous gout

34
Q

What are classical features of Chronic tophaceous gout?

A
  • Polyarticular arthritis
  • Tophi deposits in ear lobes, fingers and elbows
  • Urate kidney stones
35
Q

What joints are commonly affected in pseudo-gout?

A

Acute monoarthritis

  • Knee and shoulder
  • Precipitated by
    trauma/infection

Chronic

  • Polyarticular arthritis
36
Q

How would gout and pseudo-gout differentiated on an x-ray?

A

In gout: rat-bite erosions

Pseudogrout: Chondrocalcinosis on X-ray

37
Q

What would the crystals look in gout and pseudo-gout?

A

Gout: Urate crystals, needle shaped - negatively bierefringent

Pseudo-gout: Calcium pyrophosphate crystals,
rhomboid shaped - positively bierefringent

38
Q

How is an acute attack of gout managed?

A

Colchicine (+NSAIDs)
(Rest + ice affected joint)

binds and stabilizes tubulin subunits → inhibits microtubule polymerization → inhibits phagocytosis of urate crystals, neutrophil activation, migration, and degranulation

39
Q

How is gout chronically managed?
What is the MOA?

A

Allopurinol
Inhibition of xanthine oxidase → hypoxanthine and xanthine are not degraded into uric acid

Conservative: ↓ETOH and purine intake e.g. sardines, liver

40
Q

How is pseudo-gout managed?

A

NSAIDs or intra-articular steroids

41
Q

What is the aetiology of pseudo-gout?

A

The primary (idiopathic) form is most common, risk Factor: age

Secondary forms

  • joint trauma/ damage, e.g. surgery, JIA, OA
  • Metabolic: Hyperparathyroidism, haemochromasism others
  • Familial chondrocalcinosis
42
Q

What are different aetiologies of pseudo-gout?

A
  1. increased production: tumour lysis syndrome, inherited metabolic abnormalities
  2. Increasd intake: high dietary, alcohol intake
  3. Decreased excretion: diuretics

Year 5 Path Histopathology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions