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BMA 3 > week 9 > Flashcards

week 9 Flashcards

1
Q

what are innate defences and purpose

A 
surface barriers
internal defences eg phagocytes, inflammation, fever
• Prevent foreign substances
from entering the body
• Immobilise and eliminate invaders
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2
Q

what are adaptive defences and purpose

A

humeral immunity (B cells)
cellular immunity (T cells)
T and B lymphocytes and
protein products
• Tolerant to “self” but react against “non-self”
• Target and destroy specific substances (“antigens”)

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3
Q

what do cytotoxic T cells do

A

target infected cells, but also affects cells around

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4
Q

what happens in an autoimmune disease

A 
adaptive defences: 
attack normal body cells
antigen cannot be cleared
sustained response
 tissue and organ damage
autoimmune disease
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5
Q

define systemic disease

A

affects multiple organs/system

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6
Q

define organ specific disease

A

affects one organ/tissue

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7
Q

mechanisms of autoimmune disease

A

combination of genetic and evironemtnal factors

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8
Q

whats genetic factors autoimmune disease

A

type of “self proteins” a person has (HLA proteins)

• Women (75% of patients)àrole for estrogen? • Ethnicity

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9
Q

whats environemental factors autoimmune disease

A

Chemicals

• Viral and bacterial infections (e.g. EBV, streptococcus)

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10
Q

how does breakdown of self tolerance occur

A
  • failure to destroy self reactive T and B lymphocytes during development
  • failure of regulatory T cells to control immune response
  • antigen mimicry (foreign antigens resemble self antigens)
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11
Q

how does autoimmune disease cause tissue damage 3 ways

A

mmune complex mediated inflammation
cell mediated cytotxicity
antibody reactions

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12
Q

immune complex mediated inflammation tissue damage

A

immune complex mediated inflammation eg rheumatoid arthritis:

  • autoantibodies are common marker of autoimmune disease eg rheumatoid factor.
  • immune complexes go into the blood which attract phagocyte which realease digestive enzymes into extracellular space which leads to tissue damage
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13
Q

cell mediated cytotoxicity tissue damage

A
  • Cytotoxic T cells lyse target cells, e.g. insulin-producing pancreatic b cells in Type I diabetes
  • Phagocytesdamage/kill cells by releasing digestive TC cell
    enzymes, e.g. rheumatoid arthritis, multiple sclerosis
  • T cells release enzymes that damage target cells membranes and degrade DNA
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14
Q

antibody reactions tissue damange

A

against cell surface antigens (act as agonists) eg graves disease

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15
Q

whats rheumatoid arthritis

A

systemic disease with prominent joint involvement. Immune-mediated chronic inflammationàjoint
destruction, i.e. autoimmune disease
• Inflammatory arthritis involving pain, swelling and stiffness of symmetrical joints
• Heart, lungs, skin, eyes, central nervous system may be affected/damaged by inflammatory reactions

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16
Q

whats idiopathic means

A

cause unknown

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17
Q

how are autoimmune disease treated

A
  • relieve symptoms eg anti-inflammatory drugs (NSAID)
  • replace vital substances the body can no longer make eg hormone replacement (insulin)
  • suppress the immune system: control disease process and preserve organ function
  • dietary manipulation eg no gluten in coeliac disease
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18
Q

what is JIA

A
  • onset prior to 16 years old
  • idiopathic
  • arthritis
  • immune mediated chronic inflammation (autoimmune disease)
  • affects girls more than boys
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19
Q

genetic components of JIA

A

Markedly increased risk for close relatives
• Females > males
• Most common in Caucasians
• Emotionalissues/stressmayworsensymptoms
• Roleforsexhormones?

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20
Q

what area of immune system affected JIA

A

Elevated cytokine levels (TNF, IL-1, IL-6) and auto- reactive antibodies
• Distinct from adult RA, despite many similarities

21
Q

JIA signs and symptoms

A
  • joints pain and swelling (synovial inflammation, erosion of articular cartilage)
  • joint stiffness, flexion contracture: leads to restricted movement and physical activity
  • sleep disturbances, fatigue
  • period of remission (symptom free) and flareups
22
Q

the stages the pain cycle

A
  • pain
  • tense muscles
  • stress
  • sleep difficulty
  • fear, anger, frsutration
  • depression
  • fatigue
23
Q

three major factors that cause pain in JIA patients

A

inflammation
damage to joints
muscle tension

24
Q

extra articular manifestations JIA

A

acute phase response
serositis
uveitis
growth failure

25
Q

whats acute phase response

A

Low-gradefever,weakness,malaise,muscle and joint aches, increased BP, lack of appetite, anaemia

26
Q

whats serositis

A

autoantibodies lead to rollin pathogenesis via immune complex mediated inflammation leads to damage to:

  • pericardium= impaired function. pain
  • lung pleura= impaired fonction, pain
  • blood vessels= schema, necrosis in skin, heart and nerves
  • nerve pain (tingling or burning in hands and feet
27
Q

whats uveitis

A

inflammation of the urea membrane Easy to treat but hard to know if they have it
- long term uveitis = permanent eye damage, blindness

28
Q

whats growth faliue

A
  • overall rate of growth reduced
  • uneven limb/joint growth
  • low bone mineral density
29
Q

three major types of JIA

A

oligoarticular
polyarticular
systemic

30
Q

whats oligoartuclar JIA

A
  • less than 5 joints
  • medium-large joints affected eg knees, ankle
  • asymmetric
  • non destructive arthritis
  • 20% uveitis
31
Q

what is polyarticular JIA

A
  • more than 5 joints affected
  • usually smaller joints
  • symmetric
  • destructive arthritis
  • usually RF positive
32
Q

what is systemic JIA

A
  • more than one joint
  • any join
  • symetric
  • destructive arthrisic
  • daily fever, rash
33
Q

what is enthesitis associated JIA

A
  • typically knee, ankle
  • ethestis: inflation of tendons at muscle insertion ponts
  • increase risk of unites
  • more communion males
34
Q

whats psoriatic JIA

A
  • any joint small and large
  • increase risk of uveitis
  • nail pitting and loss
35
Q

whats undifferentiated JIA

A

does not fit into any category or fit into 2 or more categories

36
Q

diagnosis of JIA

A

usually by exclusion of other paediatric disorders

• Involving blood tests, imaging studies, clinical presentation

37
Q

three goals for treatment of JIA

A

Control pain and prevent joint damage
• Maintain normal growth, joint function and muscle strength
• Control systemic complications

38
Q

pharmacological treatment of JIA

A

non steroidal anti-inflammatory drugs (NSAID): eg nurophen, aspirin. (1ST LINE)
- reduce joint pain and swelling but DOES NOT prevent joint destruction or inhibit disease progression
corticosteroids: reduce pain, inflammation and can prevent joint inflammation. (1st LINE)
- short term treatment only
disease modifying antirhumatic drugs (DMARDS): (2ND LINE)
- long term use
- imunosupressent, reduces inflammation, progressive joint destruction
Biologics (when 1st and 2 nd line fail)
- immune suppressants

39
Q

side affects of corticserotied treatment

A

immunosupression= increased risk of infetion
grwoth retardation
decreased bone mineral density
weight gain

40
Q

non pharmacological treamtoer

A
  • exercises, stretching and strengthening
  • restnng and functional splints
    PAIN MANAGMENT:
  • breathing and relaxation techniques
  • massage
  • heat cold application
    NUTRITION:
  • vitamin D and calcium supplements (bones)
  • Omega 3 (may help reduce inflammation/pain)
    SURGERY
41
Q

three types of surgery

A

Osteotomy – removing or inserting a wedge of bone to allow more normal joint alignment
• Epiphysiodesis – removal/impairment of the growth plate to stop bone growth
• Joint replacement – not usually done until growth has stopped

42
Q

prognosis for JIA

A 
Oligoarticular
50% at 10 y post-diagnosis
Polyarticular (RF-)
25% at 10 y
Polyarticular (RF+)
<10% at 10 y
Systemic
10% if single episode
(90% will have relapsing or chronic disease)
Poor prognosis associated with:
• Early hip or wrist involvement
• Symmetrical disease, rheumatoid factor (i.e. like adult RA)
• Persistent inflammation (> 5-10 years) and/or prolonged systemic disease
43
Q

side effects of non steroidal antjnflamtory drugs (NSAID)

A

Generally well tolerated in children
• < 1% experience mild nauseaàloss of appetite, but minimised by taking with meals
• Bruising more common

44
Q

side effects of disease modifying antirhumatic drugs

A

mmunosuppressantàincreased risk of infection
• Generally well tolerated in children but …
• ~10% experience nausea and abdominal discomfort
• ~ 3% liver damageàregular blood tests (no alcohol)
• Teratogenàbirth defects

45
Q

side effects of biologics

A

Increased frequency and severity of infections e.g. UTI, pneumonia, tuberculosis, fungal infections
• Patients cannot have any live vaccines, e.g. polio, chicken pox, MMR

46
Q

causes of fatigue in JIA

A

disease activity
pain (affects sleep)
muscle weakness/ wasting
depression

47
Q

why is exercise good for JIA

A

Improve mobility and flexibility of joints, muscle strength, posture and balance

Decrease pain, fatigue (tiredness), muscle tension and stress

48
Q

should clients exercise a painful or inflamed joint

A

No. You should stop exercising if it is causing you unusual pain or increases your pain beyond what is normal for you. Exercising through this type of pain may lead to injury or worsening of your arthritis symptoms.

BMA 3 (8 decks)

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