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phase 2 medicine > rheumatology > Flashcards

rheumatology Flashcards

1
Q

what markers can measure the rate of collagen formation in the blood

A

P1NP and P1CP

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2
Q

what is cathepsin k

A

enzyme which breaks down collagen; secreted by osteoclasts

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3
Q

what type of collagen are bones, ligaments, tendons, and skin made of

A

type 1

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4
Q

what does type 4 collagen make

A

the basement membrane

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5
Q

what does type 10 collagen make

A

the growth plate

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6
Q

what are the different areas of the bone

A

epiphysis, metaphysis, diaphysis

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7
Q

woven vs lamellar bone

A

woven bone is made quickly and is disorganised
lamellar bone is made slowly and it is more organised. lamellar bone is remodelled woven bone.

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8
Q

what are osteons

A

cylinders of lamellae which contain the blood and nerve supply in the centre in a canal called the harversian canal

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9
Q

what is the difference between the type of bone in the epiphysis and the diaphysis

A

the epiphysis has trabecular bone and the diaphysis has cortical bone

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10
Q

where do osteoblasts originate from

A

mesenchymal stem cell

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11
Q

what is the function of alkaline phosphatase (ALP) in bone and why do you measure it in the blood

A

Alkaline phosphatase is produced by osteoblasts. It facilitates the deposition of minerals (mainly calcium and phosphate) in the bone matrix. The enzyme helps with bone formation and remodelling.

Measuring alkaline phosphatase levels in the blood can be a diagnostic tool to assess bone health. Elevated levels of alkaline phosphatase may indicate increased bone turnover, as seen in conditions such as bone growth (during periods of rapid bone growth, like adolescence) or in diseases that affect bone metabolism, such as Paget’s disease, osteomalacia, or certain bone tumors.

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12
Q

why do you get hyperexcitability in hypocalcaemia

A

Calcium contributes to setting the threshold for action potentials because calcium maintains a constant background gradient and the action potential is triggered by entry of sodium into the cell. When calcium levels are low, the threshold may be altered, making it easier for nerve cells to reach the threshold and generate action potentials.

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13
Q

where in the nephron is most calcium reabsorbed

A

in the proximal convoluted tube

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14
Q

FGF-23 function and what is it produced by

A

regulates Vit D levels. FGF-23 decreases Vit D to decrease phosphate gut absorption and also increases renal phosphate excretion
it is secreted by osteocytes

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15
Q

if you have a low calcium diet will you absorb less calcium?

A

no. you will synthesise more Vit D3 (calcitriol) so that you can absorb more Ca from your diet

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16
Q

effect of PTH on serum phosphate levels

A

decreases serum phosphate levels –> more excretion of phosphate in DCT

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17
Q

what is osteoid

A

unmineralised bone tissue which is secreted by osteoblasts and needs to become mineralised

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18
Q

interstitial vs appositional growth and why is it relevant

A

interstitial –> from within –> growth in length
appositional –> from the outside –> growth in width
bones grow like this so that they don’t increase in weight. they are broken down from within by osteoclasts whilst they are being built from the outside by osteoblasts

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19
Q

what is the process of how bones are built

A

formation of cartilage model from hyaline cartilage by chondroblasts
you get primary ossification in diaphysis and secondary ossification in epiphysis
ossification slowly starts replacing cartilage
fusion of growth plates marks end of growth

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20
Q

how does cartilage get its nutrients

A

diffusion

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21
Q

what is the ossification of the growth plate called

A

endochondral ossification

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22
Q

what is the ossification of the bones of the skull called

A

intramembranous ossification

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23
Q

why is exercise physiologically good for bone

A

the stress form exercise downregulates osteoclast activity –> less chance of osteoporosis

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24
Q

what are the red flags for bone cancer

A

bone pain (worse at night)
pathological fracture
soft tissue swelling

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25
Q

type 1 vs type 2 muscle fibres

A

type 1 - slow twitch fatigue resistant
type 2a - fast twitch fatigue resistant
type 2b - fast twitch fatigue sensitive (largest fibres and strongest contractions)

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26
Q

how do muscles sense stretch and tension

A

stretch: muscle spindles
tension: intrafusal muscle fibres which are wrapped around gamma nerve fibres

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27
Q

what is the storage form of calcium in bone

A

calcium hydroxyapatite

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28
Q

what protects the tendons from overstretching and explain the pathophysio

A

the Golgi tendon organ

when the muscle contracts the tendon stretches –> if the golgi tendon organ senses too much stretch it sends impulse to 1 beta neurons in spinal chord. this synapses on an interneuron which then stimulates the alpha neuron innervating the muscle, causing muscle relaxation and preventing muscle damage

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29
Q

what type of collagen is cartilage made from

A

type 2 collagen

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30
Q

what is uric acid synthesised from

A

the breakdown of purines

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31
Q

why does alcohol increase the chance of gout

A

alcohol increases purine synthesis and decreases the excretion of uric acid

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32
Q

explain how osteoblasts and osteoclasts communicate to remodel bone

A

osteoBlast expresses RANKL which binds to osteoClast RANK receptor. This activates osteoClasts.
osteoBlasts also form OPG (osteoproteginin) which downregulates RANKL to control osteoclast activation

so if you have more RANKL than OPG you get bone resorption and if you have less RANKL than OPG you have decreased bone resorption

sclerostin is secreted by osteoclasts to STOP bone formation by binding to the WNT receptor on osteoblasts

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33
Q

what is Desonumab

A

medication which stops RANKL production so stops osteoclast formation

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34
Q

what is rhomosozumab

A

medication which inhibits sclerostin to promote bone formation

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35
Q

what is the most common cause of ricket’s

A

vit d deficiency

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36
Q

what is septic arthritis

A

infection of 1 or more joints due to pathogens

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37
Q

what is the most common cause of septic arthritis

A

staph aureus

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38
Q

risk factors for septic arthritis

A

pre-existing joint disease, intravenous drug user, joint prosthesis, immunosuppression, alcohol abuse, diabetes, recent joint surgery, intra-articular corticosteroid injection

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39
Q

key presentations of septic arthritis

A

acutely hot swollen painful red joint
onset less than 2 weeks
fever
reduced motion
lethargy
sepsis: tachycardia, hypotension, cold, clammy, shaking

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40
Q

1st line and gold standard investigations for septic arthritis

A

1st line: blood culture, CRP/ESR, FBC: raised WCC

gold standard: urgent aspirate joint for MC+S

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41
Q

management of septic arthritis

A

aspirate joint
empirical antibiotic
after lab results come you change antibiotic to the strain of bacteria identified
NSAIDS for analgesia
if patient is already on steroids stop them if possible

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42
Q

what antibiotics do you give for septic arthritis caused by N. gonorrhoea

A

IM ceftriaxone + azithromycin

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43
Q

what is osteomyelitis

A

Inflammatory condition of bone and bone marrow caused by an infectious organism, most commonly staph aureus.

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44
Q

most common cause of osteomyelitis

A

staph aureus

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45
Q

risk factors for osteomyelitis

A

Previous osteomyelitis, penetrating injury, IVDU, diabetes (diabetic foot ulcers), HIV, recent surgery, infection, sickle cell, rheumatoid arthritis, chronic kidney disease, children (upper respiratory tract or varicella infection)

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46
Q

what is acute osteomyelitis and what are possible complications

A

Inflammation and Bone Edema → In the early stages of bone infection, there is an acute inflammatory response. The affected bone becomes inflamed, and there is an accumulation of immune cells and fluid, leading to bone edema

complications: chronic osteomyelitis, formation of sequestra and invlucurum

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47
Q

key presentations of osteomyelitis

A

limping, reluctance to bear weight, hot, erythema and swollen joint, dull pain, bone oedema , muscle aches

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48
Q

what representative feature of acute osteomyelitis should you see on an MRI

A

bone oedema

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49
Q

what representative feature of chronic osteomyelitis should you see on an MRI? explain what they are

A

Sequestra: areas of necrotic (dead) bone, known as sequestra, may form. These are surrounded by inflammatory tissue and pus.

Involucrum: formations of new bone around sequestra to compensate for lack of support from necrotic bone. This new bone, called involucrum, is thickened and sclerotic, serving as a protective shell.

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50
Q

investigations for osteomyelitis

A

1st line - raised WCC, CRP, ESR, blood culture, X-ray, MRI

gold standard - bone marrow biopsy and culture

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51
Q

what is charcot’s foot

A

Charcot’s foot / neuropathic arthropathy - Complication from peripheral neuropathy from diabetes.
You get progressive degeneration of the weight bearing joints of the foot due to loss of innervation which causes loss of sensation so even if you have damage to your foot you don’t feel it and this results in repetitive minor traumas to the foot → Arthropathy
All of the repetitive damage leads to chronic inflammation in the foot → you get arch collapse → structural failure of foot and ankle → foot more susceptible to soft tissue breakdown and infection

Signs: red, hot, swollen foot

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52
Q

management of osteomyelitis

A

immobilise and give antibiotics
supportive therapy
surgical removal of necrotic bone

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53
Q

give examples of some inflammatory connective tissue disorders

A

lupus, scleroderma, sjogren’s syndrome

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54
Q

risk factors to lupus

A

female (14-40)
drugs - isoniazid
HLA link
EBV
smoking
genetics

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55
Q

pathophysiology of lupus

A

In a normal person apoptosed cells should be cleared out by the immune system but if they are not cleared out then the cellular contents, including the DNA are exposed to the immune system → the immune system mounts an attack against our own proteins and nuclear material

The antibodies to a person’s nucleus are called ANA (Antinuclear Antibodies) and when they bind to the surface antigen of a cell or they form complexes which deposit in tissues and they can cause different kinds of inflammation.

Some people with lupus are also deficient of complement system proteins like C3 and C4 → apoptosis can’t happen well

When the body’s immune system autoregulation kicks in the body can slowly recover → that is why you get flare ups

Anything that causes mass cell apoptosis can trigger flare-ups:
UV light
Surgery
Infection
Pregnancy
Stress

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56
Q

key presentations of lupus

A

Face
Photosensitive (eyes)
Red malar butterfly rash

Neurological
Cognitive impairment
Seizures
Psychosis
Delirium
Peripheral neuropathies

Lungs
Pulmonary fibrosis
Pulmonary vasculitis
Pleural effusion

Cardiovascular
Pericarditis
Pericardial effusion
Myositis
Valvular disease
Hypertension → complication of nephritic syndrome

GI
Splenomegaly
Kidney
Nephritic syndrome

MSK
Arthralgia
Arthritis
Raynaud’s phenomenon → episodic cyanosis of fingers due to vasoconstriction from the cold or emotional stress
Osteopenia and osteoporosis → due to low Vit D from low sun exposure, renal osteodystrophy, long term use of steroids, age, female sex (menopause)

Non-specific symptoms
Fever
myalgia/fatigue
Hair loss
Weight loss
Mouth ulcers
Lymphadenopathy → swollen lymph nodes
Chronic anaemia
Leucopenia

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57
Q

1st line and gold standard investigations for lupus

A

FBC (anaemia, leukopenia, thrombocytopenia)
CRP, ESR → indicate inflammation but are not always high; for example when you are stable and are not having a flare-up
Kidney function → urinalysis, raised urea and creatinine, urine albumin:creatinine ratio (proteinuria), urine dipstick (haematuria, proteinuria)
LFTs
renal USS for pyelonephritis

Gold standard
Antibodies
anti-nuclear (ANA)
anti-double-stranded DNA (aDsDNA)
Complement system proteins → low complement levels C3, C4

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58
Q

what antibodies do you test for in lupus

A

anti-nuclear (ANA)
anti-double-stranded DNA (aDsDNA)

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59
Q

management of lupus

A

1st line – Hydroxychloroquine
Consider: NSAIDs (for the MSK pain), corticosteroid, immunosuppressant (methotrexate), monoclonal antibodies (rituximab)

Others: treat anaemia and reduce cardiovascular risk by decreasing hypertension

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60
Q

what is scleroderma and what are the types

A

Systemic sclerosis in which normal tissue is replaced with thick dense connective tissue. It affects skin, blood vessels and internal organs. 2 types: limited cutaneous systemic sclerosis (CREST syndrome) and diffuse cutaneous systemic sclerosis.

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61
Q

what is the cause of scleroderma

A

Autoimmune antibodies attacking connective tissue

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62
Q

risk factors for scleroderma

A

Women 30-50yo, family history, exposure to environmental substances and toxins (silica dust, solvents)

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63
Q

key presentations of scleroderma

A

CREST mnemonic
Calcinosis (calcified nodules under skin),
Raynaud’s phenomenon
Esophageal dysmotility (strictures, food gets stuck on swallowing),
Sclerodactyly (tightening and thickening of skin over fingers distal to MCP joint),
Telangiectasia (prominent dilated capillaries, especially on cheeks)

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64
Q

what is raynaud’s phenomenon

A

episodic cyanosis of fingers due to vasoconstriction from the cold or emotional stress

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65
Q

what is sclerodactyly and what disease is it associated with

A

tightening and thickening of skin over fingers distal to MCP joint
associated with scleroderma

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66
Q

what is Telangiectasia and what disease is it associated with

A

prominent dilated capillaries, especially on cheeks
associated with scleroderma

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67
Q

what are complications of scleroderma

A

Coronary artery disease, pulmonary hypertension, pulmonary fibrosis, GORD, kidney failure, malabsorption, hypothyroidism

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68
Q

gold standard investigations for scleroderma

A

Anti centromere antibodies (limited/CREST)
Anti-SCL70 (diffuse)

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69
Q

what is Sjogren’s syndrome

A

autoimmune condition affecting exocrine glands and causing dry mucous membranes

70
Q

what other diseases can have Sjogren’s syndrome as a complication

A

lupus with rheumatoid arthritis

71
Q

key presentations of Sjogren’s syndrome

A

Dry mucous membranes – dry mouth (xerostomia), dry eyes (keratoconjunctivitis sicca), dry vagina

72
Q

gold standard investigations for Sjorgen’s syndrome

A

Anti-Ro and anti-La antibodies

73
Q

management of Sjorgen’s syndrome

A

1st line – artificial tears, artificial saliva, vaginal lubricant.
Hydroxychloroquine used to halt progression

74
Q

dermatomyositis vs polymyositis

A

dermatomyositis = connective tissue disorder with inflammation of muscles and skin

polymyositis = chronic inflammation of muscles

75
Q

key presentations of dermatomyositis and polymyositis

A

SYMMETRICAL wasting of muscles of shoulder and pelvic girdle and muscle pain, fatigue and weakness
in dermatomyositis only you get
gottron lesions (scaly erythematous patches) on knuckles, elbows, and knees. Purple rash on face and eyelids. Photosensitive erythematous rash on back, shoulders and neck. Periorbital oedema. Subcutaneous calcinosis

76
Q

1st line and gold standard investigations for dermatomyositis and polymyositis

A

1st line (think about muscle damage markers)
Lactate dehydrogenase raised → cellular damage
AST and ALT raised → AST found everywhere, in liver and in muscles and kidneys
myoglobin raised → only found in muscle after muscle injury
creatinine kinase raised (>1000 U/L. Normal = <300.) → also shows muscle injury but not as accurate because it can be influenced by muscle mass; waste product produced after metabolism of creatine phosphate in muscle
Serology: anti-Jo-1 (polymyositis), anti Mi2 (dermatomyositis), anti-nuclear antibodies (dermatomyositis). Electromyograph

gold standard
muscle fibre biopsy

77
Q

management of dermatomyositis and polymyositis

A

1st - steroid
2nd - immunosuppressant
3rd - monoclonal antibody

1st line – prednisolone. Also, IV immunoglobulin
2nd line – immunosuppressant (methotrexate, azathioprine)
3rd line – rituximab or cyclophosphamide

78
Q

osteoarthritis definition

A

Degenerative joint disorder, not inflammatory. Osteoarthritis is ‘wear and tear’ of synovial joints, resulting from mechanical and biological events that destabilise the normal degradation and synthesis of cartilage.

79
Q

risk factors to osteoarthritis

A

High intensity labour, old age, women, obesity, occupation/sports, genetic

80
Q

pathophysiology of osteoarthritis

A

Due to wear and tear over time there is more cartilage breakdown than repair causing an imbalance. Chondrocytes respond by metalloproteinase secretion which degrades type 2 collagen and causes cysts. Bone underneath cartilage attempts to overcome this response by producing more type 1 collagen which leads to abnormal bony growths (osteophytes) and cysts

81
Q

what are the most commonly affected joints in osteoarthritis

A

hips, knees, distal interphalangeal joints, thumb, cervical spine, sacroiliac joints

82
Q

key presentations of osteoarthritis

A

Transient painful joints stiff for <30 mins in morning, worse throughout day. Proximal Bouchard nodes and distal Heberden nodes on fingers.
Hard asymmetrical bulky non-inflamed joint, squaring at the base of thumb (carpometacarpal saddle joint)

83
Q

Bouchard nodes vs Heberden nodes

A

signs for osteoarthritis; they are bulky non-inflamed joints
B –> proximal
H –> distal

84
Q

gold standard investigation for osteoarthritis

A

x-ray

85
Q

what x-ray changes do you see in osteoarthritis

A

L - loss of space between bones
O - osteophytes
S - subchondral sclerosis
S - subchondral cysts

86
Q

management of osteoarthritis

A

1st line - lifestyle (less weight-bearing, physio), topical analgesics (capsaicin, NSAIDs – diclofenac, methyl salicylate), + paracetamol, + opioid (PPI for gastric protection)
joint replacement surgery (arthroplasty)

87
Q

what is reactive arthritis

A

synovitis in a joint as a result of a recent infective trigger
Typically causes monoarticular synovitis → affects single joint in lower limb (mc knee).

88
Q

how do you distinguish between reactive arthritis and septic arthritis?

A

in reactive arthritis there is NO JOINT INFECTION

89
Q

what is Reiter syndrome

A

reactive arthritis

90
Q

what are the causes of reactive arthritis

A

STIs or gastroenteritis
Chlamydia trachomatis → most common
N. gonorrhoeae → although it usually causes septic arthritis not reactive arthritis
Gastroenteritis: campylobacter jejuni, salmonella enteritidis, shigella

91
Q

what are risk factors to reactive arthritis

A

HLA B27 gene → this gene is known for seronegative spondyloarthropathy
Male
preceding STI or gastroenteritis

92
Q

key presentation of reactive arthritis

A

Can’t See –> conjunctivitis
Can’t pee –> urethritis/balanitis (dermatitis of the head of the penis)
Can’t climb a tree –> arthritis

onset 1-4 weeks after infection

93
Q

what is balanitis

A

dermatitis of the head of the penis

94
Q

investigations for reactive arthritis

A

ESR and CRP raised → indicate presence of inflammation

Negative ANA (antinuclear antibodies) → rule out lupus

Rheumatoid factor negative → rules out rheumatoid arthritis

X-ray to identify structural changes to joints
sacroiliitis - inflammation of the sacroiliac joints
enthesopathy - disorder of the enthesis of bones (the enthesis connects tendon to bone)

joint aspiration negative → exclude septic arthritis and gout

stool cultures → to rule out GI infections

urine dipstick → to exclude UTI

Polarised light microscopy → rule out crystal arthropathy

95
Q

management of reactive arthritis

A

you ALWAYS assume septic arthritis until proven otherwise so first line you give antibiotics and do joint aspiration

once septic arthritis is ruled out you give
NSAIDs (naproxen, ibuprofen, indometacin)
intra-articular corticosteroid injection
DMARDs - disease-modifying anti-rheumatic drug (sulfasalazine)
or
TNF inhibitors in chronic arthritis

96
Q

rheumatoid arthritis

A

Autoimmune condition causing inflammation of the synovial lining of joints, tendon sheaths and bursa. Inflammatory symmetrical polyarthritis

97
Q

what is the population that has rheumatoid arthritis like

A

Women 30-50 (3x more likely than men premenopausal)

98
Q

causes of rheumatoid arthritis

A

Autoimmune, genetic (HLA DR4/DR1)

99
Q

pathophysiology of rheumatoid arthritis

A

autoimmune destruction of synovium via the autoantibody RHEUMATOID FACTOR which attacks IgG antibodies. This causes inflammation and damage to tendons, bones, cartilage and ligaments

Cyclic citrullinated peptide antibodies (anti-CCP) are autoantibodies which also target healthy joint tissues.

100
Q

key presentations of rheumatoid arthritis

A

Joint pain worse in morning (>30mins) gets better as day goes on and with movement
Symmetrical distal Polyarthropathy
hot inflamed joints most common in wrist/hand + feet, knee, hip.

101
Q

signs of rheumatoid arthritis

A

Swan neck thumb
ulnar deviation
boutonniere deformity
Z shaped thumb deformity; DIP joint often spared.

make sure that you can picture all of these words in your head

102
Q

investigations for rheumatoid arthritis

A

Serology: anti CCP positive, rheumatoid factor positive!!!!!
Bloods: anaemia, CRP/ESR raised
x-ray: less lost joint space, erosion, soft tissue swelling, soft bones

103
Q

management of rheumatoid arthritis

A

1st line – DMARDs (disease modifying anti-rheumatic drugs) e.g., methotrexate, leflunomide, sulfasalazine

2nd – Add biological agent
Infliximab → monoclonal antibody against TNF-a
Adalimumab → TNF inhibitor
Etanercept → TNF-a inhibitor (all of the TNF inhibitors prevent TNF from triggering inflammation)
Rituximab → monoclonal antibody that targets B cells

3rd – corticosteroid (prednisolone), NSAIDs (ibuprofen)
Pregnant: prednisolone, sulfasalazine, hydroxychloroquine

104
Q

pseudogout vs gout

A

pseudogout caused by formation of calcium pyrophosphate crystals as a result of direct injury whilst gout is caused by high blood uric acid levels which leads to monosodium urate crystal deposits in joints

pseudogout more common in females over 70 and gout more common in middle aged overweight men

105
Q

risk factors for pseudogout

A

Females over 70
hyperthyroidism
hyperparathyroidism
excess iron or calcium
diabetes
metabolic diseases

mainly think about diseases which affect calcium metabolism –> they are the primary risk factors cuz in pseudogout you get CALCIUM pyrophosphate crystals

106
Q

1st line and gold standard investigations for pseudogout

A

1st line
X ray and elevated serum calcium, iron and PTH

gold standard
joint aspiration and polarised light microscopy (rhomboid shaped crystals, positive birefringent of polarised light, calcium pyrophosphate crystals)

107
Q

what feature do you see on an x-ray of pseudogout

A

CHONDROCALCINOSIS
thin white line in the middle of joint space caused by calcium deposition

108
Q

management of pseudogout

A

1st line – NSAIDs, colchicine, corticosteroids/intra-articular steroid injection

109
Q

what is colchicine

A

antinflammatory med used specifically for gout

110
Q

risk factors for gout

A

high purine diet (meat, seafood, beer)
increased cell turnover → more uric acid production so more needed to be excreted
CKD → can’t excrete uric acid efficiently
Diuretics; especially thiazide diuretics → diuretics can compete with uric acid for excretion + dehydration causes the ECM to be more concentrated → higher chance for uric acid to form crystals

111
Q

what oxidises purines to uric acid

A

xanthine oxidase

112
Q

pseudogout and gout: are the polyarticular or monoarticular

A

pseudogout: poly
gout: mono

113
Q

what are the most common locations of gout

A

often big toe/DIPs/wrist/thumb

114
Q

what are tophi

A

subcutaneous deposits of uric acid affecting small joints and connective tissue in DIPs, elbow, ears

sign of gout

make sure that you can picture them

115
Q

1srt line and gold standard investigation for gout

A

1st line
serum uric acid levels

gold standard
joint aspiration and polarised light microscopy (needle-like crystals, negative birefringent of polarised light, monosodium urate crystals)

116
Q

what characteristics do you see in polarised light microscopy in pseudogout vs gout

A

Pseudogout
- rhomboid shaped crystals
- positive birefringent of polarised light
- calcium pyrophosphate crystals

Gout
- needle-like crystals
- negative birefringent of polarised light
- monosodium urate crystals

117
Q

what changes do you see on a gout x-ray

A

maintained joint space
Punch out lytic lesions
Overhanging sclerotic borders
soft tissue tophi

118
Q

management of gout

A

Lifestyle changes (decreased purines, more diary – antigout)
Acute flare: NSAIDs, Colchicine, corticosteroids
Prevention: allopurinol (xanthine oxidase inhibitor > reduces uric acid)

119
Q

what is allopurinol

A

xanthine oxidase inhibitor > reduces uric acid
prevention medication for gout

120
Q

which types of arthritis manifested as night pain and morning pain

A

night pain - gout
morning pain - rheumatoid

121
Q

which are the seronegative spondyloarthropathies

A

ankylosing spondylitis, reactive arthritis and psoriatic arthritis

122
Q

what is ankylosing spondylitis

A

Inflammatory condition mainly affecting sacroiliac joints and vertebral column and causing progressive stiffness and pain.

123
Q

what gene is highly associated with ankylosing spondylitis

A

HLA B27

124
Q

pathophysiology of anchylosing spondylitis

A

inflammation of spine and rib cage leads to formation of new bone and fusion of joints
syndesmophytes replace spinal bone –> spine less mobile

125
Q

syndesmophyte vs osteophyte

A

Syndesmophytes are paravertebral ossifications which bridge across the joint

osteophytes are located at the margin of a degenerative synovial joint and are non-bridging

126
Q

key presentations of anchylosing spondylitis

A

Progressively worse and chronic lower back pain and stiffness
worse with rest and improves with movement
Worse at morning and night
Sacroiliac pain
Flares of worsening symptoms.

127
Q

what is lumbar lordosis

A

the natural inward curve of the lower back

128
Q

signs of anchylosing spondylitis

A

Anterior uveitis, dactylitis, enthesitis
lumbar pathology: decreased lumbar lordosis > more kyphosis
Schober test shows decreased lumbar flexion <20cm

129
Q

what is the Schober test and how do you do it

A

used to assess decrease in lumbar spine range of motion (flexion) due to ankylosing spondylitis

Patient is standing, examiner marks the L5 spinous process by drawing a horizontal line across the patient’s back.

A second line is marked 10 cm above the first line.

Patient is then instructed to flex forward as if attempting to touch his/her toes, examiner remeasures distance between two lines with patient fully flexed.

The difference between the measurements in erect and flexion positions indicates the outcome of the lumbar flexion

if the schober test indicates lumber flexion of less than 20 cm –> ankylosing spondylitis

130
Q

1st line and gold standard investigations for anchylosing spondylitis

A

1st line
CRP and ESR raised, HLA B27 genetic test, MRI spine (bone marrow oedema in early disease before x-ray changes)

gold standard
x-ray of spine and sacrum

131
Q

what is an early MRI sign of anchylosing spondylitis

A

bone marrow oedema

132
Q

what x-ray changes do you see in anchylosing spondylitis

A

Bamboo spine (fusion of vertebral bodies)
· Sacroiliitis
· Squaring of vertebral bodies
· Subchondral sclerosis and erosions
· Syndesmophytes (bony outgrowths in spinal ligament)
· Ossification of ligaments, discs and joints
· Fusion of facet, sacroiliac and costovertebral joints

133
Q

management of ankylosing spondylitis

A

1st line – NSAIDs (naproxen, indomethacin, ibuprofen)

Steroids during flares
anti-TNF drugs e.g., etanercept.
Monoclonal antibodies against TNF (infliximab)
physiotherapy and lifestyle advice
surgery for deformities

134
Q

what conditions is HLA B27 mutation associated with

A

anchylosing spondylitis, psoriatic arthritis, reactive arthritis, IBD,

135
Q

what disorders is HLA DR3-DR4 mutation associated with

A

lupus
rheumatoid arthritis
type 1 diabetes
coeliac disease

136
Q

what is psoriatic arthritis

A

inflammatory arthritis associated with psoriasis –> red scaly rash

137
Q

key presentations of psoriatic arthritis

A

Inflammatory joint pain
plaques of psoriasis (hidden – behind ears, under nails, scalp)
onycholysis (separation of nail from nail bed)
dactylitis (inflammation of finger)
enthesitis (tendon/ligament insertion inflammation)
Nail pitting

138
Q

general key presentations of spondyloarthropathies

A

SPINE ACHE mnemonic

Sausage digits (dactylitis)
Psoriasis → red scaly patches
Inflammatory back pain
NSAIDs > good response
Enthesitis (tendon/ligament insertion)
Arthritis
Crohn’s/colitis/CRP raised → chron’s has the HLA B27 component
HLA B27
Eye (uveitis/conjunctivitis)

139
Q

1st line and gold standard investigations for psoriatic arthritis

A

1st line
CRP/ESR raised, rheumatoid factor -ve, anti-CCG negative, joint aspiration negative for crystals or bacteria

gold standard
joint x-ray

140
Q

x-ray changes in psoriatic arthritis

A

erosion in distal interphalangeal joint and periarticular new bone formation.
· Osteolysis.
· Pencil-in-cup deformity (central erosions of bone beside the joints causing one to look hollow like a cup, and one to sit in the cup)
· Periostitis (periosteum inflammation causing thickened, irregular outline of bone)
· Ankylosis (joints fuse causing stiffness)
· Dactylitis (finger inflammation appears as soft tissue swelling)

141
Q

what does seronegative stand for in seronegative spondyloarthropathies

A

-ve for serum rheumatoid factor which is the autoantibody which causes rheumatoid arthritis

142
Q

what other inflammatory conditions in the body are associated with psoriatic arthritis

A

Anterior uveitis, conjunctivitis, aortitis (inflammation of the aorta), amyloidosis (amyloid = abnormal protein → you get abnormal protein deposits on organs)

143
Q

what is the most severe complication of psoriatic arthritis

A

arthritis mutilans
caused by osteolysis which leads to shortening of bones on fingers

144
Q

how do you manage psoriatic arthritis

A

1st line – NSAIDs for pain (naproxen, ibuprofen, indomethacin), intra-articular corticosteroid injection if severe
DMARDs (methotrexate, sulfasalazine, leflunomide), TNF inhibitor or monoclonal Ab (etanercept, adalimumab, infliximab), last resort – ustekinumab (Mab targeting IL 12 and 23

145
Q

what class of medications are the meds which finish in MAB like infliximab and adalimumab and rituximab

A

monoclonal antibodies which inhibit TNF

146
Q

what are DMARDs and give an example

A

disease modifying anti-rheumatic drugs

methotrexate pt sulfasalazine

147
Q

what is etanercept

A

a TNF blocker

148
Q

what does a bamboo spine of the X-ray indicate

A

ankylosing spondylitis

149
Q

osteopenia vs osteoporosis

A

osteopenia = low bone mineral density unrelated to malnutrition or nutrient deficiency
osteoporosis = more severe decrease in bone mineral density

150
Q

causes of osteoporosis

A

50+ postmenopausal Caucasian women
SHATTERED mnemonic
steroids
hyperparathyroidism and hyperthyroidism
alcohol
thin (low BMI)
low testosterone
early menopause
renal/liver failure
erosive/inflammatory bone disease

151
Q

key features of osteoporosis

A

Fractures (proximal femur, colles wrist fracture → fracture of the radius, compression vertebral crush - kyphosis)

152
Q

1st line and gold standard investigations for osteoporosis

A

1st line
FRAX score (10-year probability of major osteoporotic fracture or hip fracture), Calcium, phosphate, ALP normal

gold standard
DEXA bone scan - T score (normal = T > -1, osteopenia = -2.5 < T < -1, osteoporosis = T < -2.5)

153
Q

why would ALP be normal in osteoporosis

A

in osteoporosis bone formation stays the same and bone resorption increases. ALP only used in bone formation so it won’t change + ALP is not a specific marker for osteoporosis; it is also in bile and liver

154
Q

what is the FRAX score

A

The FRAX score estimates the 10-year risk of major osteoporotic fracture, including the risk of fracturing the spine, hip, forearm, or shoulder

155
Q

management of osteoporosis

A

Lifestyle – exercise, weight, low alcohol and smoking. Vitamin D and calcium supplementation.
1st line –Bisphosphonates (reduce osteoclast activity), e.g., alendronate, risendronate, zoledronic acid.
2nd line – denosumab (monoclonal antibody which binds to RANK-ligand and blocks osteoclast)
Hormone replacement therapy, raloxifene (stimulates oestrogen bone receptor)

156
Q

osteomalacia vs rickets

A

Poor bone mineralisation leading to soft bone due to lack of Ca2+ in ADULTS

Rickets: inadequate mineralisation of the bone and epiphyseal cartilage in the growing skeleton of CHILDREN

157
Q

key presentations of osteomalacia and rickets

A

Osteomalacia: bone pain and tenderness. Dull ache, worse on weight-bearing exercises. Fractures (esp neck of femur), muscle weakness (waddling gait, difficulty with stairs)
Rickets: growth retardation, hypotonia, knock-kneed, bow-legged

158
Q

1st line and gold standard treatment for osteomalacia + management

A

1st line
X-ray (loss of cortical bone – defective mineralisation, looser zone), U&E (low calcium and phosphate), raised PTH, low serum 25-hydroxyvitamin D (<25 nmol/L = deficiency)

gold standard
bone biopsy (incomplete mineralisation)

Managemnet –> Vit D supplements (cholecalciferol) + calcium supplements

159
Q

what is giant cell arteritis

A

Vasculitis is a group of diseases causing inflammation of blood vessels. Giant cell arteritis affects large blood vessels
Autoimmune attacking of blood vessels

160
Q

risk factors for giant cell arteritis

A

Over 50 y.o, northern European, females, Hx of polymyalgia rheumatica

FOR THIS CONDITION THE RISK FACTORS ARE VERY IMPORTANT

161
Q

what part of the arterial system is generally affected by giant cell arteritis

A

aorta and/or its major branches

THINK CAROTID, TEMPORAL ARTERIES AND OCCIPITAL ARTEIRES

162
Q

key presentations of giant cell arteritis

A

Headache (new onset, unilateral over temporal area), scalp tenderness (hurts to brush hair), jaw claudication, visual disturbances (blurred, diplopia, amaurosis fugax – transient vision loss, blindness), thickened temporal arteries and weak pulses

163
Q

what is amaurosis fugax

A

transient vision loss, blindness

164
Q

1st line and gold standard investigations for giant cell arteritis

A

1st line
Raised CRP, Raised ESR >50mm/hr (ESR IMPORTANT IN THIS DISEASE). FBC (anaemia), LFT/RFT may be abnormal
Halo sign (wall thickening) on vascular ultrasonography of temporal and axillary artery

gold standard
Temporal artery biopsy (shows giant cells, granulomatous inflammation – patchy lesions therefore take big sample)

165
Q

management of giant cell arteritis

A

Pain in temporal region in an elderly woman is GIANT CELL ARTERITIS until proven otherwise → steroids stat otherwise she loses her vision

1st line – high dose STEROIDS (e.g., prednisolone 40-60mg)
Consider: tocilizumab, methotrexate. Amaurosis fugax – high dose IV methylprednisolone.

166
Q

what disease is giant cell arteritis highly associated with

A

POLYMYALGIA RHEUMATICA

167
Q

what is polymyalgia rheumatica

A

Inflammatory condition causing pain and stiffness in shoulders, pelvic girdle, and neck.

168
Q

risk factors for polymyalgia rheumatica

A

Females, white, always 50+, associated with giant cell arteritis

169
Q

key presentations of polymyalgia rheumatica

A

Features should be present for at least 2 weeks to make diagnosis
Bilateral shoulder pain radiating to elbow
Bilateral pelvic girdle pain
Pain worse with movement and causes insomnia
morning stiffness >45 mins
rapid response to corticosteroids

170
Q

DDx of polymyalgia rheumatica

A

Fibromyalgia
Osteoarthritis
rheumatoid arthritis
SLE
Myositis
Cervical spondylosis

171
Q

management of polymyalgia rheumatica

A

steroid –> prednisolone

172
Q
A

phase 2 medicine (15 decks)

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