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BRS/POM MOCKS > BRS MOCK 9 - PNS, early dev disorders, rheumatology 2 > Flashcards

BRS MOCK 9 - PNS, early dev disorders, rheumatology 2 Flashcards

1
Q

What do sympathetic efferent nerves target?

A

Viscera and periphery (vasculature and sweat glands).

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2
Q

What do parasympathetic efferent nerves target?

A

Only viscera.

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3
Q

Nerve layer of connective tissue?

A

Epineurium

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4
Q

Nerve fascicle layer of connective tissue?

A

Perineurium

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5
Q

Axon layer of connective tissue?

A

Endoneurium

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6
Q

What do Nociceptors detect?

A

Detect tissue damage, interpreted as pain.

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7
Q

What is a muscle spindle?

A

Proprioceptor that detecs changes in muscles length.

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8
Q

What is a golgi tendon organ?

A

Proprioceptor that detects changes in tension in tendons.

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9
Q

What do joint receptors do?

A

Proprioceptor that is found in joint capsules – detect start and end of movement.

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10
Q

What neurotransmitter is released at the preganglionic synapse?

A

Acetylcholine

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11
Q

In sympathetic neurone, what neurotransmitter is released at a postganglionic neurone?

A

Noradrenaline.

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12
Q

In parasympathetic neurone, what neurotransmitter is released at a postganglionic neurone?

A

Acetylcholine.

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13
Q

What parasympathetic nerves emerge from spinal cord?

A

Pelvic nerves. S2 to S4.

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14
Q

What cranial nerves have parasympathetic motor nerve fibres?

A

III, VII, IX and X

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15
Q

Where do sympathetic nerves emerge from in spinal cord?

A

T1 to L2.

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16
Q

Visceral sensory nerves?

A

T1-L2, S2-S4 and cranial nerves IX and X

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17
Q

What is major cause of early pregnancy loss?

A

Aneuploidy in embryo.

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18
Q

What kind of pregnancy increases exponentially in with maternal age?

A

Risk of trisomic pregnancy.

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19
Q

Why does aneuploidy of embryo increase with maternal age?

A

Loss of cohesin proteins between chromatids. This results in a loss in cohesion between chromatids. Chromatids can separate and drift during meiotic division leading to cells with wrong number of chromosomes during division of the cells.

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20
Q

What are the main cohesin proteins?

A

REC8 and SMC2.

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21
Q

Why does smoking increase risk of ectopic pregnancy?

A

Inhibits cilia function. Decreases contractility of the smooth muscle layer surrounding the fallopian tube. Smoking induces apoptosis of epithelial layer of fallopian tube by triggering expression of pro apoptosis proteins. Loss of epithelial cells results in loss of cilia and so embryo can’t move down fallopian tube properly.

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22
Q

Risk factors for ectopic pregnancy?

A

Prior ectopic pregnancy.
Prior fallopian tube surgery.
Smoking.

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23
Q

What is the proteoglycan in articular cartilage?

A

Aggrecan.

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24
Q

What is a main compound present in synovial fluid?

A

Hyaluronic acid.

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25
Q

What is the synovium made up of?

A

Type 1 collagen. Synoviocytes.

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26
Q

What is the main reason to why cartilage doesn’t heal well?

A

Cartilage is avascular (lacks blood supply).

27
Q

Describe the pattern of joint involvement in rheumatoid arthritis

A

Polyarthritis and symmetrical.

28
Q

What joints does rheumatoid arthritis commonly affect?

A

Joints in hands, wrists and feet.

Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
NOT distal interphalangeal joints
Metatarsophalangeal joints (MTP)

29
Q

What are common extra articular features present in a rheumatoid arthritis patient?

A

Fever, weight loss. Subcutaneous nodules.

30
Q

What are some uncommon extra articular features present in a rheumatoid arthritis patient?

A

Vasculitis and episcleritis.

31
Q

What causes proliferation of the synovium into a mass of tissue in rheumatoid arthritis?

A

Neovascularisation, lymphangiogenesis and recruitment of inflammatory cells. Excess of pro inflammatory cytokines.

32
Q

What is the dominant pro inflammatory cytokine in rheumatoid arthritis? How does it cause symptoms of rheumatoid arthritis?

A

Tumour necrosis factor alpha. Osteoclast activation, chondrocyte activation which results in production of MMP and pro inflammatory cytokine release.

33
Q

Example of TNF-alpha inhibitor?

A

Adalimumab.

34
Q

Rheumatoid arthritis biomarkers?

A

Normocytic anaemia (low Hb but normal MCV). Raised platelets, raised ESR and CRP.

35
Q

What biomarker can differentiate septic arthritis from rheumatoid arthritis?

A

Raise white blood cell count in septic arthritis but normal in rheumatoid arthritis.

36
Q

What are the two main biomarkers for septic arthritis?

A

Raise white cell count and CRP.

37
Q

What class of antibody is rheumatoid factor?

A

IgM.

38
Q

What are the two self antigens targeted in rheumatoid arthritis?

A

Fc portion of IgG antibodies. Citrullinated proteins.

39
Q

What are the two types of autoantibodies in rheumatoid arthritis?

A

Rheumatoid factor and anti-CCP antibody (anti-cyclic citrullinated protein antibody).

40
Q

What is the most specific test for rheumatoid arthritis?

A

Anti-CCP antibody test.

41
Q

When do bony erosions present in RA?

A

Later on in disease once its fully established.

42
Q

What would you seen in the ultrasound of a joint in a rheumatoid arthritis patient?

A

Thickening of the synovium. Increased blood flow due to neovascularisation of synovium (doppler ultrasound) and erosions (IF RA IS ESTABLISHED).

43
Q

1st line treatment for rheumatoid arthritis?

A

Glucocorticoids and DMARDs (disease modifiying anti rheumatic drugs).

44
Q

Example of a disease modifying anti rheumatic drug?

A

Methotrexate.

45
Q

Mechanism for how methotrexate works?

A

Acts as a folate antagonist by inhibiting dihydrofolate reductase.

46
Q

Examples of biological therapies for rheumatoid arthritis?

A

Anti TNF alpha, antibody against B cell antigen or CD20, antibody against IL-6 receptor, blocking of T cell co stimulation proteins.

47
Q

What is seronegative arthritis?

A

When you have inflammatory joint disease symptoms but don’t have rheumatoid factor or anti ccp.

48
Q

Types of seronegative arthritis?

A

Psoriatic arthritis, reactive arthritis, ankylosing spondylitis and IBD associated arthritis.

49
Q

Presentation of psoriatic arthritis

A

Scaly red plaques on extensor surfaces (elbows and knees). Asymmetrical pattern of joint involvement. Usually affects interphalangeal joints.
Doesn’t affect MCPJ’s unlike RA.

50
Q

What is reactive arthritis?

A

Sterile inflammation of joint following infection elsewhere in the body.

51
Q

What type of infections usually cause reactive arthritis?

A

Urogenital (chlamydia) and gastrointestinal (salmonella).

52
Q

What extra articular features might be present in reactive arthritis?

A

Enthesistis (inflammation where tendon or ligament attached to bone), skin inflammation and eye inflammation.

53
Q

What test can you do to see if someone is more likely to develop reactive arthritis?

A

HLA-B27

54
Q

What is HLA-B27?

A

MHC I class molecule.

55
Q

How does ankylosing spondylitis present?

A

Inflammation of spine. Inflammation of sacro iliac joints. Enthesistis

56
Q

Extra articular features in ankylosing spondylitis?

A

4 A’S. Anterior uveitus (iris), Apical lung fibrosis, aortitis (inflammation of aorta), amyloidosis.

57
Q

What is a big risk factor for ankylosing spondylitis?

A

HLA-B27 positive.

58
Q

Untreated ankylosing spondylitis can lead to what?

A

Bone growth between adjacent vertebrae leading to spinal fusion.

59
Q

First line treatment for ankylosing spondylitis?

A

NSAID’s

60
Q

How do NSAID’s work?

A

Reduce inflammation by blocking COX1 and COX2 resulting in inhibition of prostaglandin production.

61
Q

Why do NSAID’s cause asthma to get worse?

A

Increased production of leukotrienes which cause bronchoconstriction.

62
Q

Two types of autoantibodies produced in SLE that can be measured in the blood?

A

Antinuclear antibodies and anti-double stranded DNA antibodies.

63
Q

Which of the two autoantibodies is more specific for SLE?

A

Anti-double stranded DNA antibodies.

BRS/POM MOCKS (23 decks)

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