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YEAR 2 MED > Year 1 stuff > Flashcards

Year 1 stuff Flashcards

1
Q

Dermatomes + myotomes + plexuses (cervical, brachial, lumbosacral)

A

https://geekymedics.com/dermatomes-and-myotomes/

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2
Q

SALTER harris –> draw out

A

.

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3
Q

Allopurinol MOA

A

Xanthine oxidase inhibitor –> reduces lvls of uric acid

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4
Q

Methotrexate contraindications

A

Trimethoprim and pregnancy (swap for sulfasalazine)

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5
Q

Garden classification –> hip fractures

A
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6
Q

Weber classification –> ankle fractures

A
  • Type A: lateral malleolar fracture below level of syndesmosis, stable fracture, deltoid ligament intact
  • Type B: lateral malleolar fracture at level of syndesmosis, may be stable or unstable, deltoid ligament may be torn
  • Type C: lateral malleolar fracture above syndesmosis, unstable injury, deltoid ligament injury present, open
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7
Q

Management of NOFs + why is an intracapsular NOF bad

A
  • Intracapsular NOF –> fracture line is between femoral artery and femoral head (retinacular vessels are severed) –> risk of avascular necrosis
    .
  • Undisplaced intracapsular –> internal fixation
  • Displaced intracapsular –> hemiarthroplasty (elderly/immobile) OR total hip replacement (younger/mobile)
  • Extracapsular (intertrochanteric) –> internal fixation with dynamic hip screw
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8
Q

Ankylosing spondylitis 4As

A
  • Anterior uveitis
  • Aortic incompetence
  • Amyloidosis
  • Apical lung fibrosis
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9
Q

Cushings syndrome (too much steroids)

A

Too much steroids (caused by tapering of steroids being too slow)
- symptoms: osteoporosis, obesity, hypertension, hyperglycemia

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10
Q

Addisons disease (too little steroids)

A

Too little steroids ( (body doesn’t have enough cortisol): caused by tapering of steroids being too fast
- symptoms: nausea, headaches, fever, hypotension, hypoglycaemia

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11
Q

Autoantibodies:
- ANA
- Anti-dsDNA / Anti-Smith
- Anti-Ro/La
- Anti-CCP / Rheumatoid factor
- Anti-histone
- Anti-Jo-1
- Anticentromere
- Anti-Scl-70
- c-ANCA (PR3)
- p-ANCA (MPO)
- Anti-TTG

A
  • ANA –> non-specific (common in SLE)
  • Anti-dsDNA / Anti-Smith –> SLE
  • Anti-Ro/La –> Sjorgen’s syndrome
  • Anti-CCP / Rheumatoid factor –> RA
  • Anti-histone - drug-induced lupus
  • Anti-Jo-1 –> polymyositis/dermatomyositis
  • Anticentromere –> limited sclerosis (CREST)
  • Anti-Scl-70 –> diffuse systemic sclerosis
  • c-ANCA (PR3) –> Granulomatosis with polyangitis (Wegener’s)
  • p-ANCA (MPO) –> eosinophilic granulomatosis with polyangitis (Chrug-Strauss)
  • Anti-TTG –> coeliac disease
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12
Q

Four ethical principles/pillars?

A
  • Autonomy –> the patient has the right to make their own decisions and act upon them
  • Beneficence –> act in the patient’s best interest
  • Non-maleficence –> do no harm
  • Justice –> ensure fairness (distribute resources, including your time and skill, equitably)
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13
Q

What is paternalism?

A
  • the idea that “the doctor knows best”
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14
Q

Discuss the principles of consent to treatment in an individual who is not an adult

A
  • Gillick competence
  • If child is deemed to have capacity then can give consent without parents/guardian
  • Although, child would be unable to refuse treatment
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15
Q

How would a doctor assess whether a patient is competent to consent?

A
  • Test ability to retain and comprehend information
  • Test ability to make a decision
  • Test ability to communicate a decision
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16
Q

What do each of the germ cell layers divide into?

A
  • Ectoderm –> nervous system, epidermis (inc. hair and nails), eye, ear, and nose
  • Mesoderm –> muscle, connective tissue, bone, blood/blood vessels (Heart)
  • Endoderm –> lining of digestive and respiratory tracts
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17
Q

what is the structure of a chromosome? how many does human body have?

A
  • chromatin fibres made up of histones wrapped in DNA
  • chromosomes come in pairs, one from the father and one from the mother
    .
  • 46
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18
Q

What is apoptosis and what is it characterised by?

A
  • programmed cell death (characterised by chromatin degradation)
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19
Q

What is the role of the TP53 gene?

A
  • ‘guardian of the genome’
  • regulates cell division
  • when there is DNA damage, the p53 protein has a role in deciding whether the cell can be repaired (activates other genes to fix the damage) or needs to be destroyed (p53 stops cell from dividing and signals apoptosis to occur)
  • (therefore the TP53 gene is frequently inactivated in cancers)
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20
Q

Inheritance pattern of Duchenne’s muscular dystrophy + features

A
  • X-linked recessive
    .
  • Gower’s sign –> difficulty getting up (uses all fours), degeneration of muscle fibres, dilated cardiomyopathy
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21
Q

what are the 2 mechanisms in which NSAIDs can damage the stomach?

A
  • direct: erosion of gastric lining
  • indirect: blocks COX enzymes so decreased lvls of prostaglandins, therefore unable to make protective gastric mucus barrier against acid
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22
Q

what are the 2 main drugs used to treat osteoporosis?

A
  • bisphosphonates –> inhibit osteoclast activity
  • denosumab –> monoclonal antibody (RANKL inhibitor –> therefore reduces osteoclast activity)
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23
Q

Opioid reversal agent

A

Naloxone

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24
Q

Describe how paracetamol helps to reduce fever

A
  • Paracetamol is a COX enzyme inhibitor (thought to be selective for COX-3)
  • (COX enzymes stimulate the production of prostaglandins)
  • In fever, the temperature set point is elevated by the production of PGE2
  • Paracetamol helps to prevent PGE2 synthesis, PGE2 is the main compound that alters the homeostatic temperature set point in the hypothalamic neurons that regulate body temperature
  • PGE2 synthesis is stimulated by cytokines (IL-1, TNF-alpha) which are produced by the action of bacteria/viruses on the immune system
  • By blocking PGE2 synthesis, parace
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25
Q

During his last few months of life the patient was prescribed morphine. Describe how morphine works

A
  • Morphine attaches to opioid receptors (Mu)
  • Morphine reduces membrane excitability and hence action potential firing frequency
  • (Opioids act on the dorsal horn as well as the peripheral terminals of nociceptive afferents neurons)
  • Thus preventing pain signals travelling up the spinal column
  • Morphine also increases release of enkephalins and 5-HT (serotonin) onto dorsal horn neurons via stimulation of the periaqueductal grey matter (PAG) and the raphe nucleus
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26
Q

In which anatomical structure is cortisol synthesised and what is the precursor molecule from which it is made?

A
  • Synthesised in the zona fasciculata (ZF) of adrenal cortex/gland
  • Precursor molecule is cholesterol
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27
Q

what pathways do corticosteroids block?

A
  • they block the conversion of phospholipids to arachidonic acid
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28
Q

what drugs are prescribed for acute gout flare-ups?

A
  • NSAIDs (ibuprofen, naproxen)
  • colchicine
  • corticosteroid (local injection or oral)
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29
Q

what drugs are prescribed for chronic gout (prevention)?

A
  • allopurinol
  • (or febuxostat)
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30
Q

what is the mechanism by which bisphosphonates work?

A
  • pyrophopshate analogue
  • attach to bone crystals and inhibit osteoclast breakdown of bone
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31
Q

Nerve affected in carpal tunnel syndrome

A

Median

32
Q

What is the management for carpal tunnel syndrome?

A
  • wrist splint, corticosteroid injection
  • surgical decompression (by division of the carpal transverse ligament)
33
Q

What is radial nerve palsy (‘Saturday night palsy’)?

A
  • compression of the radial nerve at the axilla
  • wrist drop
34
Q

Foot drop –> what nerve affected

A

Common peroneal nerve

35
Q

Scapular winging –> what nerve is damaged?

A

Long thoracic nerve

36
Q

What is a prolapsed intervertebral disc and where does it usually occur in the back?

A
  • a disc prolapse occurs when part of the nucleus pulposus herniates through the annulus fibrosus and presses on a spinal nerve root
  • note: usually occurs at L4-L5 or L5-S1 level
37
Q

What are the symptoms of cauda equina syndrome (urgent MRI required)?

A
  • altered bladder/anal function (urinary retention or incontinence)
  • perineal pain/paraesthesia (saddle anaesthesia)
  • bilateral leg pain/paraesthesia/weakness
38
Q

What is spondylolisthesis, where does it usually occur, and what is the aetiology?

A
  • Spondylolisthesis = one vertebral body slipping on another (usually occurs at the L5-S1 level)
  • Aetiology: commonly fast bowlers in cricket, gymnasts
39
Q

A child has a leg which is shorter than the other, what is the likely diagnosis?

A
  • typical of DDH
  • apparent shortening will be present if there is any fixed flexion deformity
40
Q

What are the 4 typical features found on X-ray examination of osteoarthritis joints?

A
  • Loss of joint space
  • Osteophytes
  • Subchondral cysts
  • Sclerosis
41
Q

What is the management for osteoarthritis (OA)?
(there is no cure for OA, treatment is aimed at relieving pain and maintaining function)

A
  • Conservative: weight loss, exercise. physio, OT
  • Pharmacological: analgesia (paracetamol, NSAIDs), intra-articular steroid injections
  • Surgical: joint arthroplasty (relieves pain, but function not as good), joint arthrodesis (relieves pain, but function lost), osteotomy (used to correct deformity)
42
Q

Presentation of C-spine involvement in RA?

A
  • atlanto-axial joint (C1-C2) subluxation
  • any minor neck trauma needs imaging to assess C-spine
  • note: can result in spinal cord compression
43
Q

What are the 4 spondyloarthropathies (or seronegative spondyloarthropathies) associated with HLA-B27?

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthritis
  • enteropathic arthritis
44
Q

What is the management for ankylosing spondylitis?

A
  • physio/exercise (aim to maintain posture and mobility)
  • drug treatment: NSAIDs, corticosteroids, biologics (anti-TNFs)
45
Q

What is the CASPAR classification?

A
  • the classification criteria for diagnosing psoriatic arthritis
46
Q

What is the management for psoriatic arthritis?

A
  • NSAIDs
  • DMARDs (methotrexate, leflunomide)
  • biologics
47
Q

What is Reiter syndrome?

A
  • triad of arthritis, conjunctivitis, and urethritis
48
Q

What is the management for enteropathic arthritis?

A
  • treatment of the IBD is priority and will help with peripheral arthritis
  • corticosteroids and sulfasalazine help with both bowel and joint disease
  • anti-TNFs: very effective for both bowel and joint disease
  • (note: not NSAIDS, they will worsen GI symptoms)
49
Q

What are the clinical features of antiphospholipid syndrome (APLS)?

A
  • Clots: venous thrombosis (eg. DVT or pulmonary), arterial thrombosis (eg. myocardial infarction or stroke)
  • Livedo reticularis: a mottled appearance of skin on lower limbs
  • Obstretic loss: recurrent miscarriages, premature births
  • Thrombocytopenia:
50
Q

What are the investigations for suspected APLS?

A
  • antibodies: lupus anticoagulant and anticardiolipin
  • FBC: thrombocytopenia
51
Q

What are the investigations for suspected Sjorgen syndrome?

A
  • Bloods: ESR/CRP raised, Rf, anti-Ro/anti-La
  • Schirmer’s test: shows reduction in tear production
52
Q

What are the features of limited cutaneous system sclerosis (CREST syndrome)?

A
  • Calcinosis
  • Raynaud’s phenomenon
  • oEsophageal dysmotility (dysphagia)
  • Sclerodactyly (shiny/tight/swollen skin of hands/feet)
  • Telangiectasia
  • note: symptoms limited to hands/forearms, feet/legs, and head/neck
53
Q

What is the presentation of granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A

Classic triad…
- upper respiratory tract involvement: chronic sinusitis, epistaxis, saddle-nose deformity
- lower respiratory tract involvement: cough, haemoptysis, pleuritis
- Glomerulonephritis: haematuria, proteinuria (frothy urine)

54
Q

What is Marfan’s syndrome?

A
  • an autosomal dominant CTD caused by mis-sense mutation of the fibrillin 1 gene
55
Q

What is a T-score and what are the ranges for osteoporosis, osteopenia, and normal?

A
  • T-score = used to measure bone mineral density (BMD)
  • Osteoporosis = T-score < -2.5
  • Osteopenia = T-score between -1 and -2.5
  • Normal: T-score > -1
56
Q

What is Rickets and what is osteomalacia? + What is the main cause of Rickets / osteomalacia?

A
  • Both conditions are the result of failure of mineralisation of bone, increased osteoid in osteomalacia
  • Rickets: occurs in the growing skeleton
  • Osteomalacia (soft bones): occurs in adults
    .
  • vitamin D deficiency
  • Serum alkaline phosphatase (ALP): raised
57
Q

What is Osgood-Schlatter disease?

A
  • inflammation of the insertion point of the patella tendon at the tibial tuberosity
58
Q

What is the unhappy triad?

A
  • ACL injury
  • MCL injury
  • meniscal injury
59
Q

What is the difference between onset of injury between meniscal tears and ACL tears, and why?

A
  • ACL tears: swelling usually occurs within minutes to hours
  • Meniscal tears: swelling usually occurs over 24 hours
  • (this is because the ACL is more vascular than the menisci)
60
Q

Test for Achilles tendon rupture

A

Simmonds

61
Q

+ve Thomas’ test

A

fixed flexion deformity in hip

62
Q

+ve Trendelenburg’s test

A

weak hip abductors on contralateral side of pelvis

63
Q

External rotation against resistance tests for?

A

Infraspinatus

64
Q

Shoulder abduction (Empty can/Jobe’s) tests for?

A

Supraspinatus

65
Q

Patient presents with pain on palpation of the anatomical snuffbox, what is the diagnosis and what is the management?

A
  • scaphoid fracture
  • x-ray: repeat x-rays after 10 days
  • high risk of avascular necrosis (due to blood supply distally)
66
Q

Most common blood-borne virus to be transmitted in a needlestick injury

A

Hepatitis B

67
Q
A

from left to right:
- Staph A (grapes)
- Strep (chains)
- Gram-negative rods (bacilli)

68
Q

Gram positive bacteria (cocci and bacilli).

A
69
Q

Gram negative bacteria (cocci and bacilli).

A
70
Q

Do gram-positive bacteria retain the crystal violet dye?

A
  • yes
71
Q

Name four viral infections that can be spread by mosquitoes.

A
  • Yellow fever
  • Dengue fever
  • Zika
  • Japanese encephalitis
72
Q

explain the steps of PCR?

A
  • denaturation: heat to 95ᵒϹ breaks hydrogen bonds between the two strands of DNA
  • annealing: cool to 55ᵒϹ, allows primers to bind to their complementary sequences on the DNA
  • extension: heat up to 70ᵒϹ and TAQ polymerase binds to primers and uses free nucleotides to assemble new strands of DNA
73
Q

describe the gram stain and how it works

A
  • the gram stain is used to study bacteria
  • crystal violet dye and iodine bind to cell wall
  • gram positive bacteria retain the stain when acetone is added and remain purple
  • gram negative bacteria lose the purple stain when acetone is added and appear colourless until stained with a pink counterstain (safranin)
  • this is due to gram positive bacteria having a thicker peptidoglycan cell wall so retains the stain
74
Q

describe acid-fast stain and why it is used

A
  • used for organisms that do not readily take up the gram stain (eg. mycobacteria ( TB ), have waxy cell walls)
  • acid and alcohol are added to the cells after they have been stained through another method (Ziehl Neelson stain)
  • if the cells withstand decolourisation from the acid and alcohol then they are known as acid and alcohol fast
75
Q

What is the causative organism of malaria?

A
  • Plasmodium
76
Q
A

YEAR 2 MED (16 decks)

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