Brainscape's Knowledge GenomeTM

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


See full index

Sandra Phase 2a > MSK & Rheumatology > Flashcards

MSK & Rheumatology Flashcards

1
Q

Where does osteoarthritis commonly occur?

A

Synovial joint

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

Bones that form the joints are surrounded by …

A

Periosteum

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

What is the purpose of articular cartilage?

A

Absorb shock and allows gliding between thhe bones surrounding the synovial joint

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

Anatomy of a synovial joint

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

The knee joint also contains another cartilage called…

A

Meniscus (Fibrocartilage)

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

What occurs during mild osteoarthritis?

A

Have degeneration/damage of the articular cartilage in the presence of joint space narrowing

Common when youage

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

Risk factors of osteoarthritis

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

What does mild osteoarthritis progress to?

A

Severe osteoarthritis.

With severe osteoarthritis there is: bone spur formation, loss of articular cartilage, bone/bone joint space narrowing

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

Aetiology - Classification of osteoarthritis

A

Primary (Idiopathic) - no preceeding injury

Secondary - due to congenital abnormality, trauma, inflammatory arthropathy

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

Clinical Presentation of osteoarthritis

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

Findings based on clinical examination of osteoarthritis

A

Muscle Wasting
Overweight
Tenderness on joint palpation(+/- osteophytes)
Joint effusion
Crepitations

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

Differential diagnosis of osteoarthritis

A

Calcium pyrophosphate crystal deposition disease

Septic arthritis

Rheumatoid arhtritis

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

Investigations for osteoarthritis

A

MRI is good however X-ray better for initial investigation

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

Management for osteoarthritis

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

Pathophisiology of osteoarthritis

A

Progressive Loss of articular cartilage -> friction -> Inflammation -> Pain

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

What is rheumatoid arthritis

A

Systemic rheumatological disorder affecting multiple joints

Autoimmune

Progressive, symmetric joint depression

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

Clinical Presentation of rheumatoid arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diff in hand involvement in rheumatoid arthritis vs osteoarthritis

A

The disease can progress you can get other features in the hand:

Swan neck: DIP-Flex + PIP - hyper extension
Boutonniere: DIP - hyperextension, PIP - Flex
Z deformity of thumb: Ulnar deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macroscopic view of rheumatoid arthritis

A

Inflammation of the synovium of the synovial membrane (Synovitis) : Pain and swelling

Can also see angiogenesis

Bone/Cartilage Erosion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pathophisiology of rheumatoid arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pre rheumatoid arthritis: things that can contribute in the development of rheumatoid arthritis.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antibodies found in rheumatoid arthritis

A

Rheumatoid Factor (IgM ~ 75%) : Targets Fc portion of IgG. Forms immune complexes

Anti-citrullinated protein antibidy: targets citrullinated proteins such as fibrin, fillagrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Extraarticular involvement of rheumatoid arthritis

A

Result of cytokines produced within joints : TNF - alpha, IL-1, IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnosis of rheumatoid arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment for rheumatoid arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Examples of crystal arthritis

A

Gout
Pseudogout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is gout

A

Common form of inflammatory arthritis characterised by recurrent attacks of painful joint pain

Gout attack occurs suddenly often at night. The intial attack usually involves only one joint, most often in the big toe and lasts a few days. Subsequent flares may involve mutliple joints and can last for weeks, with shorter intervals of remission in between

The affected joint is swollen, red and warm to touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Causes of gout

A

Caused by deposits of monosodium urate crystals in the joints, which can happen when blood levels or uric acid are too high (>6.8mg/L)

High serum urate level may result from decreased urate excretion, increased urate production and/or over consumption of purines.

  1. Most common cause is kidney’s decreased ability to excrete uric acid: hereditary, kidney diseases, medications (diuretics), alcohol usage, lead poisoning
  2. Increased urate production: Lymphoma, leukemia, haemolytic anaemia, psoriasis, radiation therapy, obesity
  3. Purine-rich foods: red meat, organ meat, anchovies, sardines, asparagus, beer .. RARELY THE ONLY CAUSE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is uric acid

A

Waste product from the breakdown of purines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What joints are most liely affected by gout and why?

A

Joints of the extremities

Due to uric acid crystals forming more easily in cooler temperatures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are tophi

A

Crystals deposited under skin
Not usually painful

-Can limit joint motions
-Can become inflammed/ruptured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

People with gout are at an increased risk of developing ..

A

osteoarthritis

can also lead in the development of kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Risk factors of gout

A

Men (middle aged), women (menopause)
Diet
Obesity
High bp, diabetes, metabolic syndrome, heart and kidney diseases
Family History
Surgery/trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diagnosis of gout

A

Urate crystals in synovial joint fluid
High serum urate levels alone not conclusive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Treatment for gout

A

Anti-inflammatory drugs (NSAIDS, corticosteroids, colchicine)

Dissolve tophi by lowering serum urate to <5 to 6 mg/dL:
+ block urate production with xanthine oxidase inhibitors (allopurinol, febuxostat)
+ increase urate excretion (probenecid, losartan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Appeaence of monosodium urate crystals

A

Appear as yellow shaped needles with negative birefrigence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is pseudogout

A

Form of arthritis causing pain and inflammation in affected joints

There is acute onset joint pain, swelling and erythema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Causes of pseudogout

A

Buildup of calcium pyrophosphate dehydrate crystals within the cartilage and synovium of a joint

CPPD crystals appear as blue rhomboid shapes with weakly postive birefringence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Areas affected by gout vs pseudogout

A

Gout: Smaller joints e.g big toe called pedagra
Pseudogout: Larger joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Risk Factors of pseudogout

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Investigations for pseudogout

A

Joint aspiration

Xray: cartilage calcification

Blood test:
-Ca & PTH
-Iron studies
-Mg
-ACP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Management for pseudogout

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Gout vs Pseudogout table

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is osteoporosis

A

when there is a higher breakdown of bone in comparison to the formation of new bone which results in porous bones, meaning a decrease in bone density to the point of potential fracture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Structure of bone

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How often does bone remodelling take place

A

spongy bone replaced every 3-4 years
compact bone replaced every 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is bone remodelling dependent on

A

Dependent on serum Ca2+ levels:
PTH, Calcitonin, Vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What causes osteoporosis

A

when osteoclasts break down bone faster than the osteoblasts can rebuild, it results in the lowering of the bone mass and eventually in osteoporosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Osteoporosis vs. osteomalacia

A

Osteoporosis: normal mineralisation, normal cells

Osteomalacia: lack of mineralisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Abnormal findings of osteoporosis

A
  1. fewer trabeculae in the spongy bone
  2. thinning of the cortical bone
  3. widening of the Haversian canals

These bone changes increase the risk of fracture, and they are known as fragility or pathologic fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Bones at risk of fragility fractures

A

vertebrae
shoulder blades
ribs

= as they consist mainly of spongy bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Factors that increase bone mass loss, increase risk of osteoporosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Types of osteoporosis

A

Postmenopausal: decreased oestrogen levels lead to increased bone resorption.

Senile: believed that osteoblasts just gradually lose the ability to form bone, while the osteoclasts keep doing their thing unabated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Symptoms of osteoporosis

A

People with osteoporosis don’t usually have symptoms until a fracture occurs.

The most common type of fractures are vertebral fractures (compression fracture). Occurs when one or more bones in the spine weaken and shatter.

Vertebral fractures cause back pain, height loss, and a hunched posture.

Femoral neck fractures and distal radius fractures can also occur, and they’re often associated with postmenopausal osteoporosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Diagnosis of osteoporosis

A

Dual-energy x-ray absorptiometry (DEXA) scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Treatment for osteoporosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is osteopenia

A

Osteopenia and osteoporosis are two very similar conditions, but one is more severe than the other. Both conditions are decreased bone density, but osteopenia is to a lesser degree than osteoporosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is vasculitis?

A

Inflammation of the blood vessels resulting in damaged vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the complications of vasculitis?

A

Tissue ischaemia
Aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is primary vasculitis classified?

A

Size of blood vessels affected

Large/Medium/Small

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does large cell vasculitis affect?

A

Aorta and its branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Example of large cell vascultis

A

Giant cell arteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is giant cell arteritis

A

Granulomatous arteritis of the aorta and the large vessels

Location: temporal branch of carotid artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Clinical Features of giant cell arteritis

A

severe unilateral headache around temporal region

visual changes: amaurosis fugax

if facial artery is affected: jaw claudication. Lingual artery: tongue claudication

Association with polymyalgia rheumatica

Classic Presentation is an elderly female with new headache, new neck pain with a potential superficial temporal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Histopathological changes of giant cell arteritis

A

Presence of giant cells
Pan arthritis inflammation of all the vessel layers
Presence of CD4 & CD8 lymphocytes, macrophages

=all of thesecells are present in smoother muscle layers of the vessel

Skip lesions
No fibrinoid necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Investigations for giant cell arteritis

A

Increase ESR
Increase CRP

Ultrasound doppler: Halo sign, stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Diagnosis of giant cell arteritis

A

Temporal artery biopsy
Immune cell infiltration in smooth muscle layer
Evidence of pan arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Management of giant cell arteritis

A

High dose steroids
Calcium and Vit D
Bisphosphanate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Classification of Spondyloarthropathies

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteric arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is ankylosing spondycitis

A

chronic inflammatory disease of intervertebral & facet joints that affects the vertebral joints and makes the spine really stiff, but can also cause inflammation in other parts of the body like the eyes and blood vessels.

Associated with HLA-B27 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Ankylosing spondylitis is also called

A

Bechterew disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are spondyloarthropathies

A

Spondyloarthropathies are all autoimmune diseases that affect the joints, and they’re seronegative (rheumatoid factor not found in the blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Cause of ankylosing spondylitis

A

autoimmune process attacking type I and type II collagen in the joints.

Over time, the inflammation destroys the intervertebral joints, the facet joints, and the sacroiliac joints, and fibroblasts replace the destroyed joint with fibrin

ossification results in small bony outgrowths will form at the joint edges, called syndesmophytes in the beginning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Other part of the body affected by ankylosing spondylitis due to inflammation

A

Eye: anterior uveitis
Aortic valve: aortic regurgitation
tendons (like the achilles tendon) :enthesitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Symptoms of ankylosing spondylitis

A

weight loss, fevers, and fatigue.

If ankylosing spondylitis affects the sacroiliac joints it typically causes buttock pain, and if it affects the cervical or thoracic region it can cause neck or back pain and stiffness.

Because the ribs and vertebrae are involved in breathing, stiffness can cause shortness of breath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Diagnosis of ankylosing spondylitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Treatment for ankylosing spondylitis

A

Inflammation and pain:
Treated with non-steroidal anti-inflammatory drugs like ibuprofen.
The pain can also be relieved by exercise or physical therapy.

In more severe cases, disease modifying anti-rheumatic drugs, or DMARDs, like sulfasalazine and methotrexate can be helpful.

Newer therapies called biologics can also be useful, because they block the actions of cytokines like tumor necrosis factor alpha and the interleukins.

Surgery can repair damaged hip and knee joints, but spinal surgery is typically considered risky and is rarely performed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is psoriatic arthritis?

A

psoriatic arthritis is a type of joint inflammation that happens in individuals with psoriasis.

It is chronic and progressive

Associated with the HLA-B27 gene T-cell mediated attack of joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Cause of psoriatic arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Symptoms of psoriatic arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Types of psoriatic arthritis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Diagnosis of psoriatic arthritis

A
83
Q

Treatment for psoriatic arthritis

A
84
Q

What is reactive arthritis

A

Reactive arthritis, formerly known as Reiter’s syndrome, is inflammation of a joint which usually develops after an infection, and that infection is typically a sexually transmitted disease or gastroenteritis

85
Q

Tissues affected by reactive arthritis

A

Starts 2-3 weeks after infection

86
Q

What are the symtpoms of reactive arthritis

A
87
Q

Diagnosis of reactive arthritis

A

History of previous infection
Clinical exam
Positive for HLA-B27

88
Q

Treatment for reactive arthritis

A

antibodies for infection
NSAIDs

89
Q

What is septic arthritis

A

Septic arthritis, also called infectious arthritis, refers to any joint inflammation caused by a microbe - and usually it results from a bacterial infection of the joint

90
Q

Types of infective arthritis

A

Septic arthritis
Osteomyelitis

91
Q

Clinical Presentation of septic arthritis

A
92
Q

What do people presenting with an inflamed joint require?

A

History
Examination

93
Q

Causative agent for septic arthritis

A
94
Q

Pathogensis of septic arhtiris

A

Skin infection such as Staphylococcus aureus can disseminate into joint causing septic arthritis

osteomyelitis can also locally invade the joint causing septic arthritis

Lower/upper respiratory tract infections from group A streptococcus

STI

Procedures

Surgery

95
Q

Septic arthritis is considered to be a …

A

surgical emergency >24hrs -> irreversible damage

96
Q

Investigations for septic arthritis

A

X-Ray:
shows sublaxation/dislocation
shows joint space widening

97
Q

Steps taken after intial investigation in patient with septic arthritis

A
98
Q

What is osteomyelitis

A

Inflammation of the bone or bone marrow, and it typically results from an infection.

99
Q

In osteomyelitis, microorganisms, such as bacteria, reach the bone to cause an infection in a few different ways. How

A

Bacteria particularly affect certain high-risk individuals like those with a weak immune system, and those with poor blood circulation due to uncontrolled diabetes.

1.Bacteria reaches the bone through the bloodstream: contaminated needles to inject drugs or in individuals undergoing hemodialysis that may be contaminated by a bacteria or even through the dental extraction of an infected tooth.

2.Trauma
3.Surgery
4.Contiguous spread

CAN ALSO BE A COMBINATION

100
Q

Through the bloodstream, the microorganisms may reach specific places in the body, and this mostly depends on the age of the person ..

A

In older adults, for example, the microorganisms may reach the vertebrae and cause vertebral osteomyelitis. This usually affects two adjacent vertebrae and the interintervertebral disk between them.

In children, the metaphysis of long bones like the femur is commonly affected.

101
Q

Pathophisiology of osteomyelitis

A

Chronic osteomyeltis lasts months-year -> Affeted bone becomes necrotic and separates

102
Q

Occasionally, in both acute and chronic osteomyelitis the inflammation may involve the …

A

Perisoteum

103
Q

Infection of osteomyelitis can spread to:

A
104
Q

Microorganisms that cause osteomyelitis

A
105
Q

Symptoms of osteomyelitis

A
106
Q

Diagnosis of osteomyelitis

A
107
Q

Treatment for osteomyelitis

A
108
Q

What is systemic lupus erythematosus

A

Autoimmune disease mediated by antibodies and immiune complexes

It is a multi-system disorder that most commonly affects women during reproductive years

109
Q

Pathophisiology of SLE

A
110
Q

Constitutional symptoms of SLE

A
111
Q

Investigations for SLE

A

+Antinuclear Antibody (ANA):
Anti dsDNA, anti histone, anti SM , anti Ro, anti nRNP

Extractable nuclear antigens (ENA)
Anti cardiolipin
Anti RF

112
Q

Serum markers associated with disease flare ups (s
SLE)

A

Decrease in complement 3 & 4
Increase Anti dsDNA

113
Q

SLE + DRUG

A
114
Q

Complications of SLE

A
115
Q

Risk Factors for SLE

A
116
Q

Treatment for SLE

A
117
Q

What is fibromyalgia

A

Chronic condition characterised by widespread pain and hypersensitivity to pressure

118
Q

Epidemiology of fibromyalgia

A

8% of population affected
2: 1 Female to male
Most commonly diagnosed between 35-45 years

119
Q

Signs and symptoms of fibromyalgia

A
120
Q

Cause of fibromyalgia

A

Exact cause/mechanism is unknown

Thought to have central sensitisation: More sensitive to pain and therefore lower threshold for pain.

Hyperexcitation of pain sensing neurons and under activity of inhibitory pathways

Physical/enotional stress is often a trigger: Link with IBS/TMS/Chronic fatigue

121
Q

Risk Factors for fibromyalgia

A

Poor sleep
Smoking
Obesity
Sedentary lifestyle

122
Q

Diagnosis for fibromyalgia

A

unremarkable test results
widespread pain index/symptom severity score
up to 66% may have symptoms explained by other conditions:
-SLE (Lupus)
-Non coeliac gluten sensitivty
-Polymyalgia rheumatica
-Hypothyroidism
-Nerve compression syndrome

123
Q

Subtypes of fibromyalgia

A
  1. Extreme sensitivity to pain without pyschiatric association
  2. Fibromyalgia with pain related depression
  3. depression with fibromyalgia syndrome
  4. Fibromyalgia due to somatisation
124
Q

Treatment for fibromyalgia

A

No cure or treatment - symptom management

  1. Non-pharmacological:
    Exercise: reduces pain and fatigue, aerobic yoga
    CBT
    Reduce Stress
    Sleep hygiene: avoid caffeine, large meals, screen environment
  2. Pharmacological
    Anti depressants:
    -SNRI: Duloxetine, milnacipran
    -TCA: Amitriptyline

Anti convulsants
-Pregabalin

125
Q

What is Sjogren Syndrome ?

A

Autoimmune disorder

-Typically occuirng in women
-Immune cells attack exocrine glands. Primarily lacrimal & salivary glands

126
Q

Pathophisiology of Sjogren Syndrome

A
127
Q

Cause of Sjogren Syndomre

A

Exact cause is unknown

Thought to be a combination of genetic (Anti-SS-A & Anti-SS-B) and environmental factors

128
Q

Classification of Sjogren syndrome

A

Primary (Occurs alone)-> Sicca syndrome

Secondary (occurs with other autoimmune diseases) -> e.g rheumatoid arthritis

129
Q

Symptoms of sjogren’s syndrome

A
130
Q

Diagnosis of Sjogren’s syndrome

A
131
Q

Treatment for Sjogren’s syndrome

A

Suppress the immune response: Corticosteroids
Increase the exocrine secretions: Pilocarpine

132
Q

What is anti-neutrophilic cytoplasmic antibody associated vasculitis

A

Vasculitis that affects small blood vessels.

There are three diseases and are all characterised by the presence of the ANCA antibodies

This includes granulamatosis with polyangitis

133
Q

Complication of Wegener’s granulomatosis (granulomatosis with polyangiitis)

A

ANCA nephritis

134
Q

What is Wegener’s granulomatosis (granulomatosis with polyangiitis)

A

ANCA positive against proteinase 3

An anti-neutrophilic cytoplasmic antibody associated vasculitis. Most common

Small vessel vascultis characterised by the inflammation of the small blood vessels with infiltrationof immune cells forming granulomas

135
Q

Where does inflammation occur in Wegener’s granulomatosis

A

Blood vessels of:
Upper respiratory tract
Lower respiratory tract
Kidney

=Wegener’s triad

136
Q

Histopathological findings of Wegener’s granulomatosis

A

Granuloma formation
Pauci immune necrotising vasculitis

137
Q

Clinical Features of Wegener’s granulomatosis

A
138
Q

Investigations for Wegener’s syndrome

A
139
Q

Diagnosis for Wegener’s syndrome

A

Skin biopsy: Leukocytoclastic vasculitis (No compplemet or immunoglobulin)

Renal biopsy: Rapidly progressing glomerulonephritis. Crescents. Pauci immune glomerulonephritis

140
Q

Management of Wegener’s syndrome

A
141
Q

What is antiphospholipid syndrome

A

An autoimmune disease where antiphospholipid antibodies attack phospholipids in cell membrane or proteins bound to phosphlipid

More common in young females

142
Q

Classification of antiphospholipid syndrome

A

Primary: Occurs by itself

Secondary: occurs with other autoimmune diseases (esp. SLE)

143
Q

Cause of APS

A

Cause is unknown

Known genetic (HLA-DR7 Gene) and environmental factors

Environmantal trigger msut be present

144
Q

Pathology of APS

A
145
Q

Complications of APS

A
146
Q

Diagnosis of APS

A
147
Q

Treatment for APS

A
148
Q

What are the types of idiopathic inflammatory myopathies

A

Polymyositis
Dermatomyositis

149
Q

What are idiopathic inflammatory myopathies

A

Autoimmune conditions involving proximal muscle weakness and muscle inflammation

-Polymyositis does not involve the skin
-Dermatomyositis does involve the skin

150
Q

Incidence & Onset of idiopathic inflammatory myopathies

A

Incidence: approx 2 per 100,000 per year
Female - Male Ratio = 2:1
Onset 40-50

151
Q

Causes of idiopathic inflammatory myopathies

A
  1. Genetics
    HLA 8.1, PTPN22, STAT4, TRAF6
  2. Environmental trigger
    Uv rdiation, previous infections, prior lung disease
152
Q

Polymyositis vs dermatomyositis pathogenesis

A
153
Q

Polymyositis vs dermatomyositis clinical features

A

Myalgia
Dysphagia
Symmetrical proximal muscle weakness (most common)

154
Q

Associated conditions with idiopathic inflammatory myopathies

A

Instertitial lung disease
Raynaud’s phenomenon
Polyarthritis
SLE

155
Q

Features specific to dermatomyoitis

A

Heliotrope rash
Gottron’s Papules
Shawl sign: rash on shoulders, back elbows and knees
V sign: rash on neck and upper chest
Holster sign: rash on lateral thighs
Periungual erythema
Calcinosis Cutis

156
Q

Diagnosis polymyositis vs dermatomyositis

A

Diagnostic Criteria:
1. Symmetric proximal muscle weakness
2. Elevated enzymes
3. EMG abnormalities
4. Muscle biopsy findings
5. Cutaneous findings = only for dermatomyositis

157
Q

Treatment for polymyositis & dermatomyosits

A
158
Q

What is scleroderma

A

Scleroderma refers to systemic sclerosis, a rare autoimmune disorder in which normal tissue is replaced with thick, dense connective tissue. It affects the skin, blood vessels and internal organs

159
Q

Types of scleroderma

A

Limited cutaneous systemic scleroderma (CREST syndrome)
Diffuse cutaneous systemic scleroderma

160
Q

Causes of scleroderma

A

Affects women 3x more often than men

Pathology not understood
-Genetic predisposition
-Triggered by external factors: viral infection, exposure, medication

161
Q

What organs does scleroderma primarily involve

A

Skin
-First appears on fingers (sclerodactyly): swollen and doughy
-Later: tight, shiny, smooth and stiff

Lung
Heart
Kidney
GI tract

162
Q

Symptoms of scleroderma

A

With diffuse scleroderma organ damage occurs earlier

163
Q

Diagnosis of scleroderma

A
164
Q

Treatment for scleroderma

A
165
Q

Treatment for scleroderma

A
166
Q

What is polyarteritis Nodosa (PAN)

A

Necrotising vasculitis involving medium-sized vessels
ANCA negative

Association with Hep B

Systemic involvement:
-Kidneys most commonly involved organ
-Spares the lungs

167
Q

Signs and symptoms of PAN

A

Myalgias
Renal Infarts
Mononeuritis multiplex
Fever

Rash:
-Purpuric rash
-Subcutaneous nodules
-Bullous/vesticular lesions
-Livedo reticularis

168
Q

Investigations for PAN

A

Hepatitis serology
FBC
EUC
Angiogram microaneurysms

169
Q

Treatment for PAN

A

Glucocorticoids
Cutaneous polyarteritis Nodosa -> Skin limited Disease

170
Q

What is Pagat’s disease ?

A

Metabolic disease of increased bone destruction and remodelling

171
Q

Pathology of Pagat’s Disease

A

Basic pathology is overactove osteoclastic activity
Accelerated bone re-absorption is accompanied by disordered bone formation, resulting in excess bone formation, altered in shape and size

172
Q

Aetiology of Pagat’s Disease

A

Probably triggered by paramyxovirus

173
Q

Treatment for Pagat’s disease

A

Oral (risedronate) or an IV (zoledronate) bisphosphonate

174
Q

Complications of Pagat’s disease

A

General: risk of osteosarcoma, high output congestive cardiac failure

Skull: entrapment of cranial nerves leading to deafness, visual loss, headache. Cord compression, hydrocephalus

Face: cosmetic issues, dental abnormalities

Spine: spinal cord compression, radiculopathy, cauda equina syndrome, spinal stenosis

Femur: osteoarthritis at the knee and hip

175
Q

Differential diagnosis for Pagat’s disease

A

Malignancy
Osteoporotic fractures in spine

176
Q

Investigations for Pagat’s disease

A

Elevated ALP: reflects extent of disease:
-With treatment, ALP should normalise

Plain radiography of affected part: lytic, sclerotic disorganised bone

Bone scan: focal areas of increased uptake reflect extent of disease

177
Q

What is polymyalgia rheumatic (PMR)

A

Pain and stiffness of proximal extremities in the absence of muscle weakness

Commonly associated with temporal arteritis

178
Q

Polymyalgia rheumatic signs and symptoms

A

Fever
Weight Loss
Malaise

Pain and stiffness of proximal muscles symmetrically
-neck
-shoulders and hips

Gelling

Muscle tenderness nut NO weakness or atrophy

179
Q

Diagnosis of PMR

A

Age >50 years old at onset

Proximally and bilaterally distributed aching and morning stiffness (lasting at least 30mins or more) persisting for at least two weeks. Stiffness should involve at least two of the following three areas: neck or torso, shoulders or proximal regions of the arms, hips or proximal aspects of the thigh

ESR >=40mm/hour

180
Q

Treatment for PMR

A

Low dose corticosteroids such as prednisone

181
Q

What is mechanical lower back pain

A

Lower back pain that is triggered by movement and improved with rest

182
Q

Causes of mechanical lower back pain

A
  1. Lumbar spine strain/sprain (70%)
  2. Degeneration of discs/facets
    -discogenic worsens with flexion + coughing / sneezing
    -facet pain worsen with extension
  3. Disc herniation (nucleus pulposus)
  4. Spinal stenosis - osteophyte formation, ligament hypertrophy
  5. Spondylolysis
183
Q

Red flags for mechanical lower back pain

A
  1. Saddle Anesthesia
  2. Urinary Incontinence/Retention
  3. Neurological deficit
  4. Systemic Manifestations
    -Weight Loss
    -Fever
    -Night Sweats
    5.History of malignancy
    6.Immunosupression
    7.IV Drug user
    8.Osteoporosis
    9.Trauma
    10.Visible Injury
    11.Non-mechanical suggestion
    -waking from sleep
    -no improvement with rest
184
Q

Conditions to rule out with mechanical lower back pain

A
  1. Cauda Equina Syndrome
  2. Spinal Cord compression
  3. Abscess
  4. Ruptured AAA
  5. Acute Pancreatitis
185
Q

Diagnosis of mechanical lower back pain

A

History + Physical Exam mostly

Physical:
1.Inspection - deformities/abnormal curvature
2.Palpation - Focal Tenderness
-Movement:
active + passive
pain on flexion + leg radiation -> suggestive of disc herniation
pain on extension -> suggestive of facet involvement or spinal stenosis
young + reduced range of motion -> consider ankylosing spondylitis
–Provocative tests:
1. Disc herniation : striaght leg raise + femoral stretch
2. Sacroiliac joint involvement- thigh thrust, distraction, gaenslen’s test, pelvic compression, faber

  1. Neurological Exam
  2. Hip Asessment

Lab values - FBC, CRP, ESR
Imaging
-Red Flag patients/refractory: to conservative management
-Vertebral x-ray: Fractures
-MRI
-CT- Generally as part of trauma workup

186
Q

Treatment for mechanical lower back pain

A

3rd line:
Radiofrequency ablation
Injection therapy
Surgical Intervention

187
Q

What is osteomalacia

A

Bone softening caused by a faulty process of bone mineralisation or deficiency/impaired metabolism of Vit D, phospahte, calcium

Rickets = children
Osteomalacia = adults

188
Q

Causes of Vit D deficiency

A
189
Q

Symptoms of rickets/osteomalacia

A
190
Q

Diagnosis of rickets/osteomalacia

A
191
Q

Treatment for rickets/osteomalacia

A
192
Q

Examples of connective tissue disorders

A
  • Marfan’s
  • Ehlers Danlos
193
Q

What is Marfan Syndrome

A

Marfan syndrome is a genetic disorder that results in defective connective tissue, which can affect a person’s skeleton, heart, blood vessels, eyes, and lungs.

Inheritance is autosomal dominant
Mutation in FBN1:
-Fewer fibrillin microfibrils
-More TGF-Beta

194
Q

Complications of Marfan Syndrome

A

Lens dislocation
Aortic rupture
Pneumothorax

195
Q

Signs and symptoms of Marfan Syndrome

A

Skin: Stretch marks
Lungs: Bulla -> Pneumothorax
Eyes: Retinal detachment & lens dislocation
Cardiovascular:
-Aorta dilates: Aortic valve insufficiency
-Cystic medial necrosis: tunica media degenerates
-Mitral Valve Prolapse

196
Q

Features of Marfan Syndrome

A

not always present
more/less severe
usually not noticeable at birth -> show up with age
present at birth -> early - onset (neonatal) Marfan Syndrome

197
Q

Diagnosis of Marfan Syndrome

A

If has clinical features:
-aortic disease
-dislocated lens
-family history
-FBN1 Mutations

198
Q

Treatment for Marfan Syndrome

A
199
Q

What is Ehlers-Danlos syndrome

A

In Ehlers-Danlos syndrome, defective collagen leads to stretchy skin, easy bruising, and joints that are super flexible.

200
Q

Symptoms of Ehlers-Danlos syndrome

A

Overly flexible joints
Easy bruising
Elastic Skin

201
Q

Diagnosis of Ehlers-Danlos syndrome

A

Characteristic symptoms
examining joints and skin
DNA studies that identify mutation

202
Q

Treatment for Ehlers Danlos syndrome

A

Supportive care
-Physiotherapy to supporting bones and joints
–orthopedic instruments

203
Q

Connective Tissue Disorder table

A

Sandra Phase 2a (17 decks)

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