Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Rheumatology > RA and OA > Flashcards

RA and OA Flashcards

1
Q

What is the most important environmental risk factor for development of RA?

A

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What HLA is RA associated with?

A

HLA DRB1 0404
HLA DRB1 0401

Risk stacks, therefore if have both HLA DRB1 0404 and 0401 pos the high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the MHC association of RA?

A

Shard epitope in 3rd hypervariable region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most specific antibody for RA? this antibody is part of a class of RA antibodies called?

A

Anti CCP

1 of a group of antibodies called ACPAs (anti cetrulinated protein antibodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Whst is though to be the main pathogenesis of RA?

A

There is an environmental stress that causes induction of PAD enzyme
- PAD converts arginine to citrulline (citrullination)
- Autoreactivity to neoepitopes created by protein citrulination leads to teh formation of ACPAs (anti citrulinated protein antibodies) such as anti CCP

Note citrulination occurs all the time, for example in the lungs of smokers
Person without HLA B1 DR3 0404 or 0401 positive will have more resistance to this citrulination process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does protein citrulination occur in the development of RA? (where does RA begin)

A

Mucosal
Gut microbiome
Lungs

Begins in the peripheries, mucosal surfaces
Antigen presentation and T cell activation in the nodes
Then cell mediated joint attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the unifying cytokine that is increase in all connective tissue disease?

A

TNF-alpha
- thought to be IL15 because this controls production of TNF, however tests show that TNF alpha is the main driver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the most common cell in the synovial fluid of RA pts? Why is this the case?
What about the synovium?

A

Neutrophil are in teh synovial fluid
THere should not be any neutrophils in the synovium, that would not be RA (? infection)
- this is because there is a gradient of IL8 (chemoatractive)

The main cell in the synovium is the T cells (B cells <5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two types of fibroblasts in the synovial membrane? what is their role in RA?

A

Ling layer fibroblasts
- Cause bone and cartilage destructive
Sub lining layer fibroblasts
- produce cytokines for chemoattration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most important cytokine in errosive RA?

A

IL-1 (increased expression = increased errosive disease)
- IL-17 is in the synovioum and is associated with errosive disease but it is not the cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Is RA a disease of TH1 or TH2?

A

TH1, response is maintained by IL18 and 33

Thought that RA pts are deficient in TH2 cells (these are responsible for switching off the immune response)
- TH2 response sustained by IL4 and 13 which are absent in RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happen in an RA flare? (cell migration kinda stuff)

A

Naive B cell exists in the serum before a flare
B cell becomes activated
PRIME cells are recruited
PRIME cells and activated B cells migrate into the joint causing teh flare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pt comes in with arthralgia. WHat factors would make them more likely to develop RA in teh new 12 months?

A

Firs degree relative with RA
RF and anti CCP positive
MCP involvement / morning stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the main clinical aspect in the diagnostic criteria for RA?

A

Joint involvement, multiple joints involved is worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When should RF be performed?

A

Only do this if you think the person has RA. Very poor specificity meaning lots of false positives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IS RF or anti CCP a better predictor of errosive disease?

A

Anti CCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

WHat is the earliest change in RA on Hand XR? What are some other features on hand XR and neck XR?

A

Peri-articular osteoporosis
- Occurs mainly in RA, not in other condition

Errosions are a poor prognostic factor
Atlantoaxial subluxation >4mm needs to be addressed, esp prior to having surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

WHat is the triad that characterises Feltys syndrome?

A

RA, splenomegally, neutropenia (due to hypersplenism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What heart complication can RA pts classically get?

A

Constrictive pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What form of eye disease is RA most associated with?

A

Episcleritis, scleritis

Scleritis is painful and has visual abn

Episcleritis is not painful and nil visual change
- Phenylephrine topically will cause blanching. WIll not cause blanching in scleritis

21
Q

All RA pts who tolerate it should be on …?

A

Methotrexate

22
Q

What medications reduce radiological progression of RA?

A

MTX, hydroxychloroquine, leflunamide, sulfasalazine

23
Q

What are the contraindications for MTX?

A

mild seronegative disease
renal impairment
liver impairment
high eoth intake
Lung disease

24
Q

Pt with RA, CPC liver disease and ongoing alcohol. Can they have MTX?

A

No

25
Q

How does MTX penumonitis typically present? How is it managed?

A

Soon after starting MTX, pt presents with fever, SOB, dry cough, chest pain
Main DDx is PJP infection

Rx:
Cease MTX
Pred
Supprtive measures

No role for folinic acid

26
Q

What cancers is MTX associated with?

A

SKin cancers
B cell lymphomas
Lung cancer (probs due to smoking association)

27
Q

Should MTX be ceased in periop?

A

No, generally speaking just continue it

28
Q

What is the general approach if pt fails MTX alone?

A

Add sulphasalazine +/- hydroxychloroquine
- COmbination is always better than MTX alone

29
Q

What is a specific side effect of luflunamide and how is it managed?

A

P{eripheral neuropathy
- cease and allow drug to wash out

30
Q

What is the criteria for biologics in RA?

A

MTX for at least 3 months, combination with another DMARD for at least 3 months

(Basically fail conventional DMARDs)

31
Q

What is the biologic that is best / safest to use in preg for RA pts?

A

Certolizumab

32
Q

What are some of the TNF alpha inhibitors used in RA?

A

Infliximab
Adalimumab
Etanercept
Golimumab
Certolizumab

33
Q

DMARDs slow radiological progresion of RA. What effect do teh biologics have on radiological progression?

A

Cease radiological progression
- this doesnt nec means better patient scores tho

34
Q

TNF inhibitor are associated with reactivation of which latent infection?

A

TB

35
Q

Why is MS an absolute contraindication for TNF inhibitors?

A

TNF inhibitors can cause demyelination

36
Q

Aside from teh TNF inhibitors, what other biologics can be used for RA?

A

Abatercept (Soluble CTLA4 anoligue)
Tocilizumab (IL6 receptor antibody)
Rituxumab (mab for CD20)
JAK inhibitors
- Tofacitinib (JAK1, JKA6)
- Baracitinib (JK1,2)
- Upadacitinib (JK1)

37
Q

What infectious agent is most implicated in TNF inhibitors?

A

Herpes zoster
- need to give shingrex

38
Q

Pt has Hep B, new dx RA> which biologic can he have?

A

None

39
Q

Pt has solid malignancy <5yrs, new dx RA. which biologic can he have?

A

Ritux

40
Q

How is OA classified?

A

Primary or secondary

Knee OA vs multiple joint OA (most often Knee + other joints but not always)

41
Q

What are some common causes of secondary OA?

A

Anatomical abn
Trauma
Metabolic disorder (ie haemachromatosis)

42
Q

What is the biggest RF for OA?

A

Age

43
Q

Hip OA in younger person. What secondary cause?

A

Probably hip dysplasia
May also be haemachromatosis

44
Q

What is the major modifiable RF of OA?

A

Obesity
its a much bigger RF from knee OA than for hip OA

45
Q

Is exersise protective or RF for OA?

A

Normal joint at risk with lack of exersise, at risk with high impact exersise

Abn joints are at risk with exersise

46
Q

WHat are teh 4 features of OA on XR?

A

Loss of joint space
Osteophytes
Subchondral cysts
Subchondral sclerosis

47
Q

Pt with hand OA, has MCP joint involvment. What is Dx?

A

Cant be standard OA (MCP woulds not be involved)
- Have to think of RA, OA due to secondary cause it haamachromatosis, boxing etc)

48
Q

Rx of OA? What medications do not work / are not recomended?

A

Non pharm:
- Loose weight
- Exersise / tai chi

Pharm:
- Paracetamol if nil co-morbidities (First line if niol co-morbidity, not first line if have co-morbidities)
- Non seletective NSAIDs (gastroprotection needed if co-morbidities, not give to pts with significant co-comorbidities)
-> topical NSAIDs short term or for intermitent pain
- Topical capcacin
- Duloxetine - pain management if failure of NSAIDs

  • DO not use opioids - unclear benefit and significant risks
  • BPs are of unclear benefit at this stage
  • Nil good evidence for glucosamine and chondroitin (also beware shell fish allergy)
  • Intrarticular injection are not effective in the long term. Similar efficacy to placebo in the short term for symptom relief
49
Q

What medicaiton is disease modifying in OA?

A

Doxycycline
- reduces joint space narrowing

Strontium is also Disease modifying, however not used anymore due to risk of thromboemolism

Rheumatology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions