Brainscape's Knowledge GenomeTM

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


See full index

year 2 core concepts > MSK: systemic conditions > Flashcards

MSK: systemic conditions Flashcards

1
Q

What is the pathophysiology of osteoporosis?

A

more break down of bone than formation of bone causing decrease in bone density

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

what increase osteoclast/ bone resorption and breakdown?

A

PTH-> increase serum calcium-> osteoclast bone resorption

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

what increase osteoblast/ bone formation

A
  1. calcitonin: produced by C-cells in thyroid, inhibits osteoclast activity and decrease serum calcium
  2. growth hormone, estrogen, testosterone
  3. good nutrients: intake of calcium and vitamin D
  4. strength training
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the 2 main types of osteoporosis and their causes?

A
  1. type 1/ Post menopausal: decrease in estrogen-> increase bone resorption/ breakdown by osteoclast
  2. type 2/ Senile/ old age: osteoblast loose ability for bone formation
  3. secondary: corticosteorids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histological findings of osteoporosis & which change cause increase bone fragility

A
  • fewer trabeculae in spongy/ trabecular bone (inside part of the bone)
  • Thickening of cortical bone (outside part of bone)
  • Widening of the Haversian canals (hollow center space of osteons that makeup the cortical part of bone, have blood supply of innervation of bone cells): this is the reason of increase risk of fracture/ bone fragility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the risk factors of osteoporosis? Any Conditions or medication?

A

Low estrogen (after menopause)
Low serum calcium
Glucocorticoids (decrease Ca2+ absorption from gut)
Physical inactivity
Cushing’s syndrome, diabetes
Alcohol & smoking

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

What is the investigation and diagnosis for osteoporosis? and who should be investigated?

A

DEXA scan: test bone density T score: less than 2.5 or -2.5= osteoporosis
All Female 65+ and male 75+, if they are younger, screen if they have previous fragility fractures, on oral corticosteroids (ie, glucocorticoids for arterial problems)

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

what are the treatment options for osteoporosis (mode of action)

A

reduce fragility risk
1. Oral Bisphosphonates: analogue of pyrophosphate that inhibits osteoclast (ie, alendronate & risedronate)
2. Hormone replacement therapy for younger post-menopausal women

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

what are the side effects and compensations for prescribing bisphophonate

A
  • Side effects: Oesophageal ulcer & reflux, Osteonecrosis of jaw (jaw pain with no scalp tenderness), osteosarcoma (bone pain)
  • give vitamin D or calcium if blood test show deficiency
  • raised alkaline phosphatase levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the main complication of osteoporosis and its presentation? Any other complications?

A

FRACTURES
Vertebral/ compression fracture: back pain, height loss, hunches posture
Femoral neck fracture
Distal radius fracture

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

What is gout? Symptoms, site & causes

A
  • inflammatory arthritis that is severely painful, swollen, and red esp at night
  • 70% is in the first MTP but can occur in the ankle, wrist, MCP, knee
  • Drugs (thiazide, furosemide)- trauma, infection, surgery. haemolytic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the test & diagnosis for gout? what other level might also be raised?

A

Test: aspirate for synovial fluid
diagnosis: needle shaped negatively birefringent monosodium urate crystals under polarized light + Uric acid/ urate increase when symptoms settled

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

What are the treatments of gout? Any cautions/ side effects when perscribing?

A
  1. NSAID (prescribe with PPI, not for patients with peptic ulcer)
  2. Colchicine (SE: diarrhea)
  3. allopurinol: Urate lower therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the typical presentation of polymyalgia rheumatica?

A
  • Aching and pain with morning stiffness (45 min+) & worse with movement in the proximal limb muscles but no weakness (ie, painful to move but power is there)
  • Bilateral shoulder pain radiating to arm & elbow, Bilateral pelvic girdle pain
  • Low grade fever, low mood
  • Temporal arteritis symptoms
  • 60 female, white
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the diagnosis of polymyalgia rheumatica? which levels should be normal

A
  • Clinical symptoms + inflammatory marker + response to steroid- Raised ESR, plasma viscosity, CRP
  • Dramatic response to steroid should be seen (normal creatinine & anti-CCP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment of polymyalgia rheumatica? any side effects? What other medications may be necessary for long term treatment?

A
  • Prednisolone 15mg (usually a dramatic respond by 3-4 weeks with normal inflammatory marker, if not give another diagnosis)
  • Reduce dosage gradually- SE: avascular necrosis of hip
  • give bisphosphonate w/or calcium, vitamin D to reduce osteoporosis risk caused by steroid
  • Give PPI for gastric protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some related conditions to polymyalgia rheumatica? MSK/systemic symptoms?

A

Commonly associated with giant cell/ temporal arteritis (headache & tender at temple, jaw pain)
Carpal tunnel
Pitting edema

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

what is the pathophysiology of rheumatoid arthritis

A
  • Genetically predisposed individual have immune system that mistakes self-antigens (ie citrullinated protein) as foreign, and immune cells (B and T cells) produce autoantibodies that bind to these self- antigens and triggers a immune response
  • Immune response attacks synovial membrane and recruits more immune cells causing inflammation and destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms of rheumatoid arthritis?

A
  • Joint swelling, pain, w/ morning stiffness for 30 min +
  • effects MCP and PIP
  • Gradually worsen as larger joints are involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what clinical exam is positive and deformity is present in rheumatoid arthritis

A
  • positive squeeze test
  • swan neck & boutonniere deformity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the diagnostic tests for Rheumatoid arthritis?

A
  1. Rheumatoid factor
  2. anti-CCP: more specific, if rheumatoid factor is negative do this
  3. X-ray of hands and feet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is rheumatoid factor

A

circulating antibody (igM or igA) that react to Fc portion of igG

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

what is Anti-CCP

A

anti-cyclic citrullinated peptide antibodies
- formed during a self-citrulllination process in genetically predisposed individual where positively charged arginine amino acid turns into neutral citrulline and body developed Anti-CCP

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

what is considered bad prognosis for rheumatoid arthritis?

A

Positive rheumatoid factor, anti-CCP & erosions on x-ray in 2 years means poor prognosis

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

what criteria is used to measure disease activity?

A

DAS 28
- assess 28 joints for swelling and tenderness in combination with inflammatory markers

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

what is the X-ray finding of rheumatoid arthritis, who should get it?

A

LESS
L: loss of joint space
E: periarticular Erosion
S: soft tissue swelling
S: soft bones/ osteopenia

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

What are the steps of management for rheumatoid arthritis treatment?

A
  1. Monotherapy of oral methotrexate +/- short term corticosteroids: prednisolone for flare ups (oral or intramuscular)
  2. If methotrexate is not suitable or severe SE-> sulfasalazine, leflunomide, hydroxychloroquine is used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

when is TNF inhibitor used when treating rheumatoid arthritist

A

If patient have tried 2 DMRAD and still inadequate response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the first line main rheumatoid arthritis treatments, its side effects/ monitoring when prescribed?

A
  • Methotrexate, Once per week
  • prescribed w/ folic acid to be taken a day after due to myelosuppression (bone marrow)
  • hepatotoxicity, methotrexate pneumonitis
  • Monitor FBC, U&E, LFT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the mode of action of methotrexate

A

inhibit dihydrofolate reductase (enzyme for synthesis of purines & pyrimidines)

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

what should be avoided when prescribing methotrexate

A
  • Avoid trimethoprim or co-trimoxazole, and aspirin
  • avoid pregnancy for 6 months after stopping drug
32
Q

what are the pros and cons of hydroxychloroquine?

A
  • Bull’s eye retinopathy- visions loss, need annual eye screening
  • Can be used in pregnant woman
33
Q

what are some examples of TNF inhibitors, any side effects?

A
  • etanercept, infliximab
  • Risk of reactivation tuberculosis (chest x-ray & TB test first)
34
Q

what are the respiratory and cardiovascular manifestations of rheumatoid arthritis

A
  • resp: pulmonary fibrosis, pleural effusion, bronchiectasis
  • Ischemic heart disease
35
Q

what are the MSK manifestations of rheumatoid arthritis

A

MSK: osteoporosis, Carpal tunnel syndrome, De-quervain’s

36
Q

what is the triad for felty’s syndrome?

A

rheumatoid arthirist + splenomegaly + low white cell count

37
Q

what are the histological changes in osteoarthritist

A
  • Progressive damage to a synovial joint causing structure changes and pain
  • Loss of cartilage at the ends of bones
  • osteophytes (bone growth to compensate for the lost cartilage)
38
Q

what are the risk factors of osteoarthrisit

A

genetic factors
age, female
obesity
previous trauma

39
Q

What is a synovial joint? What does it consist of?

A
  • Joint that allows movement
  • enclosed by articular cartilage (end of bones) and synovial membrane on the side forms a joint cavity filled by synovial fluid
  • protected on the outside by a joint/ articular capsule.
40
Q

What are the symptoms of osteoarthritis?

A
  • Swelling of Carpometacarpal (CMC, squaring of thumb), and DIP (heberden’s nodes)
  • Bilateral Knee and hip pain
  • Joint pain on movement, relieved by resting, Morning stiffness that only last few minutes
41
Q

What is the investigation for osteoarthritis? What are the results?

A

X-ray
- Loss of Joint space
- Osteophytes (new bone formed to compensate cartilage loss)
- Subchondral sclerosis (dense bone formed in cartilage loss)
- Subchondral cysts (cyst formed beneath cartilage when it’s degenerating)

42
Q

What is the management and treatment for osteoarthritis?

A
  • Weight Loss, muscle strengthening exercise
  • Paracetamol, topical NSAIDs/ COX-2 inhibitors (avoid if patient takes aspirin, topical NSAID only for hand and knee)
  • add codeine
43
Q

What is the management for osteoarthritis of the hip?

A

Oral analgesia
Intra-articular injections
Total hip replacement (aseptic loosening is common)

44
Q

What is the cause of ankylosing spondylitis?

A
  • Having the HLA-B27 gene causing inflammation for sacroiliac joint (sacrum= below vertebrae attaching it to pelvis, ilium= pelvis)
45
Q

what is the typial patient profile and presentation of ankylosing spondylisit

A
  • Male 20-30 years of age + lower back pain/stiffness that is worse in the morning & improve with exercise
  • Pain at night that’s relieved when getting up
46
Q

What are the investigations and treatment for ankylosing spondylitis?

A
  • X-ray, clinical examinations, HLA-B27 gene (90%), raised inflammatory markers
  • Exercise like swimming, NSAID, physiotherapy
47
Q

What are the X-ray symptoms of ankylosing spondylitis?

A
  • Sacroiliitis: loss of joint space & denser bones in sacroiliac joint
  • Squaring of lumbar vertebrae
  • Syndesmophytes: bony outgrowth in edge of vertebrae
48
Q

What are the clinical examinations done for ankylosing spondylitis? What are the results?

A

Lumbar exam: reduced lateral flexion
Schober’s test: reduced forward flexion
Reduced chest expansion

49
Q

what are the ocular, MSK, and hematological manifestations of ankylosing spondylitis

A
  • Anterior uveitis: inflammation of front eye
  • Achilles tendonitis: inflammation of tendon that connects calf muscle and heel bone
  • Amyloidosis: build up of protein amyloid in organs and tissues
50
Q

what are the respiraotry and cardiovascular manifestations of ankylosing spondylitis

A
  • Apical fibrosis: scarring of apex of lung
  • Aortic regurgitation: aortic valve cant close properly
  • AV node block: delayed electrical signal at av node
51
Q

What is vasculitis? What are the 2 main types?

A

Inflammation of the blood vessels
- Primary vasculitis: inflammatory response that targets the vessel walls and has no known cause
- Secondary vasculitis: infection, drug, toxin and may occur as part of another inflammatory disorder or cancer

52
Q

What does vasculitis cause? What are some general symptoms?

A
  • Inflammation -> thickening of vessel wall-> stenosis & ischemia
  • Palpable purpura (raised, non-blanching when pressed)
53
Q

What are the symptoms & typical presentation of temporal arteritis/ giant cell arteritis?

A
  • Old female 60+ have rapid onset unilateral headache, jaw pain
  • Blurring, double vision
  • Scalp tenderness and pain esp when brushing hair
  • Patient might have polymyalgia rheumatica
54
Q

What are the investigations for temporal arteritis

A
  • Temporal artery biopsy (skip lesions is possible showing normal result)
  • Raised ESR
55
Q

what are the treatments for temporal arteritis

A
  • Urgent high dose prednisolone for no visual loss in suspected patients
  • IV methylprednisolone for evolving visual loss
  • Urgent refer to ophthalmology
56
Q

What is a major complication of temporal arteritis? What test should be done

A
  • Anterior ischemic optic neuropathy: occlusion of posterior ciliary artery (branch of ophthalmic artery) causing ischemia of optic nerve head
  • Fundoscopy: swollen pale disc and blurred margins
57
Q

What is the typical presentation of kawasaki disease

A
  • child with high grade fever for 5+ day and not responding to antipyretics
  • conjunctival injection ( red inside eyelid),
  • bright red and cracked lips with
  • strawberry tongue
    (Clinical diagnosis can be made with above symptoms)
58
Q

What are the management and complications of kawasaki disease?

A
  • High dose aspirin (rare instance its used in children)
  • Intravenous immunoglobulin
  • Coronary artery aneurysm
59
Q

what is ANCA associated vasculitis?

A

autoimmune condition affecting small blood vessels caused by ANCA (anti-neutrophilic cytoplasmic autoantibodies)

60
Q

what are the 2 types of ANCA vasculitis?

A
  1. pANCA: targets myloperoxidase protein
  2. cANCA: targets proteinase 3
61
Q

what are examples of ANCA associated vasculitis

A
  • granulomatosis w/ polyangiitis
  • eosinophilic granulomatosis w. Polyangiitis
  • microscopic polyangiitis
62
Q

what are the symptoms of ANCA vasculitist?

A
  • Renal impairment
  • resp symptoms
  • systemic
  • vasculitic rash
63
Q

what are the investigations necessary for ANCA vasculitist

A
  • Urinalysis for hematuria & proteinuria
  • U&E for renal
  • ANCA testing
  • CXR
64
Q

what is the treatment for ANCA vasculitis

A
  • Steroids
  • cyclophosphamide
65
Q

What are the symptoms, investigation and treatment of wegener’s granulomatosis (granulomatosis with polyangiitis)

A
  • Renal failure, epistaxis/ haemoptysis (nose bleed & coughing up blood)
66
Q

what are the investigations of wegener’s granulomatosis (granulomatosis with polyangiitis)

A
  • Bloods (cANCA), CXR (lesions), renal biopsy (cluster of inflammatory cells/ granulomas)
67
Q

What are the symptoms, investigation and treatment of churg-strauss syndrome (eosinophilic granulomatosis with polyangiitis)

A
  • Bizarre asthma is adult
  • paranasal sinusitis
68
Q

What are the investigations of churg-strauss syndrome (eosinophilic granulomatosis with polyangiitis)

A
  • Bloods: P-ANCA with eosinophilia
  • Biopsy: granulomatous and necrotizing vasculitis
69
Q

What is polyarteritis nodosa? Describe the typical presentation

A
  • Vasculitis in medium sized arteries
  • Common in middle age men with hepatitis B
  • Systemic nerve damage, abdominal pain, testicular pain
70
Q

What are the investigation for polyarteritis nodosa?

A
  • Angiogram, tissue biopsy
  • hepB serology might be found
71
Q

What are the treatment of polyarteritist nodosa

A
  • Corticosteroids
  • cyclophosphamide
72
Q

What is the pathophysiology of systemic lupus erythematosus?

A
  • Type 3 hypersensitivity
  • Immune system dysregulation leading immune complex deposition in variety of organs
73
Q

What are the cutaneous/ dermatological symptoms of systemic lupus erythema?

A
  • Malar rash in nasolabial folds-> butterfly rash
  • Raynaud’s phenomenon (fingers turn white or blue)
  • Mouth ulcers
74
Q

What are the MSK manifestations of systemic lupus erythematosus?

A
  • Arthritis: synovitis or tenderness at 2+ joints with 30 min morning stiffness (deformities are reducible and should not affect joint function, ie, patient can make fist)
  • Arthralgia, myalgia
75
Q

How are the investigations and monitoring used in systemic lupus erythematosus?

A
  • Antibodies: ANA and anti-dsDNA
  • Inflammatory marker (high means underlying infection)
  • Complement level C3 and C4 are low during active disease
76
Q

What are the antibodies associated with systemic lupus erythematosus?

A
  • Highly specific and sensitive: anti-dsDNA
  • anti-smith but has lower sensitivity
  • Highly sensitive: ANA (used to exclude lupus but not very specific)
77
Q

What are the treatments of systemic lupus erythematosus?

A
  • NSAID, sun block
  • Hydroxychloroquine
  • Prednisolone if internal organ involvement

year 2 core concepts (9 decks)

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