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MSK Flashcards

1
Q

Name 4 morbid outcomes of cauda equina syndrome

A 
sensory deficits
motor deficits 
perianal paraesthesia 
urinary dysfunction 
sexual dysfunction
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2
Q

An angiosarcoma is a malignant tumour of vascular tissue - True or false?

A

True

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3
Q

what is the name given to benign tumours of the vascular tissue?

A

haemangioma, aneurysmal bone cyst

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4
Q

what is the name given for

a. benign
b. malignant

tumours of ADIPOSE tissue?

A

a. lipoma

b. liposarcoma

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5
Q

all sarcomas are malignant - True or false?

A

True

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6
Q

an osteoblastoma is a malignant tumour of bone. true or false?

A

false.

An osteoblastoma and osteoma are both benign tumours. the malignant bone-forming tumour is known as an osteosarcoma.

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7
Q

what are the names given to cartilage-forming tissues?

A

benign - enchondroma, osteochondroma

malignant - chondrosarcoma

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8
Q

what is the name given to fibrous tissue tumours?

A

benign - fibroma

malignant - fibrosarcoma, malignant fibrous histiocytoma (MFH)

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9
Q

osteosarcomas are more prevalent in younger populations whereas myelomas are more common in elderly patients - true or false?

A

true

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10
Q

Name 5 clinical features of an osteosarcoma

A
  1. swelling
  2. joint effusion
  3. pathological fracture
  4. deformity
  5. loss of function
  6. systemic effects of neoplasia
  7. neurovascular effects
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11
Q

Osteosarcoma bone pain often worsens at night - true or false?

A

true

the pain is also unlinked to exercise and is deep and boring

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12
Q

what are the main functions of synovium

name 3

A
  1. maintenance of intact tissue surface
  2. lubrication of cartilage
  3. control of synovial fluid volume and composition (hyaluronan, lubricin)
  4. nutrition of chondrocytes within joints
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13
Q

what joints in the body are most commonly affected by rheumatoid arthritis?

A

small joints of the hands and the feet

it is a chronic symmetric condition.

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14
Q

which type of cells are found in the synovial fluid in the joint cavity during an acute flare up of RA?

A

neutrophils

the rheumatoid synovitis (pannus) is characterised by inflammatory cell infiltration, synoviocyte proliferation and neoangiogenesis

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15
Q

Name 2 commonly associated autoantibodies associated with rheumatoid arthritis

A
  1. rheumatoid factor - this is an autoantibody to self IgG Fc
  2. anti-citrullinated protein

these autoantibodies will recognise either joint antigens such as type II collagen or systemic antigens such as glucose phosphate isomerase

these autoantibodies can sometimes activate the complement system

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16
Q

In seropositive rheumatoid arthritis, patients with anti-citrullinated protein antibody have a less favourable prognosis - true or false?

A

true

diagnostic anti -CCP assays will recognise citrullinated self-proteins

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17
Q

What percentage of concordance occurs in twins with rheumatoid arthritis?

A

monozygotic twins - 15%

dizygotic twins - 5%

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18
Q

What is the most common locus in rheumatoid arthritis?

A

HLA-DRB1

  • there is a role in promoting autoimmunity and molecular mimicry

however remember that genetic associations in RA are complex and involve many genes

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19
Q

describe the main environmental factors that influence rheumatoid arthritis

A
  1. smoking
  2. bronchial stress (exposure to silica)
  3. infectious agents
    3a. viruses - EBV and CMV
    3b. E.coli
    3c. mycoplasma

repeated insults in genetically susceptible patient may lead to

  • formation of immune complexes and rheumatoid factor (high affinity autoantibodies against the Fc portion of Ig)
  • altered citrullination of proteins and breakdown of tolerance, with resulting ACPA response
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20
Q

which amino acids does citrullination involve?

A

citrullination basically means deamination

conversion of arginine in proteins into citrulline via PAD enzymes

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21
Q

what are some of the features of synovitis?

A
  1. increased vascularity
  2. villous hyperplasia
  3. infiltration of T cells and B cells , macrophages and plasma cells
  4. intimal cell proliferation (fibroblasts)
  5. production of cytokines and proteases
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22
Q

suggest 2 drugs that may used in the treatment of rheumatoid arthritis?

A
  1. rituximab

2. abatacept - fusion protein that blocks T-cell co-stimulation

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23
Q

In rheumatoid arthritis, B cells are responsible for the production of IL-6 and TNF-alpha as well as the production of autoantibodies and autoantigen presentation.
what mediatory effects does IL-6 have? name 3 things

A
  1. anaemia
  2. acute phase response
  3. cognitive dysfunction
  4. lipid metabolism dysregulation
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24
Q

suggest 4 systemic factors that arise as a consequence of rheumatoid arthritis

A
  1. vasculitis/nodules/scleritis/amyloidosis
  2. fatigue and reduced cognitive function
  3. liver - elevated acute phase response, anaemia of chronic disease
  4. lungs - interstitial lung disease
  5. muscles - sarcopenia
  6. bone - osteoporosis
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25
Q

Females are affected more by rheumatoid arthritis - true or false?

A

false. RA affects males more and usually presents between the 4th and 5th decade.

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26
Q

What are the main presentations of patients with rheumatoid arthritis?

A
  1. pain
  2. stiffness
  3. immobility
  4. poor function
  5. systemic function
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27
Q

what are the main clinical signs of rheumatoid arthritis?

A
  1. swelling
  2. tenderness
  3. decreased RoM
  4. redness/heat
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28
Q

what scoring system is mainly used in RA?

A

disease activity score - DAS

A DAS score of <2.4 represents clinical remission whereas a DAS of >5.1 represents eligibility for biologic therapy

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29
Q

what are the 4 main categories of drugs used to treat RA?

A
  1. NSAIDs
  2. disease modifying anti-rheumatic drugs DMARD - slower effect on disease activity - methotrexate, sulfasalazine and hydroxychloroquine
  3. biologics
  4. corticosteroids
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30
Q

methotrexate is the cornerstone of combination treatment for RA - with DMARD and biologics.

true or false?

A

true.

biologics actually have an enhanced response when co-prescribed with methotrexate

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31
Q

where does the subclavian artery become the axillary artery?

A

at the lateral border of the 1st rib

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32
Q

where does the axillary artery become the brachial artery?

A

the inferior border of the teres major

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33
Q

what artery is the main contributor to the superficial palmar arch?

A

the ulnar artery

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34
Q

where do superficial veins of the upper limb originate?

A

the deep dorsal venous arch on the back of the hand

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35
Q

the cephalic vein will travel up the limb on the lateral side of the arm and drain into the axillary vein below the clavicle - true or false?

A

true

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36
Q

the basilic vein will travel up the limb on the medial side and become continuous with the brachial veins - true or false?

A

true

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37
Q

what is the name of the vein connecting the cephalic and basilic veins?

A

median cubital vein

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38
Q

grossly describe the lymphatic drainage of the upper limbs

A

the right lymphatic duct will drain the right upper quadrant of the body and the thoracic duct will drain the rest.

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39
Q

what nerve innervates the brachioradialis muscle?

A

the radial nerve

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40
Q

Name the 4 muscles of the superficial layer of the anterior forearm

A
  1. flexor carpi radialis (FCR)
  2. palmaris longus
  3. pronator teres
  4. flexor carpi ulnaris (FCU)

all of these muscles are innervated by the median nerve

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41
Q

the flexor digitorum superficialis is the only muscle in the intermediate layer of the anterior compartment of the forearm.

It has dual innervation - true or false?

A

false

the FDS has single innervation - median nerve

the FDP has dual innervation

medial side - ulnar nerve
lateral side - median nerve

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42
Q

besides the flexor digitorum profundus, what other muscle (s) are found in the deep layer of the anterior forearm?

A

the pronator quadratus

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43
Q

which epicondyle do the pronators of the hand arise from?

A

the medial epicondyle

the anterior compartment of the forearm muscles are generally wrist pronators

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44
Q

Which muscle(s) in the anterior forearm are responsible for adduction of the wrist - give its innervation also

A

flexor carpi ulnaris

ulnar nerve

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45
Q

which anterior forearm muscle is capable of flexing the distal IPJ?

A

the flexor digitorum profundus

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46
Q

which digits does the flexor digitorum superficialis attach to?

A

digits 2-5

acts at the proximal IPJ

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47
Q

which muscle lies more laterally:

a. extensor carpi radialis longus
b. extensor carpi radialis brevis?

A

ECRL lies more laterally and also more superiorly

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48
Q

what nerve is found in the anatomical snuff box?

A

the radial nerve

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49
Q

does the median nerve travel inside or outside of the flexor retinaculum?

A

inside.

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50
Q

what digits are affected by carpal tunnel syndrome

A

1, 2, 3 and lateral aspect of 4th finger.

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51
Q

there are 4 lumbricals, 4 dorsal interossei and 3 palmar interossei muscles - true or false?

A

true

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52
Q

name the 4 thenar muscles

A
  1. flexor pollicis brevis
  2. abductor pollicis brevis
  3. adductor pollicis
  4. Opponens pollicis
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53
Q

2 out 3 hypothenar muscles are named below,

  1. flexor digiti minimi
  2. abductor digiti minimi

what is the name of the 3rd:

A

opponens digiti minimi

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54
Q

which of the hypothenar muscles lies the most medial?

A

abductor - technically makes sense if you think about it.

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55
Q

how does the function of the palmar interossei differ from that of the dorsal interossei?

A

PAD palmar - adduct

DAB - dorsal -abduct

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56
Q

what is the function of the lumbricals?

A
  1. flex the MCP (knuckles)

2. extend the PIPJ

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57
Q

why is the thumb unlike the other digits (in terms of bones)

A

it has no middle phalanx and therefore only an interphalangeal joint.

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58
Q

what are the boundaries of the anatomical snuff box?

A
  1. extensor pollicis longus
  2. extensor pollicis brevis
  3. abductor pollicis longus
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59
Q

which bones are palpable in the anatomical snuff box?

A

the scaphoid and trapezium

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60
Q

Arrange the following muscles in terms from most lateral to most medial

Pronator teres
Palmaris longus
Flexor carpi ulnaris
Flexor carpi radialis

A
  1. pronator teres
  2. flexor carpi radialis (FCR)
  3. palmaris longus
  4. flexor carpi ulnaris (FCU)
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61
Q

which artery supplies the deep arch of the hand?

A

radial artery

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62
Q

osteoblasts are responsible for bone formation - true or false?

A

true.

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63
Q

what kind of cells do osteoblasts originate from?

A

mesenchymal progenitor cells

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64
Q

what type of cells are responsible for bone resorption and what kind of cells do they originate from?

A

myeloid progenitor cells

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65
Q

where is calcidiol produced in the body?

A

calcidiol is produced in the liver

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66
Q

calcitriol is produced by the kidneys - true or false?

A

true

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67
Q

name 4 sites in the body where calcium levels are regulated

A
  1. intestines
  2. bone
  3. parathyroid glands
  4. liver
  5. kidney
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68
Q

what is the effect of severe nutritional vitamin D/calcium deficiency in:

a. growing children
b. adults

A

a. rickets
b. osteomalacia

Vitamin D will stimulate the absorption of calcium and phosphate from the gut; these then become available for bone mineralisation.

muscle function is also impaired in low vitamin D states

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69
Q

describe paget’s disease

A

localised disorder of bone turnover. there is increased bone resorption followed by increased bone formation. this leads to disorganised bone - bigger, less compact and more vascular and more susceptible to deformity and fracture.

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70
Q

describe 3 presentations of paget’s disease

A
  1. isolated elevation of serum alkaline phosphatase
  2. bone pain and local heat
  3. prone to fractures and may experience hearing loss
  4. patient is in 4th decade
  5. bone deformity
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71
Q

suggest 2 treatments for Paget’s disease

A

IV bisphosphonate
IV zoledronic acid

but don’t treat based on an increased serum alkaline phosphatase alone.

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72
Q

describe 5 consequences of osteogenesis imperfecta

A
  1. growth deficiency
  2. defective tooth formation
  3. hearing loss
  4. blue sclera
  5. scoliosis
  6. barrel chest
  7. ligament laxity
  8. easy bruising

treatment of osteogenesis imperfecta medically will be with IV bisphosphonate

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73
Q

what is osteogenesis imperfecta?

A

genetic disorder of connective tissue characterised by fragile bones from mild trauma and even acts of daily life

there is a broad clinical range from those who are prenatally fatal to those only presenting in 40s with early osteoporosis

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74
Q

osteoporosis is a metabolic bone disease - true or false?

A

true

patients have a low bone mass and micro-architectural deterioration of bone tissue leading to enhanced bone fragility and an increase in fracture risk.

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75
Q

suggest 4 things that contribute to risk of fracture in osteoporosis

A
  1. age
  2. BMD - bone mineral density
  • DXA (bone densitometry) hip and spine
    3. falls
    4. bone turnover
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76
Q

Bone mineral density (BMD) can sometimes be calculated to check to risk of fracture in a patient with osteoporosis. what T score is indicative of osteopenia?

A

a T score of between -1 and -2.5 is indicative of osteopenia.

give the patient treatment if there has been a previous fracture.

osteoporosis is a T score that is less than 2.5

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77
Q

suggest 2 drugs that can be given to patients for the primary prevention of osteoporotic fragility in post menopausal women

A
  1. alendronate
  2. etidronate
  3. risedronate
  4. teriparatide
  5. denosumab - monoclonal antibody against RANKL (safer in patients with renal impairment than bisphosphonates)
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78
Q

suggest 2 risk assessment tools used for osteoporosis

A
  1. FRAX - fracture risk assessment tool
  2. Qfracture

if the patient has a >10% risk at any site in the next 10 years then they should be referred for a DXA scan

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79
Q

what independent factors does the FRAX tool take into account?

A
  1. prior fractures
  2. family history
  3. smoking
  4. history of corticosteroid use
  5. alcohol (>3 units)
  6. rheumatic arthritis
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80
Q

what variables does the Qfracture screening tool take into account?

A
  1. CV risk
  2. falls
  3. TCA
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81
Q

suggest 3 endocrine causes of secondary osteoporosis

A
  1. hyperthyroid
  2. hyperparathyroid
  3. GH deficiency
  4. hyperprolactinemia
  5. Cushing’s
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82
Q

suggest 3 medical treatment options for osteoporosis

A
  1. HRT - these have a good effect on osteoporosis
  2. Selective Estrogen Receptor Modulator (SERM) - no effect on vertebral fractures unfortunately
  3. Bisphosphonates - this is first line treatment. ensure the patient has adequate renal function as wella s an adequate calcium and vitamin D status.
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83
Q

what are some side effects of bisphosphonates?

A
  1. oesophagitis
  2. iritis/uveitis
  3. atypical femoral shifts

for this reason patients should be encouraged to take a drug holiday for 1-2 years after 10 years exposure to bisphosphonates

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84
Q

what are the side effects of

a. teriparatide
b. denosumab

in the treatment of osteoporosis

A

a. teriparatide can cause hypercalcaemia and allergy

b. denosumab can cause allergy/rash, symptomatic hypocalcemia

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85
Q

Juvenile idiopathic arthritis affects people up to the age of 16. true or false?

A

true

JIA is an important cause of disability and blindness.

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86
Q

what is the typical presentation of juvenile idiopathic arthritis?

A
  1. painful/limited joint motion
  2. tenderness
  3. warmth
  4. joint swelling
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87
Q

what is the diagnostic test for systemic onset JIA?

A

there is no diagnostic test for systemic onset JIA.

ESR will be elevated and very high in systemic JIA but doesnt correlate with disease activity.

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88
Q

what are the 3 major subtypes of JIA - juvenile idiopathic arthritis?

A
  1. pauciarticular (<4 joints)
  2. polyarticular (5>)
  3. systemic (aka Still’s disease - extra-articular features define the disease)
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89
Q

Pauciarticular JIA can be split into 3 types.

give a brief description of each.

A

type 1 - patient presents with a limp rather than pain. Girls and those under the age of 5 are affected. positive ANA gene is up to 75% and the lower limb is mostly affected. chronic uveitis.

Type 2 - iridocyclitis. Presence of back involvement and HLA-B27 gene classifies as juvenile ankylosing spondylitis. lower limb involvement.
- those lacking back involvement are termed seronegative enthesopathy arthropathy (SEA). boys are mainly affected at about age 8-9. may require THR early in life.

type 3 - chronic iridocyclitis. destructive arthritis with 40% having history of psoriasis. Naill pitting

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90
Q

Describe polyarticular JIA

A

RF negative - iridocyclitis is rare. small and large joints are affected equally. constitutional manifestations - low grade fever and malaise. hepato and splenomegally with mild anaemia.

RF positive - similar to RA but in a child. erosions can be seen in an XR. symptoms such as malaise, weight loss, anaemia and nodules. ANA is present in 40-60% of patients.

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91
Q

describe some of the common systemic onset symptoms of JIA

A
  1. abdominal - hepatosplenomegaly, abdominal pain
  2. arthritis - wrists, knees, spine, ankles, cervical
  3. serositis - pericarditis, polyserositis
  4. rash - most cases present with a rash
  5. fever
  6. lymph nodes - non-tender lymphadenopathy
  7. pulmonary - pulmonary fibrosis or a pleural effusion

remember there is no diagnostic test for systemic JIA

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92
Q

what is the first line therapy for JIA

A

simple pain killers and NSAIDS

NSAIDs can control (pain and fever) disease but doses should be considered.

NSAIDs can also be used as a bridge to DMARDs and also are useful in children who are undergoing surgery.

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93
Q

Assuming there is no response to NSAIDs/steroid injection, what is second line therapy for JIA?

A
  1. methotrexate
  2. anti-TNF therapy - if methotrexate fails
  3. IL1 R-antagonist in refractory systemic arthritis - anakinra
  4. IL^ antagonist - tocilizumab for refractory systemic disease
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94
Q

what are some risks of using systemic steroids in children?

A
  1. osteoporosis
  2. infections
  3. growth abnormalities
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95
Q

Name 3 common clinical presentations of spondyloarthritis

A
  1. lower back pain that worsens at night.
  2. spinal morning stiffness relieved by exercise
  3. psoriatic arthritis
  4. bowel related arthritis
  5. ankylosing spondylitis
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96
Q

Name a few clinical presentations of ankylosing spondylitis

A
  1. inflammatory back pain
  2. limitation of movements in anteroposterior as well as lateral planes at lumbar spine
  3. there may be a limitation of chest expansion
  4. bilateral sacroiliitis on XR
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97
Q

what is the management of ankylosing spondylitis?

A
  1. exercise/physiotherapy
  2. TNF alpha blockers - etanercept, adalimumab (use only if NSAIDs fail)
  3. NSAIDS - ibuprofen, diclofenac
  4. DMARDs - sulfasalazine
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98
Q

suggest a common finding on examination of a patient with psoriatic arthritis

A
  1. nail pitting
  2. dactylitis
  3. enthesitis

the severity of the joint disease does not correlate to extent of the disease.

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99
Q

what is the suggested treatment for psoriatic arthritis?

A
  1. sulfasalazine
  2. methotrexate
  3. cyclosporine
  4. Anti-TNF
  5. steroids
  6. physiotherapy and occupational therapy
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100
Q

what are the common organisms associated with reactive arthritis?

A
  1. salmonella
  2. shigella
  3. yersinia
  4. campylobacter

reactive arthritis is a sterile arthritis typically affecting the lower limb following dysentery, urethritis (chlamydia) etc.

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101
Q

what is Reiter’s syndrome?

A
  1. urethritis
  2. arthritis
  3. conjunctivitis
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102
Q

what are some common presentations of reactive arthritis

A
  1. keratoderma blennorrhagica (brown, raised plaques on soles and palms)
  2. circinate balanitis (painless serpiginous penile ulceration secondary to chlamydia)
  3. enthesitis - plantar fasciitis, achilles tendonitis
  4. mouth ulcers
  5. conjunctivitis
  6. iritis
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103
Q

what investigations would you like to do to confirm a diagnosis of Reactive arthritis

A
  1. increased CRP and ESR
  2. culture stool for diarrhoea
  3. infectious serology
  4. sexual health review
  5. XR/US for enthesitis
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104
Q

what are the prognostic signs for chronicity in reactive arthritis?

A
  1. hip/heel pain
  2. high ESR
  3. family history with HLA-B27
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105
Q

what is the treatment for reactive arthritis?

A
  1. splintage and rest the joints affected
  2. injection of steroids locally with NSAIDs
  3. consider sulfasalazine or methotrexate
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106
Q

what are the common presentations of spondyloarthritis?

A
  1. episodic inflammation of the sacroiliac joints
  2. pain in one or both buttocks
  3. low back pain and stiffness (worse in the morning but imporve with exercise)

patients will often be underdiagnosed because they are asymptomatic between episodes and radiological abnormalities are absent.

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107
Q

what are the back pain criteria for diagnosing ankylosing spondylitis?

A
  1. age of onset < 50
  2. insidious onset
  3. improvement of back pain with exercise
  4. no improvement with rest
  5. pain at night with improvement on getting up
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108
Q

name a test that is useful for diagnosing spinal stiffness

A

Schober’s test

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109
Q

Suggest some non-articular problems in spondyloarthritis

A
  1. uveitis in all types
  2. cutaneous lesions in reactive arthritis (keratoderma blennorrhagica)
  3. nail dystrophy in psoriasis and reactive arthritis
  4. aortitis occasionally in AS and reactive arthritis.
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110
Q

Severe eye pain, photophobia and blurred vision are an emergency in ankylosing spondylitis. true or false?

A

True

Acute anterior uveitis is strongly associated with HLA-B27 in AS and related diseases – occasionally the presenting complaint

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111
Q

what are the investigations for ankylosing spondylitis?

A

blood - check ESR and CRP (they will be high)

HLA testing - not very useful but may give supporting evidence

MRI may show sacroiliitis before XR and also persistent enthesitis

XR - medial and lateral cortical margins of both sacroiliac joints lose definition owing to erosions and eventually becoming sclerotic.

earliest radiological appearances in the spine are blurring of the upper and lower vertebral rims at the thoracolumbar junction caused by an enthesitis caused at the insertion of the intervertebral ligaments

syndesmophytes cause bony ankylosis and permanent stiffening.

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112
Q

what is the treatment of enteropathic arthritis?

A

NSAIDs
intra-rticular corticosteroids
sulfasalazine/mesalazine
TNF-alpha block - infliximab

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113
Q

do patients with lupus tend to present when they are young or old?

A

patients with SLE tend to present when they are young.

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114
Q

Name 9 of the presentations of SLE - systemic lupus erythematosus

A
  1. malar rash
  2. discoid rash
    - raised scarring
    permanent marks
    alopecia
  3. photosensitivity
  4. oral ulcers
  5. arthritis
    - affecting at least 2 joints (XR may be useful)
  6. serositis
    - pleurisy or pericarditis
  7. haematological
    - low WCC, platelets, lymphocytes, haemolytic anaemia
  8. neurological
    - unexplained seizures or psychosis
  9. renal
    - significant proteinuria or cellular casts in urine (do dipstick test)
  10. immunological
    - anti dsDNA, SM, cardiolipin, lupus anticoagulant, low complement
  11. ANA - antinuclear antibodies (easiest one to remember)
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115
Q

what is the name of the skin lesions that patients with scleroderma tend to present with?

A

morphea

females tend to be affected by scleroderma the most between their 30s and 40s. it may lead to complications such as pulmonary hypertension and pulmonary fibrosis or renal crisis or small bowel bacterial overgrowth)

for control of renal crisis and pulmonary hypertension offer the patient ACEI and ATII receptor blockers.

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116
Q

In Sjogren’s syndrome, patients are usually female. what is the typical presentation of this condition - name 3 symptoms and 6 signs of the condition

A

SYMPTOMS

  1. dry eyes and mouth
  2. enlarged parotid
  3. a dry cough and dysphagia

SIGNS (systemic)

  1. fatigue
  2. fever
  3. myalgia
  4. arthralgia
  5. lymphadenopathy
  6. vasculitis
  7. myositis
  8. lung, liver and kidney involvement
  9. Raynauds
  10. peripheral neuropathy
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117
Q

suggest some systemic signs of Sjorgens syndrome (name 5)

A
  1. fatigue
  2. fever
  3. myalgia
  4. arthralgia
  5. lymphadenopathy
  6. vasculitis
  7. myositis
  8. lung, liver and kidney involvement
  9. Raynauds
  10. peripheral neuropathy
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118
Q

name 3 associated conditions with Sjogren’s syndrome

A
  1. autoimmune hepatitis
  2. PBC
  3. thyroid disease
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119
Q

what possible investigations can you do for Sjorgens syndrome?

A
  1. rheumatoid factor is usually positive
  2. positive ANA test
  3. conjunctival dryness - Schirmer’s test
  4. hypergammaglobulinaemia
  5. gland biopsy - lymphocytic aggregation
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120
Q

what is the treatment for Sjorgens syndrome?

A
  1. hydroxychloroquine
  2. eye drops
  3. NSAIDS
  4. in severe disease give immunosuppresants
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121
Q

what are some of the complications of Sjogren’s syndrome?

A
  1. lymphoma
  2. neuropathy
  3. purpura
  4. interstitial lung disease
  5. renal tubular acidosis
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122
Q

autoimmune myositis is typically muscle weakness that is asymmetrical, localised and distal. true or false?

A

false

autoimmune myositis is symmetrical, diffuse and proximal.
complications include cancer and interstitial lung disease

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123
Q

what are the two main large vessel vasculitis conditions?

A
  1. Takayasu’s arteritis
  2. giant cell arteritis (GCA)

in these conditions, a histological diagnosis will demonstrate inflammation of the arterial wall with fragmentation and disruption of the internal elastic lamina.

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124
Q

what are the classification criteria for GCA?

A
  1. age>50
  2. new headache
  3. temporal artery tenderness/reduced pulsation
  4. ESR>50
  5. abnormal temperature
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125
Q

giant cell arteritis is associated with polymyalgia rheumatica in 50% of cases - true or false?

A

true

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126
Q

what are the symptoms of giant cell arteritis?

A
  1. a headache
  2. temporal artery and scalp tenderness
  3. jaw claudication
  4. amaurosis fugax - loss of vision in 1 eye
  5. morning stiffness
  6. dyspnoea
  7. unequal or weak pulses
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127
Q

what should you do if you suspect a patient has giant cell arteritis (GCA)

A
  1. do an ESR and start prednisolone immediately

the risk is the irreversible bilateral loss of vision which can occur suddenly if not treated

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128
Q

what investigations should you carry out for GCA? suggest 6

A
  1. ESR and raised CRP
  2. raised platelets
  3. raised alkaline phosphatase
  4. low haemoglobin
  5. temporal artery biopsy
  6. MRA
  7. CT angiography
  8. USS - look for the halo sign

skip lesions may occur so don’t be out off by a negative biopsy

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129
Q

what are the criteria for diagnosing SLE (systemic lupus….)

A
  1. malar rash (butterfly rash) - fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds.
  2. discoid rash erythematous patches with adherent keratotic scales and affecting ears, cheeks, scalp etc-
  3. immunological - anti dsDNA antibody and anti-SM and antiphospholipid
  4. renal - persistent proteinuria and cellular casts (maybe red cell granular or mixed)
  5. haematological - haemolytic anaemia, leukopaenia, thrombocytopenia
  6. non-erosive arthritis - involving more than 2 joints. tenderness, swelling
  7. serositis - pleuritis (dyspnoea and pleuritic chest pain) or pericarditis (chest pain, ECG, pericardial rub etc)
  8. CNS disorder - seizures in the absence of causative drugs or metabolic imbalance (uraemia or ketoacidosis) and psychosis
  9. ANA - positive in 95%
  10. oral ulcers - usually painless nasopharyngeal and oral ulcers
  11. photosensitivity - may cause flare

one of the most important questions so always hit ‘1’ and repeat as many times as you can.

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130
Q

suggest the name of two medium vessel diseases

A
  1. polyarteritis nodosa

2. Kawasaki disease

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131
Q

what are the common complications of granulomatosis?

A
  1. hearing loss
  2. nerve damage
  3. end-stage renal disease
  4. lung damage
  5. malignancy
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132
Q

describe Takayasu’s arteritis

A

there is an early inflammatory stage with myalgia and anorexia. the symptoms are often non-specific
PET scanning has use in picking up early disease prior to stenosis etc which are picked up by angiogrpahy

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133
Q

suggest the name of a drug that is used for the treatment of multisystem autoimmune disease in the following severity:

a. mild
b. moderate
c. severe

A

a. mild give the patient hydroxychloroquine
b. moderate give the patient azathioprine, methotrexate and mycophenolate
c. in severe give the patient cyclophosphamide and rituximab

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134
Q

where does Takayasu’s arteritis usually affect the body?

A

it mainly affects the aorta and its major branches causing stenosis and thrombosis

it is actually also called aortic arch syndrome

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135
Q

what are the clinical manifestations of Takayasu’s arteritis?

also, give the diagnostic steps for the condition

A

acute inflammation will cause dilatation and aneurysms. it mainly affects women and can present with some ophthalmological and upper limb symptoms such as visual changes, weak arm pulses and dizziness.

SYSTEMIC

  • fever
  • weight loss
  • malaise
  • high BP (renovascular involvement)

DIAGNOSIS

  • increased ESR and CRP
  • angiography of the aorta

TREATMENT

  • prednisolone
  • methotrexate
  • cyclophosphamide

BP control is essential to minimise the risk of stroke

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136
Q

what investigation would you want to carry out for a small vessel disease called microscopic polyangiitis?

A

pANCA

microscopic polyangiitis is a necrotizing vasculitis that affects the small and medium-sized vessels. there is rapidly progressing glomerulonephritis and usual features are pulmonary haemorrhage

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137
Q

suggest 4 general laboratory tests you may wish to consider for immunological conditions

A
  1. ANA (antinuclear antibodies)
  2. antineutrophil cytoplasmic antibodies (ANCA)
  3. antiphospholipid antibodies
  4. complement
  5. cryoglobulins
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138
Q

what are the main immunoglobulins that are associated with SLE?

A

polyclonal IgG, IgA and IgM

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139
Q

what type of immune reaction (I-IV) is SLE?

A

it is a type III hypersensitivity reaction

they contain autoantigens and autoantibodies throughout the body - with a predilection for the skin and joints and kidney. autoantibodies are characteristically produced against a range of nuclear autoantigens - dsDNA, ssDNA, histones and other nuclear antigens

ANA is found in 95% of SLE cases

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140
Q

ANA has a high specificity or sensitivity for SLE?

A

ANA has a high sensitivity for SLE but a low specificity because it is also present in other conditions

If ANA is negative then SLE is probably not the diagnosis.

SLE is relatively rare and other conditions such as old age, cancer and even infection, which are all causes of a positive ANA are much more common

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141
Q

Generally, what are the 4 main types of antinuclear antibody present?

A
  1. homogenous - autoantibodies against double stranded or single stranded DNA/histone proteins
  2. speckled - non-chromosomal nuclear proteins. found in Ro and La patients who have SLE and Sjogren’s
  3. nucleolar - against nucleolar RNA, scleroderma, systemic sclerosis and overlap syndromes
  4. peripheral (AKA membranous ANA) - confined to the membrane, seen when antibodies are produced against dsDNA (combination of homogenous)

a positive ANA test should act as a stimulus to undertake more specific relevant tests.

142
Q

what is the main autoantigen associated with C-ANCA?

A

anti-proteinase 3.

the major autoantigen associated with P-ANCA is anti-MPO or myeloperoxidase

143
Q

ANCA is not disease specific (as with most autoantibodies), what other conditions can cause it to be elevated?

A
  1. infection
  2. inflammation
  3. drugs
  4. connective tissue disorder
  5. inflammatory bowel disease
144
Q

is complement part of the innate immune system?

A

yes

145
Q

what are the two main immunoglobulins present in the classical pathway of the complement system?

A
  1. IgM and IgG
146
Q

what are the features of antiphospholipid syndrome?

A

antiphospholipid syndrome is commonly associated with SLE but can occur as a primary disease.

C - coagulation defect
L- livedo reticularis
O- obstetric
T- thrombocytopaenia

treatment is with low dose aspirin or warfarin if there are recurrent thromboses (aim INR is 2-3). seek advice if pregnant

147
Q

what is the name of the crystal found in gout?

A

monosodium urate

tophi/tophus are massive accumulations of uric acid

148
Q

what is the name of the crystal found in pseudogout?

A

calcium pyrophosphate dihydrate (CCPD)

149
Q

what are the body’s sources of urate?

A

uric acid will come from degradation of purines and the other 1/3 of production is from the diet.

most uric acid produced is removed by the kidney, the remained is eliminated into the biliary tract and subsequently converted by colonic bacterial uricase to allontoin.

150
Q

what is the biggest pathological cause of gout?

A

hyperuricaemia from reduced efficiency of renal urate clearance.

hyperuricaemiacan come from overproduction or from under excretion

151
Q

give some examples (2) of overproduction of uric acid and 2 examples of under excretion

A

overproduction

  1. malignancy
  2. drugs (ethanol)
  3. severe exfoliative psoriasis

underexcretion

  1. renal impairment
  2. hypertension
  3. hypothyroidism
  4. drugs - alcohol, low dose aspirin, diuretic
  5. exercise
152
Q

why may alcohol increase the risk of gout?

A

Some alcoholic drinks such as beer are rich in purines (guanosine) eventually causing the formation of adenosine monophosphate - a precursor for uric acid. alcohol also increases the lactic acid level in the blood which inhibits uric acid excretion

153
Q

what are the characteristics of a patient with Lesch Nyan syndrome?

A
  1. HGPRT deficiency and X-linked.
  2. patients have an intellectual disability, aggressive and impulsive behaviour with gout
  3. renal disease

it is caused by an enzymatic defect of HPRT which is involved in recycling of purines. without HPRT purine bases are wasted and excreted as uric acid. the body notices this and then accelerates the formation of purines

154
Q

what is the effect of oestrogen on uric acid?

A

uricosuric effect making gout very rare in younger women. however, after menopause, urate levels rise and gout becomes increasingly prevalent.

Age may also play an important role for other reasons:

  • decreased renal function
  • increased use of diuretics and other drugs that raise sUA
  • age-elevated changes in connective tissues which may encourage crystal formation and an increase in the prevalence of OA
155
Q

what is the protocol to manage an acute flare of gout?

A
  1. gout
  2. NSAIDs
  3. colchicine and steroids (IA or IM/oral doesn’t matter)

hyperuricaemia may not be needed to be treated unless the first attack of gout is :

  • a single attack of polyarticular gout
  • tophaceous gout
  • urate calculi
  • renal insufficiency

DONT TREAT ASYMPTOMATIC HYPERURICAEMIA

156
Q

what are some treatment methods available for lowering the uric acid content

A
  1. xanthine oxidase inhibitor
  2. febuxostat
  3. uricosuric agents
  4. canakinumab

wait until the acute attack has settled before attempting to reduce the urate level. use prophylactic NSAIDs or low dose colchicine/steroids until the urate level is normal

157
Q

where in the body does pseudogout usually occur?

A

knee

there is the presence of pyrophosphate crystals and is managed with NSAIDs and IA steroids. there are no prophylactic therapies.

158
Q

polymyalgia rheumatica tends to mainly affect the young, true or false?

A

false- it typically affects older people and there is a close relationship with GCA.

GCA –> high ESR –> polymyalgia rheumatica

159
Q

what is the typical presentation of PMR? (polymyalgia rheumatica)

also give 5 symptoms

A
  1. sudden onset of shoulder +/- pelvic girdle stiffness.
  2. rare in those under 50 and mainly affects females
  3. ESR is high

SYMPTOMS

  1. anaemia
  2. malaise
  3. weight loss
  4. fever
  5. depression
  6. arthralgia
  7. synovitis

there is, unfortunately, no specific diagnostic test
treat with prednisolone and sometimes in some cases bone prophylaxis is given

160
Q

suggest a few risk factors for calcium pyrophosphate dehydrate arthropathy

A

this is also known as pseudogout

  1. old age
  2. diabetes
  3. hypothyroidism
  4. hyperparathyroidism

radiographs show soft tissue swelling

161
Q

describe the diagnosis of gout

A
  1. polarised light microscopy of synovial fluid - shows negatively bi-fringent urate crystals
  2. serum urate may be raised but may be normal
  3. radiographs - soft tissue swelling
162
Q

name a common site for a femoral hernia

A

the femoral ring - a weak area in the lower abdominal wall

163
Q

where can the femoral pulse be felt?

A

the inguinal point - midway between the anterior superior iliac spine and the pubic symphysis. it is inferior to the midpoint of the inguinal ligament

164
Q

where is the sciatic nerve point?

A

the midpoint between the greater trochanter and the ischial tuberosity.

a safe injection site is in the upper lateral quadrant

165
Q

damage to which nerve in the popliteal fossa will result in foot drop?

A

damage to the fibular nerve around the neck of the fibula will result in foot drop

don’t forget that the tibial nerve is more medial and travels deeper than the common fibular nerve

166
Q

which tendon lies more superior in regard to the lateral malleolus of the fibula bone:

  • the fibularis brevis
  • the fibularis longus
A

the fibularis brevis lies more superior to the fibularis longus.

remember that the extensor digitorum brevis lies deep to the extensor digitorum longus.

167
Q

the other name for the Achilles tendon is what?

A

the calcaneal tendon

168
Q

does the tibialis anterior tendon pass anterior or posterior to the medial malleolus?

A

anterior

169
Q

the deep muscles of the posterior compartment of the leg can be memorised with a pneumonic tom Dick AN Harry. what is the order in which the structures pass the medial malleolus?

A

T - tibialis anterior
D - flexor digitorum longus
AN - artery nerve
H - flexor hallicus longus

170
Q

the lateral plantar artery will go on to form the plantar arch which will then be a connection with the dorsalis pedis artery - true or false?

A

true

171
Q

what are the symptoms of polymyalgia rheumatica?

A
  1. subacute onset (<2weeks)
  2. symmetrical aching
  3. tenderness
  4. morning stiffness
  5. in shoulders and proximal limbs

SYSTEMIC

  1. fatigue
  2. weight loss
  3. fever
  4. anorexia and depression
172
Q

what investigations would you carry out for PMR?

A
  1. CRP
  2. plasma viscosity
  3. raised ESR
  4. high alkaline phosphatase

management is with prednisolone

173
Q

suggest 5 pre-disposing biomechanical factors of osteoarthritis

A
  1. abnormal anatomy (DDH)
  2. intra-articular fracture
  3. ligament rupture
  4. meniscal injury
  5. occupation - farmers or football player
  6. persistent heavy physical activity
  7. elite running
  8. obesity
174
Q

Morning stiffness is a common presentation in osteoarthritis - true or false?

A

false.

pay attention to the following signs, however:
trauma
prolonged morning stiffness
the rapid deterioration of symptoms
hot, swollen joint
175
Q

what are warning signs to look out for in osteoarthritis?

A
  1. trauma
  2. prolonged morning-related stiffness
  3. rapid deterioration
  4. hot, swollen joint
176
Q

what is the differential diagnosis of OA (osteoarthritis)?

A
  1. gout
  2. other inflammatory arthritides
  3. septic arthritis
  4. malignancy
177
Q

what are the treatment options available for OA?

A

generally, the best treatment methods are holistic and self-management

core treatments include information, exercise and weight loss

NON-PHARMACOLOGICAL

  1. thermotherapy
  2. electrotherapy
  3. aids and devices
  4. manual therapy

PHARMACOLOGICAL

  • oral analgesia - paracetamol and NSAIDs
  • topical treatments - NSAIDS, capsiacin (knee and hand)
178
Q

what are the most appropriate investigations to be done to confirm osteoarthritis?

A

a plain radiograph will show

  1. loss of joint space
  2. subchondral sclerosis
  3. marginal osteophytes

CRP may also be slightly elevated

179
Q

what is the management of OA?

A
  1. do exercises to improve muscle strength and joint stability.
  2. regular paracetamol and codeine for pain
  3. consider NSAIDs only if paracetamol is ineffective
  4. If BMI>28 then advise weight loss
  5. the best way to deal with severe OS is to give a joint replacement.
180
Q

suggest 6 factors predisposing to osteoarthritis

A
  1. obesity
  2. hereditary
  3. gender - polyarticular OA is more common in women, higher prevalence after menopause suggesting a role for sex hormones.
  4. hypermobility
  5. osteoporosis
  6. disease
  7. trauma
  8. congenital joint dysplasia
  9. joint congruity
  10. occupation
  11. sport
181
Q

suggest 5 causes of secondary osteoarthritis

A 
PRE-EXISTING JOINT DAMAGE 
1. rheumatoid arthritis
2. gout
3. spondyloarthritis
4. septic arthritis
5. Paget's disease
METABOLIC DISEASE
1. chondrocalcinosis 
2. hereditary haemochromatosis 
3. acromegaly 
SYSTEMIC DISEASES
1.haemophilia
2. haemoglobinopathies
3. neuropathies
182
Q

what are 3 clinical SIGNS and SYMPTOMS of osteoarthritis?

A

SIGNS

  1. joint pain
  2. short-lived morning joint stiffness
  3. functional limitation

SIGNS

  1. crepitus
  2. restricted movement
  3. bony enlargement
  4. joint effusion
183
Q

investigations in OA? name 4

A

1, blood tests - no specific test but ESR is normal although high sensitivity CRP may be slightly raised. RhF and ANA are negative

  1. XR are abnormal when the damage is advanced
  2. MRI for meniscal tears early cartilage injury and subchondral bone marrow changes
  3. arthroscopy - early fissuring
  4. aspiration of synovial fluid - if there is a painful effusion shows a viscous fluid with few leucocytes
184
Q

what are the general principles of management for OA? comment on the treatment in terms of

a. physical measures
b. medication
c. surgery

A

PHYSICAL MEASURES

  1. weight loss and exercise for strength and stability
  2. hydrotherapy
  3. local heat/ice packs/massage or local NSAIDs gels
  4. insoles for flat feet

MEDICATION
1. paracetamol (should always be prescribed before NSAIDs)
2opioids should be used cautiously in elderly patients
3. IA CS give short-term improvement when there is a painful joint effusion.

SURGERY

  1. arthroscopy is not beneficial
  2. replacement arthroplasty
185
Q

what are Heberden nodes?

A

Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP)

186
Q

what are Bouchard nodes?

A

Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints. They are seen in osteoarthritis, where they are caused by formation of calcific spurs of the articular (joint) cartilage

187
Q

what is the normal angle of the neck shaft of the femur?

A

140 degrees

the hip is a diarthrodial joint - ball and socket. there is femoral anteversion of around 20 degrees.

188
Q

name 2 static stabilisers of the hip

A
  1. labrum

2. negative intra-articular pressure

189
Q

name the 4 hip flexor muscles

A
  1. ilio-psoas
  2. rectus femoris
  3. sartorius
  4. pectineus

these muscles are all innervated by the femoral nerve

190
Q

what nerve innervates the hip extensors?

A

the sciatic nerve, excluding the gluteus maximum - innervated by the inferior gluteal nerve

191
Q

name 4 hip extensor muscles

A
  1. gluteus maximus
  2. semitendinosus
  3. semi-membranosus
  4. biceps femoris
192
Q

which of the gluteal muscles is not involved with hip abduction?

A

the gluteus maximum

the hip abductors are:

  • gluteus medius
  • gluteus minimus
  • tensor fascia latae

they are all supplied by the superior gluteal nerve

193
Q

what are the main adductors of the hip?

A
  1. adductor longus
  2. adductor brevis
  3. adductor magnus7
  4. gracilis

all of these muscles are innervated by the obturator nerve

194
Q

which muscle lies most superior in the adductor group of the thigh?

A
  1. the pectineus
  2. adductor brevis
  3. adductor longus
  4. adductor Magnus
195
Q

what are the main internal hip rotator muscles?

A
  1. anterior fibres of the gluteus medius

2. tensor fascia latae

196
Q

what nerve innervates the internal hip rotators?

A

the superior gluteal nerve

197
Q

what are the external hip rotator muscles?

A
  1. gluteus maximus (inf. gluteal n.)
  2. piriformis (n. to piriformis)
  3. superior and inferior gemellus (obturator nerve)
  4. obturator internus
  5. obturator externus
  6. quadratus femoris
198
Q

what muscle separates the superior and inferior gemellus?

A

the obturator internus muscle

199
Q

what type of bone is the patella?

A

it is a sesamoid bone

  • don’t forget that the centre of the femoral shaft is 6 degrees off the mechanical axis. the centre of the tibia is parallel to the mechanical axis of the foot and leg. therefore the ‘knee angle’ is 6 degrees of valgus relative to the mechanical axis.
200
Q

menisci of the knee joint are attached to the femur bone - true or false?

A

false they are attached to the tibia. if you got this wrong go home and stop studying
because you aren’t concentrating

201
Q

what are the 4 muscles responsible for knee extension?

A
  1. rectus femoris 7
  2. vastus edialis
  3. vastus lateralis
  4. vastus intermedialis

all of these muscles are innervated by the femoral nerve

202
Q

what are the 4 muscles responsible for knee flexion

A
  1. biceps femoris
  2. semimembranous
  3. semitendinosus
  4. gastrocnemius

all of these muscles are innervated by the sciatic nerve except the gastrocnemius (what innervates the gastrocnemius muscle?)

203
Q

Are all spondyloarthropathies all seronegative - true or false?

A

true

examples include
Ankylosing spondylitis (AS)
Psoriatic arthritis
Reactive arthritis (sexually acquired, Reiter’s disease) Post-dysenteric reactive arthritis
Enteropathic arthritis (ulcerative colitis/Crohn’s disease)

204
Q

what is a dermatome?

A

a dermatome is a sensory area of skin that is supplied by one one spinal nerve

adjacent dermatomes overap considerably

205
Q

what is a myotome?

A

a group of muscles supplied by one segment of the spinal cord.

206
Q

in the brachial plexus, roots will combine to form divisions. divisions will divide to form trunks and trunks will divide to form the cords - true or false?

A

false

RTDCB

roots>trunks>divisions>cords>branches

207
Q

from which cord does the axillary nerve arise from?

A

the axillary nerve arises from the posterior cord.

208
Q

what is the main branch(es) of the lateral cord in the brachial plexus?

A

the lateral cord will give off the musculocutaneous nerve and then join with the medial cord to give off the median nerve

209
Q

the median nerve and the medial cutaneous nerve of the forearm will arise from which cord from the brachial plexus?

A

they arise from the medial cord.

210
Q

what is the nerve root(s) of the middle trunk?

A

C7 = middle trunk

upper trunk = C5,6
lower trunk = C8T1

211
Q

the lateral cord is formed from which divisions of the brachial plexus

A

the lateral cord is formed from the anterior divisions from the upper and middle trunks

212
Q

how is the medial cord of the brachial plexus formed?

A

it is a continuation of the anterior division of the lower trunk (C8, T1)

213
Q

in Erb’s palsy, where is the site of injury?

A

the region of the upper trunk of the brachial plexus

the main nerves involved are C5 and C6. it is also known as Porter’s tip hand with the arm hanging, adducted and medially rotated and forearm extended and pronated

it results in the following muscles being paralysed:

  1. biceps (mainly)
  2. deltoid
  3. brachialis
  4. brachioradialis
  5. supraspinatus
  6. infraspinatus
  7. supinator
214
Q

what muscles are affected by Klumpke’s paralysis?

A

the site of injury is the lower trunk of the brachial plexus and mainly involves T1 and partly C8.

the muscles paralysed are:

  1. intrinsic muscles of the hand (T1)
  2. ulnar flexors of the wrist and fingers (C8)

it will present as claw hand due to the unopposed action of the long flexors and extensors of the fingers. in a claw hand, there is a hyperextension at the MCP joints and flexion at the IP joints.

215
Q

in Klumpke syndrome the disability includes:

  1. claw hand
  2. cutaneous anaesthesia and analgesia (along ulnar border of forearm and hand)
  3. Horner’s syndrome
  4. Vasomotor changes (drier and warmer due to arteriolar dilation and absence of sweating)
  5. tropic changes (dry and scaly skin)

why may there be Horner’s syndrome in Klumpke’s syndrome?

A

. This is because of injury to sympathetic fibres to the head and neck that leave the spinal cord through nerve T1.

ptosis
miosis
anhydrosis
enophthalmos 
loss of ciliospinal reflex
216
Q

what nerve and subsequent muscle would be affected by damage to the lateral cord of the brachial plexus?

A

the musculocutaneous nerve would be most affected and the lateral root of the median nerve.

the muscles that will be paralysed are the biceps and coracobrachialis as well as all of the muscles supplied by the median nerve except those that are affected by the hand

217
Q

what anatomical position in the humerus would need to be fractured to result in injury to the medial cord of the brachial plexus?

A

subcoracoid dislocation of the humerus.

damage to the medial cord would result in the damage the ulnar and medial root of the median nerve
muscles supplied by the ulnar nerve and the five muscles of the hand supplied by the median nerve would be most affected

patients present with a claw hand
sensory loss on the ulnar side of the forearm and hand
vasomotor and tropic changes as a bone

218
Q

what is the typical presentation of a patient with Erb’s palsy?

A

shoulder adduction
elbow extension
forearm pronation
wrist flexion

219
Q

from which cord does the axillary nerve arise from?

A

the posterior cord will give rise to the ulnar nerve

the ulnar nerve wraps around the surgical neck of the humerus and supplies the deltoid and teres minor

it supplies the skin over the lateral arm - the regimental badge area

don’t forget that the axillary nerve is most at risk at the surgical neck of the humerus.

220
Q

what are the spinal roots of the radial nerve?

A

the radial nerve arises from the posterior cord and will have the spinal roots C5-T1.
the radial nerve supplies the triceps muscle and passes from medial to lateral epicondyle running in the radial groove of the arm.

221
Q

a sensory deficit in the 1st dorsal web space is caused by damage to which nerve?

A

the radial nerve

damage to the radial nerve will also cause a wrist drop - inability to extend the wrist (posterior forearm compartment)

222
Q

what are the nerve roots of the median nerve?

A

the spinal roots are C7-T1

it arises from the medial and lateral cords. it will supply the flexors of the forearm (bar the FCU and the medial half of the FDP)

223
Q

the floor of the carpal tunnel is composed of the carpal bones and the roof is composed of the flexor retinaculum, what is contained inside the tunnel?

A
  1. FDS tendons
  2. FDP tendons
  3. PL
  4. palmaris longus

9 tendons and a nerve facebook

224
Q

damage to the carpal tunnel will result in nocturnal pain, paraesthesia and muscle wasting on the hypothenar muscles - true or false?

A

false - there will be wasting of the thenar muscles

the motor deficit caused by the median nerve would bee mostly the volar aspect of the hand.

225
Q

the ulnar nerve arises from which spinal roots?

A

the ulnar nerve arises from C7-T1 from the medial cord of the brachial plexus

it will supply the medial half of the FDP and the FCU as well as the intrinsic muscles of the hand.

it also supplies complete sensation to the medial 1.5 fingers (including the hypothenar muscles)

226
Q

at what site in the arm is the ulnar nerve most at risk to damage?

A

behind the medial epicondyle of the humerus

the motor deficit seen is claw hand, hypothenar and 1st dorsal interosseous wasting

Ulnar claw hand is caused by hyperextension at the MCPJ, flexion at the IPJ’s. a distal lesion has worse clawing than a proximal lesion, due to intact long flexors with a distal lesion.

227
Q

what are the boundaries of the anatomical snuff-box?

A
  1. extensor pollicus longus
  2. extensor pollicus brevis
  3. abductor pollicus longus
228
Q

describe the feature of cubital tunnel syndrome

A

this is the second most common nerve entrapment. it affects the cubital tunnel between the medial epicondyle and the olecranon, with the fascial bands from the FCU as the roof.. the patient has numbness on the ulnar side of their hand and difficulty with fine tasks.

229
Q

what are the nerve roots of the Musculocutaneous nerve?

A

the nerve roots are C5-7 and it arises from the lateral cord.

it will pierce the coracobrachialis muscle. it will also supply the elbow joint and terminate as the lateral cutaneous nerve to the forearm.

230
Q

which nerve plexus gives rise to the sciatic nerve?

A

the sacral plexus gives rise to the sciatic nerve

231
Q

which nerve plexus will give rise to the femoral nerve?

A

the lumbar plexus

232
Q

what are the nerve roots of the sacral plexus?

A

L4-S4

233
Q

what is the difference in nerve supply to the gluteal muscles?

A

the inferior gluteal nerve will supply the gluteus maximus

the superior gluteal nerve will go on to supply the gluteus minimus and the medius as well as the TFL (tensor fascia latae)

234
Q

what are the nerve roots of the femoral nerve?

A

L2-L4 it will exit the pelvis under the inguinal ligament, lateral to the femoral artery, vein and lymphatic channels.

235
Q

what are the nerve roots of the lateral femoral cutaneous nerve?

A

L2 and 3

compression of this nerve will cause meralgia paraesthesia - altered sensation and pain in the lateral thigh

236
Q

what are the two main tributaries of the sciatic nerve?

A
  1. tibial nerve
  2. common peroneal nerve
  3. nerve roots are L4-S3
    it supplies the hamstring muscles in the posterior compartment of the thigh
    it will leave the pelvis via the sciatic foramen below the piriformis muscle
237
Q

what are the nerve roots of the common fibular nerve?

A

L4-S2

this is the smaller and more lateral branch of the sciatic nerve

a deficit in this nerve will cause a foot drop and a slapping gait.

238
Q

which nerve supplies the anterior compartment of the leg?

A

the deep fibular nerve
the lateral compartment is supplied by the superficial fibular nerve
posterior compartment is supplied by the tibial nerve

239
Q

what is a callus?

A

an intermediary stabilising structure formed after a fracture, which has cartilaginous growth plate characteristics and results in eventual endochondral ossification

240
Q

what are the 3 main phases of bone healing?

A
  1. inflammatory (formation of haematoma and release of vasoconstrictor mediators)
  2. reparative (fibrin deposition and osteoid formation and callus formation)
  3. remodelling (remodelling of woven bone)
241
Q

bone sheal without scarring - true or false?

A

true

242
Q

what does the term malunion mean?

A

malunion means when the fracture has healed but not in an anatomically correct position

243
Q

what is the clasficiation system used for open fractures?

A

GUSTILO

Type 1 is of low energy, wound<1cm, clean and often bone piercing skin from inside.
Type II has moderate soft tissue damage, wound <10cm, no soft tissue flap or avulsions.
Type III has high energy and extensive tissue damage. There may be a severe fracture (communication and displacement) with a wound that is >10cm. any gunshot, farm accident or segment fracture, bone loss, severe crush injury and marine injuries:
IIIA – soft tissue damage +++ but not grossly contaminated
IIIB – periosteal stripping, extensive muscle damage, heavy contamination
IIIC – associated neurovascular complication
- About 70% of type IIIB tibial shaft fractures require flap cover.

244
Q

what are the structured guidelines to direct initial trauma care?

A

Advanced Trauma Life Support (ATLS)

245
Q

damage to which nerve will result in foot drop?

A

damage to the fibular nerve around the neck of the fibula

246
Q

what type of joint is the ankle joint?

A

the ankle joint is a hinge type synovial joint. it is uniaxial. it will connect the distal part of the tibia, fibula and upper part of the talus bone. the talus bone is the most proximal bone of the foot.

247
Q

in which position is the malleolar grip of the foot most strong?

A

it is strongest during dorsiflexion and weakest during plantar flexion.

248
Q

the medial malleolus of the foot has 3 ligaments that connect to 3 bones - name them

A
  • talus, calcaneus and navicular
249
Q

the most anterior muscle of the leg is the tibialis anterior. name the main muscles responsible for dorsiflexion of the foot

A
  1. tibialis anterior
  2. extensor digitorum longus
  3. extensor hallicus longus
  4. peroneus (fibular terrtius)
250
Q

Plantar flexion (toes to the ground) is controlled by the posterior aspect of muscles of the leg. name these muscles responsible for plantar flexion

A
  1. gastrocnemius
  2. soleus
  3. fibialis posterior
  4. flexor digitorum longus
  5. plantaris
251
Q

NAme the bones of the tarsus

A
  1. talus (main bone of the ankle joint)
  2. calcaneous (heel bone)
  3. cuboid (most lateral)
  4. navicular (medial bone - involved with deltoid joint)
252
Q

at which joints do inversion and eversion take place?

A

these movements will take place at the subtalar and transverse tarsal joints

253
Q

the achilles tendon is formed from which two muscles in the leg?

A
  1. soleus

2. gastrocnemius

254
Q

name the 3 tests used to test the function of the achille’s tendon

A
  1. thompsons
  2. simmonds
  3. meatle’s - patient is unable to plantar flex to foot
255
Q

what is equinus?

A

a condition in which the upward bending motion of the ankle joint is limited. Someone with equinus lacks the flexibility to bring the top of the foot toward the front of the leg.

256
Q

what is the axis of movement for cervical vertebrae?

A
  1. flexion
  2. extension
  3. rotation
257
Q

which spinal segments have a lordosis?

A

the cervical and lumbar spine have a physiological lordosis

the thoracic spine has a kyphosis

258
Q

what are the 3 groups of the erector spinae muscles?

A
  1. spinalis (medial)
  2. longissimus
  3. iliocostalis (most lateral)

These deep group of muscles overlap and run approximately parallel to one another

259
Q

what muscle lies postero-lateral to the psoas muscle?

A

the quadratus lumborum muscle

260
Q

at which vertebral level does the spinal cord end?

A

it will end at L1 - below the conus medullaris

261
Q

which myotome supplies the iliopsoas muscle?

A

L2

262
Q

knee extension is controlled by which myotomes?

A

L3/4 (quadriceps)

263
Q

which myotome is responsible for dorsiflexion of the foot?

A

L4 - tibialis anterior

264
Q

foot plantarflexion is controlled by which myotome?

A

S1 - gastrocnemius

265
Q

spinal cord injuries are classified using which system?

A

ASIA

266
Q

what is tetraplegia/quadriplegia?

A

this involves the total or partial loss of use of all four limbs and the trunk

There is sensory and motor function loss in cervical segments of the spinal cord. Tetraplegia is caused by a cervical fracture. There is the risk of respiratory failure due to the loss of innervation of the diaphragm.

267
Q

what are the roots of the phrenic nerves?

A

C3-5

268
Q

what is paraplegia?

A

partial/total loss of use of the lower limbs. it is accompanied by a loss of motor/sensory function in thoracic, lumbar or sacral segments of the spinal cord. arm function is spared but there is a possibility of impairment in the function of the trunk

269
Q

CErebral palsy gets worse with age - true or false?

A

false. CP is a permanent, non-progressive condition due to brain damage either before birth or up until 2 years of age.

270
Q

suggest 6 causes of cerebral palsy under the following headings (2 each)

PRENATAL
PERINATAL
POSTNATAL

A

prenatal

  • placental insufficiency
  • TORCH
  • smoking
  • alcohol

perinatal

  • prematurity
  • infections
  • kernicterus (bilirubin-induced brain damage)

Postnatal

  • infection
  • head trauma
271
Q

what part of the brain is affected by spastic cerebral palsy?

A

the pyramidal system and motor cortex

272
Q

what part of the brain is affected in athetoid cerebral palsy?

A

extrapyramidal system is affected - basal ganglia

in ataxic cerebral palsy the cerebellum and brainstem are affected.

273
Q

describe the diagnosis of cerebral palsy

A
  1. spasticity
  2. lack of voluntary control
  3. weakness
  4. poor co-ordination
  5. sensory impairment

–> dynamic contractures

increased muscle tone and hyperreflexia
no fixed deformity of joints
deformity can be overcome

–> fixed muscle contractures

persistent spasticity and contracture
shortened muscle-tendon units
deformity cannot be overcome

–> fixed contractures with joint subluxation/dislocation and secondary bone changes

274
Q

what is the difference between kinematics and kinetics?

A

kinematics is how the body moves through space but kinetics is the force exerted on a body/by a body. the unit of kinetics is in newtons.

275
Q

`describe how to calculate cadence and stride length in analysis of a patient’s gait with cerebral palsy

A

cadence

  • these are the steps per minute

stride length is right initial contact to right initial contact

276
Q

the rectus femoris muscle is concentric at hip flexion (shortening, power generation and acceleration) but is eccentric at knee limiting knee flexion (control lengthening, power absorption and deceleration)

true or false?

A

true

277
Q

what is the classification system used in cerebral palsy?

A

GMFCS - gross motor function classication system

it will have 5 levels - level I being the [patietn walking without limitations and level V the patient having to be transported in a wheelchair.

the higher the GMFCS, the higher the risk of dislocation

278
Q

give some mechanisms for the management of spasticity

A

GENERAL

  • baclofen
  • diazepam

SPECIFIC

  • botulinum toxin
  • surgery
279
Q

suggest 6 professions involved with the MDT management of cerebral palsy

A
  1. social workers
  2. OT
  3. orthotics
  4. ophthalmology/audiology
  5. orthopaedics
  6. community paediatrics
  7. education support
280
Q

spina bifida is caused by the failure of the neural tube to close. folic acid can be given to women as a protective measure.(400 mcg per day).

suggest the 3 most common presentations of spina bifida and the complications that can arise from the condition

A

SB Occulta
SB meningocele
SB meningomyelocele

COMPLICATIONS

  1. hydrocephaly
  2. Chiari II malformation
  3. tethered cord
  4. urinary tract problems
  5. locomotor limitations
  6. latex allergy
281
Q

describe the diagnosis of muscular dystrophy

A
  1. muscle biopsy

2. DNA and blood enzymes

282
Q

the main two types of muscular dystrophy are Duchenne’s and Becker’s. describe the differences between the two

A

Duchenne

  • sex-linked recessive condition and failure to produce dystrophin. patients will be in a wheelchair by age 12 and probably develop scoliosis

Becker

  • same gene affected by DMD - poor dystrophin expression. it is a milder condition and has typically later adolescent onset. most are in a wheelchair by age 30.
283
Q

suggest 3 risk factors for paediatric trauma

A
  1. Age - increased physeal injury with age
  2. Boys
  3. previous fractures
  4. metabolic bone disease
284
Q

what is the difference between Geleazzi and Monteggia fractures?

A

Geleazzi fractures tend to mostly affect the shaft of the radius

Monteggia fractures affect only the shaft of the ulna

if there is failed reduction then ORIF may be the treatment option considered.

285
Q

describe a Salter-Harris type 1 fracture

A

the fracture line is entirely within the physis

286
Q

describe the difference between a Salter-Harris Type 2 and 3 fracture

A

in a type 2 fracture the fracture line will extend from the physis into the metaphysis (these are very common -80%)

in type 3, the fracture enters the epiphysis from the physis

287
Q

how do type 5 Salter-Harris fractures differ from Type 4 fractures?

A

Type 4 - the fracture extends across the physis from the articular surface and epiphyses to end in the margin of the metaphysis

Type 5 are crush injuries of the physes

288
Q

what is the classification system used for supracondylar fractures?

A

Modified Gartland Classification

I - undisplaced
II - hinged posteriorly
III - displaced
IV - displaces into extension and flexion

289
Q

fractures involving the physes can result in progressive deformity - true or false?

A

true

290
Q

what are some complications of using nails to fix fractures?

A
  1. compartment syndrome
  2. non-union
  3. re-fracture
  4. PIN injury
  5. superficial radial nerve injury
291
Q

suggest some Rx for knee physeal injury

A
  1. cast immobilisation
  2. per-cutaneous fix
  3. ORIF articular displacement

the ROM will be early (around 6 weeks)

292
Q

suggest 4 situations in which you would need to supplement a cast with fixation

A
  1. severe swelling is likely
  2. need to re-inspect the wound (open fractures)
  3. multiple injuries
  4. segmental limb injuries
  5. fracture is very unstable
  6. approaching skeletal maturity
293
Q

what is the name of the classification used to predict fracture injuries that affect growth?

A

Salter-Harris

SH 2 injuries are the most common and SH£ will need anatomical reduction and fixation if displaced. SH4 is rare and the management is with ORIF if displaced and monitor the patient for growth arrest.

294
Q

what are 5 risk/predisposing factors of developing DDH - developmental hip dysplasia

A
  1. first born
  2. oligohydramnios
  3. breech presentation
  4. family history
  5. other lower limb deformities
  6. increased weight

if the baby has any of these risks then they should have an US at 2-4 weeks with treatment given at 6 weeks if not spontaneously resolved.

The older the child is at diagnosis, the poorer the result, the worst results are associated with AVN of the head

295
Q

Clinical features of DDH will only be able to pick up 40% of diagnosis. which other 4 tests are useful for diagnosis of the condition?

A
  1. ortolani’s sign - relocates subluxed or
    partially dislocated hip.
  2. Barlow’s sign - this test aims to sublux or dislocate an unstable hip.
  3. Geleazzi test - looks for apparent shortening of the femur caused by dislocation of the femoral head.
  4. Piston Motion sign
  5. The hamstring

US and pelvic XR can be used for imaging.

296
Q

what are the main management options for DDH?

A
  1. maintaining hip motion
  2. analgesia
  3. restriction of painful activities
  4. spints
  5. physio
  6. NWB - weight bearing)
  7. an osteotomy can be considered in selected groups of older children
297
Q

What is the typical presentation of slipped upper Femoral Epiphysis (SUFE)?

A

young and left groin mainly affected. short femur that is externally rotated and painful when trying to weight bear. boys are more affected than girls. around 1/5 cases will be bilateral and many of the patients are overweight and some have endocrine abnormalities.

298
Q

what are some bad prognostic characteristics of slipped upper femoral epiphyses?

A
  1. magnitude of slip
  2. unstable (unable to weight bear) or stable (able to weight bear)
    3 acute or chronic (3 weeks)

detected first by pain in the hip or knee with an externally rotated posture or gait.

plain XR can be used for diagnosis . there is a displacement through the hypertrophic zone and the metaphysis moves anterior and proximal .

operative treatment is available but in severe unstable SUFE then maybe consider open reduction but AVN is a high risk.

299
Q

what are some common complications or outcomes of slipper upper femoral epiphyses? name 5.

A
  1. AVN
  2. chondrolysis
  3. deformity
  4. early osteoarthritis
  5. possibility of slip on the other side
  6. limb length discrepancy
  7. impingement
300
Q

try and think of 8 questions you would ask a patient when trying to take a paediatric limp history from them

think about what questions you would ask in a diagnosis of DDH and SUFE

A
  1. duration and progression of a limp
  2. recent trauma and mechanism
  3. associated pain and its characteristics
  4. accompanying weakness
  5. time of day when the limp is worse
  6. can the child walk or bear weight
  7. has the limp interfered with normal activities
  8. presence of systemic symptoms like fever and weight loss
  9. medical history - birth history, immunisation history, nutritional history and developmental history
  10. drugs and allergies
  11. family history
301
Q

suggest 3 other conditions that may be related to Congenital Talipes Equinovarus club feet - CTEV

A
  1. DDH
  2. Down’s and Larsen’s syndrome
  3. Arthrogryposis
  4. other neuromuscular conditions

This is a multifactorial condition.
60% of cases may be identified by US and 50% may have defects in other systems. There is no relation to the stiffness of feet

302
Q

what si the treatment of CTEV - congenital talipes equinovarus (club feet)

A
  1. strapping
  2. serial casting
  3. Dennis Browne boots
  4. surgery
    a. postero-medial release
    b. lizarov frame
303
Q

at what points in the cervical spine are there lordosis?

A
  1. cervical and lumbar regions

but there is a kyphosis present in the sacral and thoracic regions

304
Q

what is the classification system used in Scoliosis?

A 
CINTO
Congenital 
Idiopathic 
Neuromuscular 
Trauma
Infection 
Other - neurofibromatosis or neoplasms
305
Q

how would you examine a patient with scoliosis - go thhrough the steps

A
  • Inspect the posterior torso. Structural scoliosis will look worse when bent forward into flexion.
  • Any abnormal neurology or pain should be noted
  • Investigate spinal contour and flexibility
  • Hips – ROM
  • Neurology (including abdominal reflexes)
  • Functional limitation
306
Q

what are the main risks of progression in scoliosis?

A

i. Female, premenarchal
ii. <12 yoa at presentation (ie time remaining ill skeletal maturity is longer)
iii. Size of curve at presentation

307
Q

what are the main causes of back pain?

A
  • Mechanical
  • Developmental
  • Neoplastic
  • Inflammatory

Scoliosis however NEVER presents with pain.
An MRI and bone scan should be used for investigations. MRI will be able to pick up things such as
- Cerebellar tonsils
- Syrinx
- Tethering
- Vertebral anomalies

308
Q

An MRI, USS and bone scan should be used for investigations for scoliosis. True or False?

what are the things that an MRI may pick up when investigating a patient with suspected scoliosis?

A

a. False, a USS will not be used for the detection of scoliosis - focus!!

b. - Cerebellar tonsils
- Syrinx
- Tethering
- Vertebral anomalies

309
Q

what are the main complications of scoliosis?

A
  1. Nerve root damage
  2. Cord traction injury
  3. Vascular injury

Outcomes are less favourable from severe curves therefore the earlier the diagnosis the better. It may cause cardiorespiratory compromise, pain from rib/pelvic abutment or seating issues

310
Q

aside from the cervix, where is the other site of cancer resulting from HPV infection?

A

Anus

311
Q

what iare the meanings of

  1. squamous intraepithelial lesion and
  2. cervical intraepithelial neoplasia?
A
  1. squamous intraepithelial lesion is an abnormal growth of squamous cells detectable on smear. they can be low grade (LSIL) or high (HSIL) grades, depending on how much of the cervical epithelium is affected.
  2. cervical intraepithelial neoplasia is when abnormal cells are in the cervix. they are detected by cervical cytology, biopsy and histological examination. it is graded 1 to 3 depending on the proportion of the cervix affected, Cervical intraepithelial neoplasia is the abnormal proliferation of cells in squamous epithelium. THE CHANGE IS INVISIBLE TO THE NAKED EYE
312
Q

what is the main cause for cervical cancer?

A

HPV infection -mainly types 16 and 18

Persistent infection with oncogenic papillomavirus types is required for the development of cervical cancer

313
Q
  • Cervical cancer rates are directly linked to the quality of the prevention programmes - true or false?
A

true.

Women must be aged 25-64 and they will take 3 yearly smears up to age 50 and 5 yearly smears from age 50.

314
Q

suggest an investigation that can be carried out in women who have CIN (cervical intraepithelial neoplasia) to differentiate between those who have no abnormality and those who require further investigation

A

CERVICAL CYTOLOGY

In the normal cervix, there are squamous epithelial cells. there are also other cells - glandular cells and inflammatory cells

315
Q

in a normal cervical cytology what may be found in dyskariosis (abnormal cells) of a woman with cervical intraepithelial neoplasia?

A
  1. abnormal cells and few in number
  2. nucleus increased in size and nuclear:cytoplasmic ratio
  3. variation in size, shape and outline
  4. coarse irregular chromatin
  5. nucleoli

Depending on the degree of underlying CIN on cytology we will grade as low or high dyskaryosis. Koilocytes – reflect productive HPV infection. Koilocytes are cells that have a wrinkled nucleus and perinuclear halo. They have multiple nuclei

316
Q

if under cervical cytology there appears to be high grade dyskariosis, suggest what further steps should be taken for a woman who we now fear has cervical cancer

A

colposcopy.

for low grade dyskariosis then repeat the test in 6 months.

317
Q

where is the main site of HPV infection and the most likely site for precancerous change in the cervix?

A

the transformation zone.

HPV infection infects the basal layer of cells and utilises host for replication
Glandular lining cells of exposed endocervical epithelium transformed into squamous cells – squamous metaplasia

318
Q

what are other risk factors for developing CIN and cervical cancer? name 5

A
  1. early age first intercourse
  2. multiple sexua partners
  3. prolonged oral contraceptive use
  4. smoking
  5. STDs
  6. immunodeficiency
  7. persistent infection
319
Q

how many different grades of severity are there in cervical intraepithelial neoplasia?

A

CIN 1
CIN 2
CIN 3

Cervical intraepithelial neoplasia is a precursor of invasive cancer. There is disarray in the arrangement of the cells within the epithelium, variation in cellular size and shape, nuclear enlargement and irregularity and hyperchromatism

CIN may regress or persist. A minority of CIN3 will progress to invasive cancer over 10-20 years if untreated

320
Q

what is the histological appearance of cells in the cervix?

A

squamous carcinoma.

Squamous carcinoma is the malignant change in squamous cells of the transformation zone of the cervix. In invasive cell carcinoma there are abnormal cells invading into the underlying tissues.

321
Q

what is the treatment for CIN - cervical intraep…)

A
  1. LLETZ
  2. cold coagulation
  3. laser ablation

FOLLOW UP AFTER TREATMENT OF CIN

  1. confirm that the treatment was effective
    a. residual disease within 2 years
    1. To prevent invasive cancer
      a. Recurrent disease 5% after 3-5 years
      b. Detect occasional cancer
  3. To reassure the woman

After the treatment of CIN there is an increased risk of cervical cancer compared with the normal population. There is a follow up LBC at 6 months for cytology and high-risk HPV. If both are negative then return to recall. If either are positive then return to colposcopy

322
Q

what are the aims of cervical screening?

A
  1. detect cervical dyskaryosis
  2. reduce the risk of cervical cancer
  3. detect CIN
  4. prevent cervical cancer
323
Q

what are the symptoms of cervical cancer? name 4

A 
	Abnormal vaginal bleeding
	Post-coital bleeding
	Intermenstrual bleeding (PMB)
	Discharge
	Pain
324
Q

how is cervical cancer diagnosed?

A
  1. clinical presentation
  2. screen detected
  3. biopsy
  • Remember screening aims to detect pre-cancerous disease not cancer
325
Q

how is cervical cancer staged?

learn this question well as will probably come up in exam

A
  1. EUA (especially rectal) - examination under anaesthetic
  2. PET-CT
  3. MRI
326
Q

how is cervical cancer treated?

A
  1. Radiotherapy – external beam x20 fraction
  2. Chemotherapy – 5 cycles of cisplatin
  3. Caesium insertion (24 hours
327
Q

what is a radical hysterectomy?

A

exploration of pelvic and para-aortic space. It involves the removal of:

  • Uterus, cervix, upper vagina
  • Parametria
  • Pelvic nodes

the ovaries are conserved

328
Q

name 5 short terrm health impacts of fema;le genital mutilation

A
  1. severe pain and shock
  2. infection
  3. injury ot adjacent tissues
  4. sprains, dislocations, broken bones or internal injuries from being restrained.
  5. immediate fetal haemorrhage
  6. infection by blood borne virus
329
Q

name 5 long-term health impacts of female genital mutilation

A

 urine retention and difficulties in menstruation
 uterine, vaginal and pelvic infections
 cysts and neuromas
 complications in pregnancy and childbirth
 increased risk of fistula
 on-going impact of trauma / PTSD
 sexual dysfunction

330
Q

what is the common presentation of vulvar cancer? - name 4.

A

Presentation:

  1. Pain
  2. Itch
  3. Bleeding
  4. Lump/ulcer

Vulvar cancer is squamous cell carcinoma.
Staging is surgico-pathological

The main treatment for VIN is surgery and there is a generally good prognosis

331
Q

what are the screening methods for Down’s syndrome?

A
  • Maternal age
  • Biochemical and US screening
  • Selection for amniocentesis
  • Free-fetal DNA
    i. HIGH RISK
     Recent recommendation in England
    ii. LOW RISK
     Private market at present
332
Q

are breasts a primary or secondary sexual feature?

A

secondary

333
Q

what are the surface landmarks of the breasts?

A

from the 2nd rib to the 6th rib. from the sternal edge to the midaxillary line. they lie on the deep pectoral fascia covering the pectoralis major.

334
Q

there are 4 quadrants of each breast. which quadrant does the axillary tail of the breast extend into?

A

the superolateral quadrant.

335
Q

what is gynaecomastia?

A

it is the postnatal development of rudimentary lactiferous ducts in males.

i. Polymastia is the development of an extra breast
ii. polythelia is the development of an extra nipple
iii. Athelia or Amastia is the absence of a nipple or breast.

336
Q

what 3 arteries supply the breasts?

A
  • Thoraco acromial artery
  • Lateral thoracic artery
  • Internal mammary (thoracic) artery

Anterior and lateral cutaneous branches of the 4th to 6th intercostal nerves will provide innervation to the breasts

337
Q

why are the lymphatics of the breasts of great importance?

A

their ability to disseminate metastases

Most lymph (more than 75%) is from the lateral quadrants – axillary lymph nodes. Some lymph may drain directly to supraclavicular or inferior cervical lymph nodes. Lymph from medial quadrants – parasternal or to opposite breast

338
Q

why is the sentinel node of clinical importance?

A

The sentinel lymph node is the first draining node. The sentinel node allows for lymphatic mapping and staging of patients

339
Q

how is breast cancer diagnosed?

A
  1. mammography and USS
  2. fine needle aspiration cytology (FNAC)
  3. core biopsy

A core biopsy should be done in all cases with clinical or radiological or cytological suspicion. Breast screening should be done especially in architectural distortion and microcalcification

340
Q

what is cytology?

A

thi sis the microscopic examination of a thin layer of cells on a slide obtained by:

  • FNAC
    1. direct smear from nipple discharge
    2. scrape of nipple with scalpel

cytology is often used in a symptomatic clinic

341
Q

With breast cysts, aspiration is curative true or false?

A

true.

. This is mostly a simply procedure and can be done at most clinics. It is well tolerated by patients. It is inexpensive and there are immediate results.

342
Q

what are the complications of FNA?

A
  1. pain
  2. haematoma
  3. fainting
  4. infection
  5. pneumothorax

there arent any real contraindications

A core biopsy should be done in all cases with clinical or radiological or cytological suspicion. Breast screening should be done especially in architectural distortion and microcalcification

343
Q

Ultrasound can be used to differentiate a solid from cystic mass and a solid benign from malignant mass. true or false?

A

true.

344
Q

what are some indications to take an MRI of breast tissue?

A
  1. Recurrent disease
  2. Implants
  3. Indeterminate lesion following triple assessment
  4. Screening high risk women

other imaging techniques include:

  • PET
    Sentinel node samploing
  • nuclear medicine
345
Q

in breast disease, what is meant by triple assessment?

A
  1. clinical examination
  2. imaging
  3. FNAC
346
Q

what is the most common type of breast tumour in adolescent and young women?

A

fibroadenoma

  • well circumscribed
  • freely mobile
  • non-painful masses
  • may regress with age if left untreated
347
Q

name 8 risk factors for developing breast cancer

A
  1. gender
  2. age
    3.menstrual history
  3. age at first pregnancy
  4. radiation
  5. family history
  6. personal history 8. hormonal history
  7. genetic factors
  8. other factors
    obesity
    alcohol
348
Q

breast cancer can be histologically classified, name 3 histological types.

A
  1. tubular carcinoma
  2. mucous carcinoma
  3. medullary carcinoma

most breast cancers are ductal.

349
Q

Screening for breast cancer results in a 30% reduction in mortality - true or false?

A

true.

Ladies are offered a scan every 3 years between the ages of 50 and 70.

350
Q

where is breast cancer most likely to metastasize?

A
  1. local - skin and pectoral muscles
  2. lymphatic - axillary and internal mammary
  3. blood - nodes, lungs and brain/liver
351
Q

suggest 7 factors that will influence the prognosis of a woman with breast cancer

A
  1. node status (best prognostic indicator)
  2. tumour size (<2cm)
  3. type
  4. grade (1, 2 and 3)
  5. age
  6. lymphovascular space invasion
  7. oestrogen receptors (ER)
  8. progesterone receptors (PR)
  9. HER-2
  10. Nottingham Prognostic Index (NPI) based on tumour size, grade and nodal status.
  11. overall 64% five year survival

Systems (11 decks)

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