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M2 Pathology > MSK (LL) Autoimmune, Metabolic, Iatrogenic, Congenital, Degenerative > Flashcards

MSK (LL) Autoimmune, Metabolic, Iatrogenic, Congenital, Degenerative Flashcards

1
Q

State the 4 common autoimmune conditions of the LL

A
  1. myasthenia gravis
  2. SLE
  3. RA
  4. Ankylosing spondylitis
  5. Psoriatic arthritis
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2
Q

State the features and complications of SLE (systemic lupus erythematosus)

A

SLE (SYSTEMIC LUPUS ERYTHEMATOSUS)

Features
- systemic (fever, fatigue, lymphadenopathy)
- mucocutaneous symptoms (malar rash sparing nasolabial folds, photosensitive lesons, sores, alopecia)
- arthralgia (joint pain that is migratory or symmetrical)
- cardiovascular symptoms (pericardiits, raynaud’s phenomenon, vasculitis, thromboembolic diseases)
- renal involvement - lupus nephritis

Complication - pleuritis, pneumonitis

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3
Q

State the investigations and management used for SLE (systemic lupus erythematosus)

A

SLE (SYSTEMIC LUPUS ERYTHEMATOSUS)

Investigations
- positive for anti-nuclear antibodies (ANA)
- positive for DsDNA
- positive for anti-smith
- positive for anti-RNP

Management
- avoid sun exposure and smoke
- anti-malarial therapy (hydroxycholorquine)
- corticosteroids (prednisolone)
- immunosuppressants (cyclosporine, azithioprine, methotrexate)

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4
Q

State the common causes of peripehral neuropathy

A
  1. DM
  2. B12 deficiency
  3. Guillain-barre syndrome
  4. Chronic idopathic demyelinating polyradiculoneuropathy (CIDP)
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5
Q

State the presentation of peripheral neuropathy

A

PERIPHERAL NEUROPATHY

Since peripheral neuropathy is usually a LMN problem –> leads to LMN symptoms

Presentation
- wasting and fasciculations
- hypotonia
- absent reflexes
- foot drop
- symptoms worse in the night –> sleep disturbances
- glove and stocking distribution
- numbness and weakness

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6
Q

State the causes and presentations of peripheral neuropathy

A

PERIPHERAL NEUROPATHY

Causes
- vitamin b12 deficiency
- guillain-barre syndrome
- DM
- chronic idiopathic demyelinating radiculoneuropathy (CIDP)

Presentation
- LMN symptoms - hypotonia, absent reflexes, wasting, fasciculations, foot drop
- glove and stocking distribution
- numbness and weakness
- symptoms worse at night –> sleep disturbances

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7
Q

State the 3 variations/presentation of guillain-barre syndrome

A
  1. affects nerve roots - ascending paralysis
  2. miller fisher type - affects eyes
  3. bickerstaff - encephalitis
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8
Q

State the treatment for guillain-barre syndrome

A

IVIG + supportive treatment

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9
Q

State everything you know about guillain-barre syndrome
(causes, presentation, treatment)

A

GUILLAIN-BARRE SYNDROME

Causes
- campylobacter jejuni

Presentation
- glove and stocking distribution of numbness and weakness
- ascending paralysis
- affects repsiratory and heart tissues –> aphyxiation
- if miller fisher type –> affects eye
- if bickerstaff –> encephalitis

Treatment
- IVIG + supportive treatment

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10
Q

State the pathogenesis of vitamin b12 defiency

A

VITAMIN B12 DEFICIENCY

Pathogenesis
- gastrectomy or iliectomy (Intrinsic factor produced by parietal cells int he stomach bidns and preserves vitamin b12 for absorption in the terminal ileum)
- cholestyramine
- vegitarianism
- pernicuous anaemia (antibodies are produced aagainst parietal cells and intrinsic factor)

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11
Q

State the presentation and investigations of vitamin b12 deficiency

A

VITAMIN B12 DEFICIENCY

Presentation
- glove and stocking distribution of reduced sensation to light touch and vibration (DCML)

Investigation
- vitamin b12 measurement

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12
Q

State everything you know about vitamin b12 defiency
(causes, presentation, investigation, treatment)

A

VITAMIN B12 DEFICIENCY

Causes
- gastrectomy or iliectomy (intrinsic factors produced by parietal cells in the stomach binds and preserves vitamin B12 for absorption in terminal ileum)
- vegetarianism
- cholestyramine
- pernicous anaemia (Ab against parietal cells and intrinsic factors)

Presentation
- glove and stocking distribution of reduces sensation to light touch and vibration (DCML)

Investigation
- vitamin b12 measurement to confirm cause of peripheral neuropathy

Treatment
- mecobalamin B12

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13
Q

State the pathogenesis and clinical features of osteomalacia

A

OSTEOMALACIA

Pathogenesis
- defective bone mineralisation while bone density may still be normal

Presentation
- persistent bone pain, weakness and fatigue
- maintained muscle strength but reduced endurance during exercise and ROM limited by pain

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14
Q

State the investigation and treatment for osteomalacia.

A

OSTEOMALACIA

Investigation
- test for liver and kidney functions as both are involved in the activation of vitamin D
- pancreative enzymes (GGT, ALP) to test for pancreatitis which leads to malabsorption of vitamin D

Treatment
- vitamin D3 replacement therapy
- encouraging sun exposure
- anti-resorptive drugs + calcium supplement

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15
Q

State everything you know about osteomalacia
(pathogenesis, features, investigations, treatment)

A

OSTEOMALACIA

Pathogenesis
- defective bone mineralisation with no change in bone density
- due to vitamin D malabsorption or underproduction

Features
- persistent bone pain, weakness and fatigue
- maintained muscle strength but reduced endurance during exercise and ROM due to pain

Investigations
- liver and kidney test (involved in activation of vitamin D)
- pancreatic enzymes (GGT and ALP) to test for pancreatitis as it may lead to malabsorption of vitamin D

Treatment
- vitamin D3 replacement therapy
- encouraging sun exposure
- anti-resorptive drugs + calcium supplements

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16
Q

State the features of femoral artery pseudoaneurysm

A
  1. painful pulsatile mass at femoral triangle with bruit heard over area
  2. slight diminished popliteal and dorsal pedis pulse on affected limb
17
Q

State the common visual deficit due to paget’s disease

A

monocular blindness - complete vision loss in one eye (optic N compression)

18
Q

State the pathogenesis of hallux valgus.

A

HALLUX VALGUS

Pathogenesis
- deformation of the bones of the big toe leading to protrusion of the 1st metatarsal phalangeal joint

19
Q

State the features and management of hallux valgus.

A

HALLUX VALGUS

Features
- tender prominence over the first MTPJ with no redness or swelling
- big toe deviated laterally
- exacerbated by tight footwear

Management
- proper footwear and orthotics
- NSAIDs
- surgery

20
Q

State the pathogenesis of pes cavus

A

PES CAVUS

Pathogenesis
- idiopathic abnormally high medial longitudinal arch
- congenital (clubfoot) or secondary to neuromuscular damage (poliomyelitis)
- symptomatic with increasing age due to diminisehd ability for shock absorption

21
Q

State the clinical features and management of pes cavus

A

PES CAVUS

Features
- pain in the foot which radiates up lower limb due to high stress placed on hindfoot during heel strike

Management
- proper footwwear and orthotics to support the foot and reduce the weght it has to bear

22
Q

State the pathogenesis of pes planus

A

PES PLANUS

Pathogenesis
- weakness of muscles supporting the longitudinal arches (tibialis anteiror, tibialis posterior, flexor digitorum longus, flexor digitorum brevis, intrinsic foto muscles)
- flat foot during infancy is normal

23
Q

State the clinical features and management of pes planus

A

PES PLANUS

Features
- foot and ankle pain precipiated by prolonged standing or activity

Management
- arch supporting inserts for shoes
- exercises

24
Q

State the pathogenesis and clinical features of statin-induced myopathy

A

STATIN-INDUCED MYOPATHY

Pathogenesis
- myopathy induced by the statin class of anti-lipid drugs

Features
- muscle weakness that is more pronounced in proximal muscles of lower limbs
- muscle cramps triggered by exercise and relieved by rest

25
Q

State the investigations, complicaitons and management of statin-induced myopathy

A

STATIN-INDUCED MYOPATHY

Investigations
- elevated blood CK due to myocyte lysis

Complication
- kidney damage

Management
- discontinue statin
- coenzyme q10 supplementation

26
Q

State the pathogenesis of duchenne muscular dystrophy

A
  • X-linked recessive disease that predominantly affect men
  • Due to a mutation in the dystrophin gene, resulting in abnormalities in the protein dystrophin
  • Normally, dystrophin is used to anchor the sarcolemma to actin fibres and to the extracellular matrix
  • With a mutated dystrophin gene, the sarcolemma is no longer anchored to the ECM and the actin fibres, muscle contraction will lead to progressive tearing of the sarcolemma → scarring and eventual replacement with fatty tissue
27
Q

State the clinical features and complications of duchenne muscular dystrophy

A

DUCHENNE MUSCULAR DYSTROPHY

Features
- gower sign
- lordotic
- waddling gait
- normal presentation in early childhood
- calf muscle pseudohypertrophy from fibrosis and fatty transformation
- life expectancy - 20-30 years old

Complication
- cardiac and respiratory failure

28
Q

State the investigations and treatment of duchenne muscular dystrophy

A

DUCHENNE MUSCULAR DYSTROPHY

Investigations
- elevated blood CK
- DNA testing positive for dystrophin gene mutation
- muscle biopsy and IHC positive for dystrophin protein

Management
- corticosteroids
- physiotherapy
- supportive treatement - respiratory support

29
Q

State the pathogenesis and clinical features of myotonic dystrophy

A

MYOTONIC DYSTROPHY

Pathogenesis
- autosomal dominant mutation

Clinical features
- frontal balding
- bilateral facial muscle weakness
- delayed muscle relaxation after handshake
- cataracts
- excessive daytime sleepines

M2 Pathology (20 decks)

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