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Medicine - Year 1 > Fractures & Dislocations - Pathology > Flashcards

Fractures & Dislocations - Pathology Flashcards

1
Q

a) Name the reversible injures a cell can undergo
b) Name the irreversilbe injuries a cell can undergo

A

a)

  • Adaptation
  • Normal cell

b)

  • Necrosis
  • Apoptosis
  • Necroptosis & Pyroptosis
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2
Q

a) What are the features of Necroptosis?
b) What are the features of Pyroptosis?
c) When and how does pyroptosis occur?

A

a) Has features of both necrosis and apoptosis

b) Pyroptosis is a mixture of pyrexia (abnormal rise of body temp)and apoptosis

c) Happens in inflammation through activation of inflammasone and is associated with pyrexia (fever) due to release of interleukin 1

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3
Q

What are the characteristics of reversible cell injury?

A
  • Cell swelling
  • Fatty change
  • Eosinophilia (higher than normal levels of eosophils)
  • Cell membrane blebbing/ blunting/ loss of microvilli
  • Mitochondrial swelling
  • Dilation of endoplasmic reticulum with detachment of ribosomes
  • Chromatin clumping – nuclear alterations
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4
Q

a) What is cell adaptation?

b) What are the types of cell adaptation?

A

a) Reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environments

b) Hypertrophy, Hyperplasia, Atrophy, Metaplasia

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5
Q

Describe hypertrophy

A
  • Increase in the size of cells that cause an increase in the size of the affected organ
  • May be physiological or pathological
  • Related to increased workload
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6
Q

Muscles have a limited capacity for division. When do they undergo hypertrophy?

A

In response to increased workload

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7
Q

a) Provide an example of where physiological hypertrophy seen?

b) Provide an example of where pathological hypertrophy most seen?

A

a) Can be seen in the uterus during pregnancy

b) Most seen in the myocardium in the context of hypertension or valvular heart disease

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8
Q

Describe hyperplasia

A
  • Increase in the number of cells in an organ/tissue in response to a stimulus – usually a hormone or growth factor
  • Can only take place if the cells are capable of dividing
  • Can be physiological or pathological
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9
Q

Provide 3 examples of hyperplasia

A
  • Number of breast cells increase during pregnancy to make more breast milk.
  • The remaining liver will undergo hyperplasia if a lobe is resected, restoring the original size of the organ
  • If blood is lost, the growth factor, erythropoietin causes bone marrow hyperplasia increasing the production of red blood cells by 8 folds.
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10
Q

Which two adaptations can take place together?

A

Hypertrophy and hyperplasia

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11
Q

Describe pathological hyperplasia

A
  • Excessive or inappropriate actions of hormones or growth factors acting on target cells
  • Growth factors can drive mature cells or can increase output of new cells from stem cells
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12
Q

a) What is a stimulus of hyperplasia

b) What occurs when the stimulus is removed?

A

a) Hormones and Growth factors

b) Hyperplasia regresses

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13
Q

Describe atrophy

A
  • Reduction in the size of an organ or tissue due to a decrease in cell size and number
  • Can Physiological and pathological
  • Decrease in cell size and decrease in size of organelles
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14
Q

a) What pathway is activated in atrophy?

b) What natural celluar mechanism is activated in atrophy? and desrcibe what it is

A

a) Ubiquitin-proteosome pathway

b) Autophagy - cell eating its own organelles to reduce nutrient demand and meet the supply

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15
Q

Give 6 examples where pathlogical atrophy occurs

A
  • Disuse atrophy
  • Denervation atrophy
  • Diminished blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure atrophy
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16
Q

Describe disuse atrophy

A
  • Prolonged bed rest can lead to skeletal muscle atrophy due to disuse (disue atrophy)
  • This can be accompanied by osteoporosis
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17
Q

Describe denervation atrophy

A

Damage to nerves supplying a muscle

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18
Q

Give an example of diminished blood supply causing atrophy

A

Atherosclerosis of blood vessels ( where arteries become clogged with fatty substances called plaques/atheroma) can cause atrophy

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19
Q

Describe malnutrition causing atrophy

A

Body uses skeletal muscle as a source of protein as fat is depleted causing cachexia/muscle wasting

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20
Q

Describe pressure atrophy

A

An expanding tumour can put pressure on blood vessels causing atrophy of tissues supplied by those vessels

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21
Q

Describe loss of endocrine stimulation atrophy using the example osterogen

A

Loss of the hormone oestrogen can cause atrophy of the female genital tract and breast

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22
Q

Desrcibe metaplasia

A

A reversible change in which one differentiated cell type is replaced by another cell type

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23
Q

a) What types of response is metaplasia?
b) What is the repacememnt cell able to do in context of the adverse environmrnt?

A

a) An adaptive response
b) The replacement cell type is able to withstand the adverse environment

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24
Q

What is metaplasia caused by?

A

Reprogramming of stem cell

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25
Q

a) What is dysplsia?
b) What can occur if dysplasia progesses over time

A

Disordered growth in the epithelium

b) Invasive carcinoma

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26
Q

a) Where is the site of squamous metaplasia?

b) What stimulus causes squamous metaplasia?

c) What is the native cell? and what is the metaplastic cell (replacement cell)?

d) What is the tumour risk?

A

a) Respiratory tract

b) Cigarette smoke

c) Native cell: columnar cell

Metaplastic cell: squamous cell

d) Squamous cell carcinoma

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27
Q

a) Where is the site of intestinal metaplasia?

b) What stimulus causes intestinal metaplasia?

c) What is the native cell? and what is the metaplastic cell (replacement cell)?

d) What is the tumour risk?

A

a) Lower oesophagus

b) Acid reflux from stomach

c) Native cell: squamous cell

Metaplastic cell: goblet cell

d) Adenocarcinoma

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28
Q

a) Describe necrosis

b) What is necrosis caused by?

A

a)
- Accidental/ unregulated form of cell death
- Damage to membranes and lysosomal enzyme digestion of cell
- Leakage of cell contents causing inflammatory reaction
- Passive process
- Always pathological

b) Caused by ischaemia, toxins, infections, trauma

29
Q

Describe the role of mitochondrial damage in necrosis

A

Causes formation of a channel in the mitochondrial membrane called the mitochondrial permeability transition pore (MPTP)

This leads to a loss of mitochondrial inner membrane potential and that leads to failure of oxidtive phospharylation and eventually mitochondrial swelling and rupture

30
Q

Describe the role of calcium influx in necrosis

A

Opens the mitochondrial permeability transition pores which leads to depeletion of ATP and can also activate enzymes causing membrane, protein, nuclear and DNA damage

31
Q

Describe apoptosis

A
  • A cell death pathway that’s induced by tightly regulated suicide programme in which cells destined to activate enzymes that can degrade the cells own DNA and proteins
  • Damage to either DNA or proteins
  • Cell kills itself by dissolving nucleus and fragmenting its cytoplasm – no loss of membrane integrity
  • No inflammatory reaction
  • Serves many normal functions
  • Active process
32
Q

What are the two apoptosis initiation pathways?

A
  1. Intrinsic (mitochondrial) pathway
  2. Extrinsic (death receptor initiated) pathway
33
Q

Describe the intrinsic (mitochondrial) pathway

A
  • Triggered by cell injury, DNA damage or decreased hormonal stimulation
  • Inactivation of BCL-2 (anti-apoptotic molecule)
  • Lack of BCL-2 allows cytochrome c to leak from the inner mitochondrial matric into the cytoplasm and activate caspases (proteases which can breakdown cell proteins)
  • Initiator = caspase 9
34
Q

What is the intrinsic pathway triggered by?

A

Cell injury, DMA damage or decreased hormonal stimuli

35
Q

What is the initiator of the intrinsic (mitochondrial) pathway?

A

Caspase 9

36
Q

Describe the extrinsic (death receptor initiated) pathway

A
  • Activated by FAS ligand, binds FAS death receptor (CD95) on the target cell, activating caspases
  • Triggered by Tumour Necrosis Factor (TNF) binds TNF receptor on target cell receptor, activating caspases
  • Initiators = caspase 8 (activation blocked by FLIP) + caspase 10
37
Q

What is the extrinic (death receptor initiated) pathway triggered by?

A

FAS ligand

Tumour necrosis factor (TNF)

38
Q

What are the initiators of the extrinsic (death receptor initiated) pathway?

A

Caspase 8

Caspase 10

39
Q

Describe the differences between necrosis and apoptosis

A

Necrosis - Passive process

Apoptosis - Active process

40
Q

List the functions of bone

A
  • Mechanical support
  • Transmisson of forces generated by musles
  • Protection of vital organs
  • Mineral homeostasis
  • Production of blood cells
41
Q

Label the structures of the bone

A
42
Q

What two types of bone can be seen under the microscope?

A

Woven and lamellar

43
Q

How is woven (primary - spongy) bone made?

A

When bone is being made rapidly, type 1 collagen fibres are laid down and then mineralised as crisscross woven bone

44
Q

a) Describe the structure of collagen fibres in lamellar (compact) bone
b) How does this help bone?

A

a) The collagen fibres are nearly parallel. They run in opposite directions in alternating layers of lamellar bone
b) This helps the bone resist torsion forces

45
Q

What are the differences between woven bone and lamellar bone?

A

Woven bone

  • Made rapidly (such as in the unborn child, a healing fracture or in some diseases)
  • Type I collagen fibres are laid down and then mineralised as criss-cross woven bone
  • This is able to withstand stress equally well in all directions.

Lamellar bone

  • The collagen fibres are nearly parallel
  • Takes longer to make but is much stronger.
  • The collagen fibres run in opposite directions in alternating layers of lamellar bone, helping the bone to resist torsion forces
46
Q

What are the two ossification methods by which bone normally forms?

A
  • Intramembranous ossification
  • Endochondral ossification
47
Q

a) Describe endochondral ossification
b) Give some examples of bones which form by this method.

A

a)

  • In endochondral ossification, bone develops by replacing hyaline cartilage.
  • Cartilage serves as a template to be completely replaced by new bone (and this takes much longer than intramembranous ossification)

b) Bones at the base of the skull and long bones form via endochondral ossification.

48
Q

a) Describe intramembranous ossification
b) Give an example of bones which form by this method.

A

a) During intramembranous ossification bone develops directly from sheets of mesenchymal (undifferentiated) connective tissue.
b) The flat bones of the face, most of the cranial bones and the clavicles (collarbones) are formed via intramembranous ossification.

49
Q

Describe the structure of an osteon/Haversian system.

A
  • Compact bone is organized as parallel columns known as Haversian systems or osteons which run lengthwise down the axis of long bones
  • These columns are composed of lamellae - concentric rings of bone surrounding a central channel or Haversian canal that contains nerves blood vessels and the lymphatic system of bone.
  • The parallel Haversian canals are connected to one another by the perpendicular Volkmann’s canals.
50
Q

How do osteocytes communicate with the haversian canal?

A

Osteocytes communicate with the haversian canal through cytoplasmic extensions that run through canaliculi (small interconnecting canals)

51
Q

Describe the bone remodelling process

A
  1. Activation - Osteoclast precursors arrive at bone surface and differentiate into mature osteoclasts
  2. Absorption - Mature osteoclasts secrete acid and proteases onto bone surface, excavating a pit known as Howship’s lacuna. Absorption phase ends with osteoclast apoptosis
  3. Reversal - Osteoblasts activated and replace excavated bone
  4. Formation - Newly secreted matrix called osteoid becomes mineralised to form mature bone
  5. Termination - Cycle end when new bone is complete
  6. Quiscence - Osteoblasts are incorporated into new bone as osteocytes or become quiescent surface bone lining cells
52
Q

Describe how osteoprotegrin (OPG) is involved in osteoclast regulation

A

Stromal cells also secrete osteoprotegrin (OPG) which acts as an inhibitor for RANKL preventing it from binding the RANK receptor on osteoclast precursors

Therefore OPG prevents bone resorption by inhibiting osteoclast differentiation.

53
Q

What systemic factors can affect the RANK:OPG ratio?

A

Systemic factors that affect this balance include horomes, Vitamin D, inflammatory cytokines (e.g., IL-1) and growth factors

54
Q

a) Describe the effect parathyroid hormone (PTH) has on osteoclast differentiation and bone turnover

b) Describe the effect steroids have on osteoclast differentiation and bone turnover

c) Describe the effect bone morphogenetic proteins (BMPs) have on osteoclast differentiation

d) Describe the effect sex hormones have on osteoclast differentiation

A

a) Promote osteoclast differentiation and bone turnover.

b) Promote osteoclast differentiation and bone turnover.

c) Inhibit osteoclast differentiation or activity by favouring OPG expression

d) Inhibit osteoclast differentiation or activity by favouring OPG expression

55
Q

Describe fracture healing (stage 1 and 2)

A

Fracture healing stage 1

  1. Inflammatory phase
    - Formation of haematoma which fills the fracture gap
    - The blood clot provides a fibrin mesh to seal the fracture site
  2. Reparative phase
    - Degrandulating platelets and inflammatory cells release platelet derived growth factor (PDGF), transforming growth factor beta (TGF-B), fibroblast growth factor (FGF) and other factors which activate osteoprogenitor cells in the periosteum, medullary cavity and surrounding soft tissue. This stimulates osteoclast and osteoblast activity
    - End of 1st week = soft callus/procallus (mass of mostly uncalcified tissue which provides anchorage between the ends of the fractures bones)
    - End of 2nd week = soft callusis transformed into bony callus
  3. Remodelling phase
    - The activated osteoprogenitor cells deposit woven bone
    - In some cases, the activated mesenchymal cells in the soft tissues and bone surrounding the fracture line also differentiate into chondrocytes that make fibrocartilage and hyaline cartilage
    - The newly formed cartilage along the fracture line undergoes endochondral ossification (to form a contingous network of bone and newely deposited bone trabeculae in the medulla and beneath the periosteum)
    - In this way, the fractured ends are bridged

Fracture healing stage 2
- As the callus matures and subjected to weight-bearing forces portions that are not physically stressed are resorbed
- This remodelling reduces the size of the callus until the shape and outline of the fractures bone are re-established as lamellar bone
- The healing process is complete with restoration of the medullary cavity

56
Q

Describe bone issues that can cause impaired healing

A

Displaced/comminuted fractures - lead to deformity

Inadequate mobilisation - prevents normal callus maturation causing delayed union or non-union

Non-union - Malformed callus can undergo cystic degeneration and become lined by synovial-like cells, creating a false joint (pseudo-arthrosis)

Open-fractures - risk of infection

Malnutrition and skeletal dysplasia

Myoglobinuria - occurs if there has been significant muslce injury

Fat emboli - can cause petechial haemorrhages , cerebral ischaemia and/or pulmonary insufficiency

57
Q

a) What is osteonecrosis

b) List some risk factors

c) What are some major complications of osteonecrosis?

A

a) Ischaemic necrosis of bone and bone marrow

b)

  • Alcohol abuse
  • Bisphosphonate therapy (jaw bones)
  • Connective tissue disorders
  • Steroid treatment
  • Chronic pancreatitis
  • The ‘bends’
  • Gaucher disease
  • Infection
  • Pregnancy
  • Radiotherapy
  • Sickle cell disease
  • Trauma
  • Tumours

c) Osteoarthritis and fractures

58
Q

a) What is osteomyeleitis

b) Who is it often seen in and where in the body?

c) What type of organism is it usually caused by and how?

d) What is the most common organism causing osteomyeleitis

e) In adults, which part of the body does haematogenously spread osteeomyelitis usually affect

f) Which organisms can cause haematogenous
osteomyellitis in patients who are immunosuppressed?

g) What may you see on x-ray

h) What develops if treatment of acute osteomyelitis is only partially successful?

A

a) Infection of bone or bone marrow

b) Children and metaphysis of femur, tibia and humerus (long bones)

c) Usually bacterial - hematogenous spread

d) Mostly caused by staphylococcus aureus

e) Vertebrae

f) Fungi and mycobacterium

g) Lytic focus and sclerosis

h) Chronic osteomyelitis develops

59
Q

a) What are the clinical features of acute osteomyelitis?

b) What are the clinical features of chronic osteomyelitis?

c) What are the risk factors?

A

a) Fever, pain, swelling, erythema of the affected site.

b)
- A long history of pain
- Persistently draining sinus tract or wound, and soft tissue damage.
- Risk factors such as diabetes and PVD also increase the likelihood of this

c)
- Diabetes melitis
- Peripheral vascular disease
- Malnutrition
- Immunosuppression
- Malignancy
- Extremes of age
- Local factors e.g chronic lymphedema, vasculitis, neuropathy etc.

60
Q

a) Describe the definite and supportive diagnostic tests for osteomyelitis

b) Describe the managment for osteomyelitis

A

a))

Definitive diagnosis
- Bone biopsy (for pathology and culture)

Supportive diagnostic tests
- Blood inflammatory markers,
- X-ray: may be negative early on as periosteal reaction cannot be seen until about 7 days and bone necrosis after 10 days. It is useful in the diagnosis of chronic osteomyelitis
- MRI: good for viewing bone and soft tissue. Imaging modality of choice.
- CT: good for identifying necrotic bone and for guiding needle for biopsy.
- Blood cultures, and culture of any expressed pus (but note that samples from sinus tracts are unreliable)

d) Antibiotics for a minimum of 4-6 weeks, surgical debridement

61
Q

List four factors which predispose to osteomyelitis.

A
  1. Trauma.
  2. Ischaemia.
  3. Presence of foreign bodies.
  4. Pressure ulcers.
62
Q

What is an osteoid?

A

Osteoid is unmineralized bone matrix and is composed of type I collagen and glycosaminoglycans (GAGs)

63
Q

Describe the layers of a long bone beginning at the external surface and moving towards the centre of the bone.

A

The layers of a long bone, beginning at the external surface are:

  1. Periosteum.
  2. Outer circumferential lamellae.
  3. Compact bone (Haversian systems).
  4. Inner circumferential lamellae.
  5. Endosteal surface of compact bone.
  6. Trabecular bone.
64
Q

Describe the regulation of osteoclast activity by the Receptor Activator of Nuclear Factor Kappa Beta (RANK) and Osteoprotegrin (OPG)

A

RANK ligand binds to its receptor RANK located on the cell surface of osteoclast precursors.

This interaction, in the background of macrophage colony-stimulating factor (M-CSF), causes the precursor cells to produce functional osteoclasts.

Stromal cells secrete osteoprotegrin (OPG) which prevents RANKL, from binding to the RANK receptor on osteoclast precursors.

Consequently OPG prevents bone resorption by inhibiting osteoclast differentiation.

Bone resorption or bone formation can be favoured by altering the RANK:OPG ratio.

Parathyroid hormone and steroids promote osteoclast differentiation and bone turnover.

In contrast, bone morphogenetic proteins and sex hormones block osteoclast differentiation or activity by favouring OPG expression.

65
Q

What would you see if you examined a fracture under the microscope on day 1?

A

An organising haematoma.

66
Q

What would you see if you examined a fracture after 2-3 weeks?

A

The soft callus is transformed into bony callus.

The activated osteoprogenitor cells deposit woven bone.

In some cases the activated mesenchymal cells in the soft tissues and bone surrounding the fracture line also differentiate into chondrocytes that make fibrocartilage and hyaline cartilage.

The newly formed cartilage along the fracture line undergoes endochondral ossification forming a contiguous network of bone with newly deposited bone trabeculae in the medulla and beneath the periosteum.

In this fashion the fractured ends are bridged.

67
Q

What would you see if you examined a fracture after 12 weeks?

A

As the callus matures and as it is subjected to weight-bearing forces, portions that are not physically stressed are resorbed.

This remodelling reduces the size of the callus until the shape and outline of the fractured bone are re-established as lamellar bone.

The healing process is complete with restoration of the medullary cavity.

68
Q

List the conditions which are known to be associated with osteonecrosis.

A
  • Alcohol abuse
  • Bisphosphonate therapy (jaw bones)
  • Connective tissue disorders
  • Steroid treatment
  • Chronic pancreatitis
  • The ‘bends’
  • Gaucher disease
  • Infection
  • Pregnancy
  • Radiotherapy
  • Sickle cell disease
  • Trauma
  • Tumours

Medicine - Year 1 (61 decks)

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