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Z 2021 Phase 2 Limbs and Back Others > limbs and back week 4 > Flashcards

limbs and back week 4 Flashcards

1
Q

describe the joint capsule

A

it is connected to the periosteum
lined with synovium

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2
Q

Describe synovium

A

a few cells think
vascular
smooth and non-adherent surface
permeable to proteins and crystalloids
no microscopic gaps
able to maintain normal joint fluid under pressure

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3
Q

Describe synoviocytes

A

macrophage and fibroblast like
cell to cell interactions mediated by cadherin-II

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4
Q

What do synoviocytes do?

A

secrete hyaluronic acid into the joint same to retain fluid in the joint

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5
Q

Describe synovial fluid

A

highly viscous, similar consistency to plasma
glycoproteins ensure a low coefficient of friction between the cartilaginous surfaces

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6
Q

What are also lined by synovium?

A

tendon sheaths and bursae

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7
Q

Does hyaline cartilage have a blood supply?

A

no it is avascular

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8
Q

where does hyaline cartilage receive its nutrients from?

A

diffusion of molecules from the synovial fluid

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9
Q

why type of collagen is in cartilage?

A

type II

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10
Q

what is the structure of hyaline cartilage?

A

the type II collagen forms a meshwork enclosing giant macromolecules such as keratin and chondroitin sulphate (aggrecans).
These molecules have a negative charge and retain water om the structure

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11
Q

Why is “loading” essential for healthy cartilage?

A

it encourages the movement of water, minerals and nutrients between the cartilage and the synovial fluid.

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12
Q

What do chondrocytes secrete?

A

collagen and proteoglycans

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13
Q

What is rheumatoid arthritis?

A

a progressive inflammatory autoimmune disease with articular and systemic effects

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14
Q

What are common symptoms of RA?

A

pain and stiffness of the small joints of the hands and feet
the wrists, elbows, shoulders, knees and ankles are also affected
In most cases many joints are involved

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15
Q

When is the pain of RA worse?

A

significantly worse in the morning
sleep is often disturbed

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16
Q

what do joints with RA look like?

A

warm and tender with joint swelling
deformities and non-articular features if disease can not be controlled

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17
Q

Describe presentations of RA

A

palindromic
transient
remitting
chronic persisting - most common
rapidly progressive

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18
Q

what are some of the complications of RA?

A

ruptured tendons
ruptured joints (baker’s cysts)
spinal cord compression
joint infection
amyloidosis (rare)

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19
Q

What are some of the non-articular manifestations of RA?

A

soft tissues surrounding the joints can be affected
lung problems
vasculitis
heart and peripheral vessels
the nervous system
the eyes
the kidneys

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20
Q

What are the investigations for RA?

A

blood count
the ESR and or CRP are raised in proportion to the activity of the inflammatory processes
serology - ACPA is present earlier in the disease (and may predate it by years)
X-rays show soft tissue swelling in early disease
MRI indicates synovitis and early erosions
aspiration - if effusion is present. Aspirate looks cloudy due to presence of leukocytes
doppler ultrasound is a very good way of demonstrating persisting synovitis when deciding on the need of DMARDs or their efficacy

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21
Q

What is the cause of RA?

A

its exact cause is unknown
genetic and environmental factors contribute

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22
Q

What inflammatory cells are involved in the pathophysiology of RA?

A

Differentiation of T cells into Th17 - production of Il17
B cells - antibody and cytokine production
mononuclear cells

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23
Q

What are the main cytokines involved in RA?

A

IL-17, TNF alpha, IL6, IL1

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24
Q

What is the pannus and what does it do in RA?

A

the osteoclast rich portion of the synovial membrane destroys the bone

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25
Q

What do enzymes secreted by the synoviocytes do?

A

Degrade the cartilage

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26
Q

What is rheumatoid factor?

A

the autoantibody that was first found in RA
the antibody against the Fc portion of IgG (an antibody against an antibody)
RF and IgG join to form an immune complex that contributes to the disease pathogenesis

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27
Q

What are the physical measures for the treatment of RA?

A

constant advice and support from physiotherapists and nurses
combination of rest and exercise
exercise in hydrotherapy pool
advice on managing daily living
shoe-wear
psychosocial support

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28
Q

What are the surgical options for the treatment of RA?

A

useful role in long term management
less needed as therapeutics improve
prophylactic objectives - prevent joint destruction
reconstructive -restore function

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29
Q

Describe the drug therapy of RA

A

There is no curative agent available for RA but drugs are now available that prevent the disease deterioration.
Symptoms are controlled with analgesia and NSAIDs

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30
Q

Describe the use of corticosteroid therapy in RA

A

there is evidence to suggest that the early use of corticosteroids slows down the course of the disease
corticosteroids are the most common cause of secondary osteoporosis
when treating for extended periods calcium and vitamin D supplements as well as biphosphonates are required

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31
Q

Describe the use of DMARDs in RA treatment

A

Disease-modifying anti-rheumatic drugs
mainly act through cytokine inhibition reduce inflammation
their beneficial effect is not immediate and may be partial or transient

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32
Q

When are DMARDs used in RA?

A

As early as possible

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33
Q

Give examples of DMARDs

A

Sulfasalazine
methotrexate
hydrochloroquine
leflunomide

34
Q

What drugs have recently become available for the treatment of RA?

A

Cytokine modulators

35
Q

What do cytokine modulators do?

A

block TNF alpha

36
Q

Why are DMARDs still usually tried before DMARDs?

A

The cost

37
Q

What are examples of cytokine modulators

A

etanercept
adalimumab
infliximab
certolicumab
retuximab
abatacept

38
Q

Name the carpal bones of the hand

A

scaphoid
trapezium
trapezoid
capitate
hamate
pisiform
triquetral
lunate

39
Q

Describe the intrinsic muscles of the hand

A

All For One And One For All
abductor pollicis brevis, flexor policis brevis, opponens pollicis, adductor pollicis brevis, opponens digiti minimi, flexor digiti minimi, abductor digiti minimi

PAD, DAB
Palmar interossei Adduct
Dorsal interossei ABduct

40
Q

Name the 10 structures that pass through the carpal tunnel

A

median nerve
flexor digitorum profundus (4 tendons)
flexor digitorum superficialis (4 tendons)
flexor policis longus

41
Q

What is the carpal tunnel covered by?

A

the flexor retinaculum

42
Q

What does the radial nerve innervate in the dorsum of the hand?

A

skin of dorsum of thumb, index, middle and radial half of ring fingers as far as the distal interphalangeal joints

43
Q

What does the ulnar nerve innervate in the dorsum of the hand?

A

ulnar half of ring finer and adjacent part of the dorm of the hand

44
Q

What does the ulnar nerve innervate on the palmar side of the hand?

A

sensory to skin of ulnar digits
motor to muscles of the hypothenar eminence
motor to ulnar 2 lumbricles
motor to 7 interossei muscles
motor to adductor policis

45
Q

What does the median nerve innervate on the palmar side of the hand?

A

sensory aspect of the thumb, index, middle and radial half of ring fingers including skin on the dorsal aspect of the phalanges
motor on thenar eminence
motor to two radial lumbricles

46
Q

What are some examples of autoimmune diseases?

A

rheumatoid arthritis
psoriasis
systemic lupus
cardiovascular disease

47
Q

What is autoimmunity?

A

the immune system mistakenly attacks self, targeting cells, tissues, and organs of a person’s body

48
Q

What is organ specific autoimmune disease?

A

autoimmune attack on self antigens in specific organ

49
Q

Give examples of organ specific AI disease

A

hashimoto thyroiditis
thyrotoxicosis
addison’s disease
juvenile diabetes mellitus
Multiple sclerosis
Guillain - Barre syndrome

50
Q

What is non-organ specific IA?

A

widespread self antigens are target for autoimmune attack

51
Q

Give examples of non-organ specific IA

A

systemic lupus
rheumatoid arthritis
mixed connective tissue disease
sjogren’s syndrome

52
Q

What are some ways the AI is thought to occur?

A

infections trigger autoimmune reactions
autoimmunity prevented by infection (type 1 diabetes, MS) “the hygiene hypothesis”

53
Q

What is the target of the autoantibodies in Grave’s disease?

A

TSH receptor

54
Q

What is the target of the autoantibodies in Myasthenia graves?

A

ACH receptor

55
Q

What is the target of the autoantibodies in idiopathic thrombocytopenia purpura (ITP)

A

PLatelets

56
Q

What is the target of the autoantibodies in Guillain-BArre syndrome?

A

gangliosides

57
Q

What are some of the autoimmunity theories?

A

leak theory
cryptic self hypothesis
self ignorance
molecular mimicry
modified self theory
defective apoptosis
polyclonal activators
NO overriding theory!!!

58
Q

What are the main signs of inflammation?

A

heat
redness
swelling
pain
loss of function

59
Q

what is septic arthritis?

A

septic infection of the joint

60
Q

what do neutrophils contain?

A

reactive oxygen intermediates, extremely toxic to bacteria however can cause damage to tissue when released

61
Q

What do neutrophils do to get to the site of infection?

A

They roll, adhere to the epithelial surface then undergo diapedesis to allow them to get to the site of infection

62
Q

What is the standard response to a bacterial infection?

A

increased production of neutrophils from the bone marrow
stimulating factors; granulocyte colony stimulating factor
increase the number of circulating neutrophils

63
Q

What is opsonisation?

A

bacteria coated with activated compliment component c3b
neutrophil has C3b receptor
encourages phagocytosis

64
Q

What are the principle mechanisms of innate immunity against viruses?

A

inhibitions of infection of other cells by type 1 interferons and NK-cell mediated killing of infected cells

65
Q

What are the the principle mechanisms of the adaptive immune response to viruses?

A

mediated by antibodies, which block virus binding and entry into host cells and by cytoxic T lymphocytes which eliminate the infection by killing infected cells

66
Q

Describe the role of antibodies in the fight against viral infections

A

antibodies are only effective against visions - the extracellular virus
bind to virus capsids or envelope proteins to neutralise them by changing the receptor shape and prevent them from binding to and infecting other cells
can opsonise virus particles - phagocytic clearance

67
Q

How do cytoxic T lymphocytes control viral infection?

A

kill cells
triggered by T cell recognition of infected cell expressing MHC viral peptide complex
perforin and granzyme molecules destroy infected cell

68
Q

What are some viral evasion strategies?

A

disarm innate immunity
regulate MHC molecules responsible for antigen presentation
alter antigen presentation
interfere with CTL and NK cells
Go and hide

69
Q

What is immunodeficiency?

A

a time when the immune response fails

70
Q

what are primary immune deficiencies?

A

congenital, resulting from genetic defects, inherited, deficiency causing disease

71
Q

What are secondary immune deficiencies?

A

acquired - result of other diseases or conditions - HIV, malnutrition, immunosupression

72
Q

How are the genetics of most immunodeficiencies?

A

most are recessive
many are X-linked

73
Q

how do primary immunodeficiencies usually present?

A

recurrent infection in young
and
allergy
autoimmunity
abnormal lymphocyte proliferation
cancer

74
Q

What different immune cells are involved in immunodeficiencies?

A

humoral defect (B cells and antibodies)
combined humeral and cellular defences (t and b)
defects in cell-mediated immunity (T)
phagocytic dysfunction
complement deficiency
cytokines / receptors can be at fault

75
Q

What do NSAIDs do?

A

inhibit the COX1 and COX2 pathways which stops the release of prostaglandins thereby reducing inflammation

76
Q

What does aspirin do?

A

Irreversibly blocks COX pathways
permanently stops platelets from producing thromboxane

77
Q

What does paracetamol do?

A

no significant anti-inflammatory effect
mild analgesic effect
antipyretic action
high doses severe hepatotoxitcity

78
Q

what are common side effects of NSAIDs?

A

GI problems due to the inhibition of prostaglandins normally stimulated by COX1 which stimulates the mucosal cells to produce the mucosa of the stomach

79
Q

What are some of the therapeutic uses of corticosteroids?

A

RA
lupus
asthma
fibrosis interstitial lung disease
sarcoidosis
anaphylaxis
rhinitis
transplantation
Chrohns
ulcerative colivitis
acute leukaemia
psoriasis

80
Q

What are some of the side effects of corticosteroids?

A

euphoria
buffalo hump
hypertension
thinning of the skin
thin arms, legs, muscle wasting
poor wound healing
easy bruising
increased abdominal fat
osteoporosis

81
Q

What are biological agents?

A

Usually antibodies against specific targets
extremely expensive

Z 2021 Phase 2 Limbs and Back Others (6 decks)

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