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Musculoskeletal > Pathology > Flashcards

Pathology Flashcards

1
Q

Describe type 1 muscle fibres

A

Red, large mitochondria and increased myoglobin

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2
Q

Describe type 2 muscle fibres

A

White, small mitochondria & large motor end plates

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3
Q

What are some indications for performing a muscle biopsy?

A

Evidence of muscle disease-weakness, atrophy, fasciculation, elevated CK, presence of neuropathy (+nerve biopsy), presence of vascular disorder (vasculitis)

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4
Q

Describe high, medium and low CK levels

A

High: 200-300x normal (dystrophies). Medium:20-30x (inflammatory myopathy). Low : 2-5x (neurogenic disorder)

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5
Q

Describe some dystrophic changes in histology

A

Variability in muscle fibre size, endomysial fibrosis, fatty infiltration and replacement, myocyte hypertrophy & fibre splitting, increased central nuclei, segmental necrosis, regeneration, ring fibres

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6
Q

What occurs to muscles and CK in DMD?

A

Proximal weakness, pseudohypertrophy of calves. Raised CK

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7
Q

What mutation occurs in DMD?

A

Mutations in dystrophin gene on long arm of ChX

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8
Q

What changes occur regarding cell structures in DMD?

A

Alterations in anchorage of actin cytoskeleton to basement membrane. Fibres liable to tearing, uncontrolled Ca2+ entry

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9
Q

What histological changes occur in DMD?

A

Muscle fibre necrosis & phagocytosis
Regeneration
Chronic inflammation and fibrosis
Hypertrophy

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10
Q

Describe the onset, mutation and progress of BMD

A

Later onset, mutation in dystrophin (like DMD), slower progress

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11
Q

What are the most common types of myotonic dystrophy?

A

DM1 (distal), DM2(proximal)

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12
Q

What symptons occur in myotonic dystrophy?

A

Muscle weakness, myotonia, non-muscle features- cataracts, frontal baldness in men, cardiomyopathy, low intelligence

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13
Q

What inheritance occurs in myotonic dystrophy?

A

Autosomal dominant-Ch19/3

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14
Q

What areas are affected by myotonic dystrophy?

A

Adolescence- face, distal limbs. Later-respiratory muscles

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15
Q

What histological changes occur in myotonic dystrophy?

A

Atrophy of type 1 fibres, central nuclei, ring fibres, fibre necrosis, fibrofatty replacement

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16
Q

What is polymyositis?

A

Cell-mediated immune response to muscle antigens

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17
Q

What pathological changes occur in polymyositis?

A

Endomysial lymphocytic infiltrate, invasion of muscle by CD8+ T cells, segmental fibre necrosis

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18
Q

What is the difference between dermatomyositis and polymyositis?

A

Dermatomyositis is polymyositis plus skin changes

19
Q

What changes occur in dermatomyositis?

A

Upper body erythema, swelling of eyelids with purple discolouration

20
Q

What are the pathological changes that occur indermatomyositis?

A

Immune complex and complement deposition within and around capillaries within muscle. Perifascicular muscle fibre injury. B-cells/CD4+ T cells > polymyositis

21
Q

What is MND?

A

Progressive degeneration of anterior horn cells. Denervation atrophy, fasciculation and weakness

22
Q

What is the genetic mutation behind spinal muscular atrophy?

A

Inherited autosomal recessive-Ch5

23
Q

What occurs in spinal muscular atrophy?

A

Degeneration of anterior horn cells in spinal cord, and denervation of muscle

24
Q

What type of disorder is Myasthenia Gravis?

A

Autoimmune

25
Q

What symptoms occur in Myasthenia Gravis?

A

Weakness, proptosis, fatigue and dysphagia

26
Q

Who does myasthenia gravis commonly effect?

A

Women between 20-40

27
Q

What percentage of people with Myasthenia Gravis have thymoma, and what may others have alternatively?

A

25%- others may have thymic hyperplasia

28
Q

What is Rhabdomyolysis, and what occurs systemically?

A

Breakdown of skeletal muscle- myoglobinuria, hyperkalaemia, necrosis and shock

29
Q

What is the outcome of rhabdomyolysis?

A

Acute renal failure, hypovolaemia, hyperkalaemia, metabolic acidosis, disseminated intravascular coagulation

30
Q

What is SLE?

A

AI multisystem disorder, involving ANA’s, has genetic factors and may be drug induced (hydralazine and pracainamide). F-M 9:1

31
Q

What symptoms/conditions occur as a result of SLE?

A

Butterfly rash, discoid lupus erythematosus (DLE), arthralgia, glomerulonephritis, psychiatric symptoms, focal neurological symptoms, peri/myocarditis, necrotizing vasculitis, lymphadenopathy, splenomegaly, pleuritis, pleural effusions, anaemia, leucopenia, thrombophilia

32
Q

What hypersensitivity presentations occur in SLE?

A

Visceral lesions (Type III), Haematological effects (Type II)

33
Q

What is polyarteritis nodosa (PAN)?

A

Inflammation and fibrinoid necrosis of small/medium arteries?

34
Q

What is the aetiology of PAN?

A

Unknown

35
Q

What are the target organs of PAN?

A

Kidneys, heart, liver, GI tract, skin, joints, muscles, nerves, lungs

36
Q

What are the clinical features of PAN?

A

Non-specific +/- organ specific features- HT, haematuria, abdo pain, melaena, diarrhea, mononeuritis multiplex, rash, cough, dyspnoea

37
Q

How is PAN diagnosed?

A

Biopsy; fibrinoid necrosis of vessels. Serum contains pANCA (perinuclar antineutrophil cytoplasmic autoantibody)

38
Q

How does polymyalgia rheumatica present?

A

In elderly commonly- pain, stiffness in shoulder & pelvic girdles. No muscle weakness

39
Q

What is Temporal arteritis?

A

Inflammation affecting cranial vessels.

40
Q

What are the symptoms of temporal arteritis?

A

Headache and scalp tenderness. Risk of blindness if terminal branches of ophthalmic artery affected

41
Q

How is temporal arteritis diagnosed?

A

Raised ESR- temporal artery biopsy; inflammation, +/- giant cells, fragmentation of internal elastic lamina

42
Q

What is scleroderma?

A

Excessive fibrosis of organs and tissues (excessive collagen production)

43
Q

What symptoms/conditions occur due to scleroderma?

A

Skin is tight, tethered, decreased joint movement. GIT-fibrous replacement of muscularis. Pericarditis and myocardial fibrosis. Interstitial fibrosis. Kidneys-affects arteries > HT, MSK- polyarteritis and myositis

44
Q

What syndrome is scleroderma associated with?

A

CREST

Musculoskeletal (16 decks)

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