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Flashcards in Rheumatology Deck (55)
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1
Q

What is arthralgia?

A

When a joint hurts but there is no sign of inflammation

2
Q

when is monoarticular arthritis typically seen?

A

infections, crystal-induced arthritis, or trauma, septic arthritis, gout, pseudogout, traumatic arthritis, mechanical derangement of joint, osteochondritis dissecans

3
Q

What is oligoarticular arthritis and when is it typically seen?

A

seen in several joints (2-4)

often associated with the axial arthropathies such as ankylosing spondylitis, psoriatic arthritis, or reactive arthritis.

often asymmetrical and involves the large joints (although not invariably).

4
Q

what is polyarticular arthritis and when is it typically seen?

A

Involves multiple joints, often SYMETRICALLY, and usually
affects both the small and large joints.

** rheumatoid arthritis, systemic lupus erythematosus, and certain viral syndromes.

5
Q

What is hyaline cartilage composed of?

A

type II collagen, proteoglycans and chondrocytes which produces collagen and proteoglycans

matrix proteins: metalloproteinases (MMP)

6
Q

what are polyarticular diseases which can present as a Monoarticular disease?

A

juvenile rheumatoid arthritis, Reactive arthritis, Sarcoid arthritis, psoriatic arthritis, pseudogout

7
Q

what are joints involved in osteoarthritis?

A

-distal interphalangeal joints (DIP), proximal interphalangeal joints (PIP), first carpometacarpal joint (CMC), cervical spine,
lumbosacral spine, hips, knees, first metatarsophalangeal joint (MTP)

8
Q

which arthritis is worse with rest or in the morning?

A

rheumatoid arthritis or axial arthropathies.

9
Q

what arthritis is worse with use?

A

osteoarthritis

10
Q

What genetic factor is associated with rheumatoid arthritis?

A

HLA-DR4 & 1

**QKRAA sequence

11
Q

How does PRPP synthetase contribute to Gout?

A

overactivity of PRPP leads to increase uric acid

PhosphoRibosyl-PyrophosPhate

12
Q

How does HGPRT contribute to gout?

A

deficiency in HGPRT leads to increase uric acid

Hypoxanthine Guanine PhosphoRibosylTransferase used to convert hypoxanthine –>guanine

13
Q

Which type of arthritis is noninflammatory?

A

Osteoarthritis

14
Q

What cytokines are associated with osteoarthritis?

A

Interleukin 1 –> MMP, prostaglandins, nitric oxide
nitric oxide –> increases MMP production and chondrocyte apoptosis
Prostaglandins: increase production and activation of MMP
complement activation
adipokines–> cytokines released from fat cells

15
Q

How does rheumatoid factor contribute to rheumatoid arthritis?

A

IgM Rheumatoid factor attacks Fc portion of IgG

16
Q

What other antibodies are associated with rheumatoid arthritis other than RF?

A

anti citrulline antibodies

These citrulline peptides should not be made and are specifically present in patients with rheumatoid arthritis

17
Q

What type of cells are present in RA synovium?

A

CD4+ Tcells, Th17 cells, B cells, and plasma cells
B cells produce antibodies to RF and CCP
macrophages induced to release MMP

18
Q

What are the joints involved in gout?

A

1st MTP

cool, peripheral joints of lower and upper extremities

19
Q

Are majority of gout patients underexcreters of uric acid or overproducers?

A

UNDEREXCETERS

20
Q

What treatment would you use to inhibit the conversion of xanthine to uric acid?

A

allopurinol and febuxostat

21
Q

How does MSU trigger immune response?

A

binds to TLR2 and 4

also engages in caspase 1 that activates NLRP3 inflammasome –> production of IL-1beta

22
Q

Describe the self limiting process of gout?

A

IgG coats the MSU and triggers phagocytosis by PMNs –> immune response

eventually apolipoprotein B coats it, now inhibiting phagocytosis and the immune response in suppressed.

23
Q

Describe calcium pyrophosphate dihydrate deposition disease?

A

You have an abnormal production of pyrophosphate (PPi) due to the over productions of nucleoside triphosphates –> PPi

Nucleoside triphosphate (NTP) is hydrolyzed by NTPPPH generating NMP and PPi

24
Q

Describe the genetic component with CPPD

A

there is an ANK GENE mutation that results in a transmembrane PPi transporter protein that allows excess PPi to leave the chondrocyte

25
Q

What are the important characteristics of CPPD?

A

rhomboid shape

POSITIVELY birefringent

26
Q

What is the genetic component of seronegative sponyloarthropathies?

A

HLA-B27

27
Q

Which important cytokine would be found in the synovium for seronegative spondyloarthropathies?

A

tumor necrosis factor

28
Q

What arthritis has a 20% chance of developing if you have a family history with one first degree relative?

A

seronegative spondyloarthropathy

29
Q

Which arthritis is asymmetric, oligoarticular, and affects lower extremities?

A

reactive arthritis

30
Q

What is Reiter’s syndrome?

A

can’t see, pee, or climb a tree

conjunctivitis, urethritis, arthritis

31
Q

What are some of the hypotheses for reactive arthritis?

A

molecular mimicry
arthriogenic peptide hat is uniquely presented by HLA-B27
HLA-B27 heavy chains combine and activate NK cells
**unfolded protein hypothesis: ER stress response

32
Q

Which arthritis is most likely explained by a misfolded protein (ERAP-1) in the ER that stimulates production of IL-23?

A

seronegative spondyloarthropathy

33
Q

What is the fundamental defect in systemic lupus erythematosus (SLE)?

A

misdirected recognition of self as foreign.

A T cell AND B cell process

34
Q

What is the strongest genetic association with lupus?

A

HLA-DR3 and C4A null allele

35
Q

What is the hallmark of systemic lupus erythmatosus?

A

positive ANA

36
Q

What type of antibodies are produced in lupus/

A

anti-dsDNA
anti histone
anti-smith, SSA, SSB

37
Q

What is the significance of anti-phospholipid antibodies in lupus?

A

it blocks the prothrombin activation in clotting but INCREASES CLOTTING (counterintuitive)

probably neutralizes the anti-coagulating effect of beta 2 GP1

38
Q

What is the major target organ in SLE?

A

The kidneys

39
Q

What is the classic clinical presentation of Vasculitis?

A

palpable purpura

40
Q

What is the presentation of giant cell vascultitis?

A

temporal : temporal arteries, vessels originating from the aortic arch, other arteries less common; temporal headache, jaw claudication, scalp tenderness, visual loss (ophthalmic artery)

**carotid artery

41
Q

What is Takayasu’s arteritis?

A

giant cell vasculitis affecting vessels branching from the aortic arch claudication of upper > lower extremities, CNS events; granulomatous
panarteritis

42
Q

medium vessel vasculitis affects which arteries?

A

muscle arteries

43
Q

Polyarteritis nodosa

A

medium vessel vasculitis that affects small and medium-sized arteries; may affect any organ, but skin, joints, peripheral nerves, gut, and kidney are most commonly involved; focal but panmural necrotizing arteritis with a predilection for involvement at the vessel bifurcation

44
Q

Kawasakis disease

A

medium vessel vasculitis - fever, conjunctivitis, erymatous rash of palms and soles, lymphadenopathy

45
Q

What are ANCAs?

A

Antineutrophil cytoplasmic antibodies

46
Q

What vasculitis is associated with cytoplasmic ANCA?

A

granulomatosis with polyangiitis

47
Q

What does c-ANCA stain positive for?

A

proteinase - 3

48
Q

What vasculitis is associated with perinuclear ANCA?

A

microscopic polyangiitis

49
Q

What does perinuclear ANCA stain positive for?

A

myeloperoxidase (MPO)

50
Q

What are signs of polymyositis/dermatomyositis?

A

muscle weakness that is proximal

low endurance

51
Q

What skin rashes seen with dermatomyositis?

A
gottron's papules
Heliotrope rash
V-sign and shawl sign
mechnic's hands
periungual changes/erythema
52
Q

What disease does PM or DM typically present with?

A

interstitial lung disease 60%

53
Q

What antibodies are associated with PM or DM?

A

anti-synthetase antibodies “ANTI-JO-1” which is an ANTI-HISTADYL TRNA SYNTHETASE

54
Q

What t cell is associated with polymyositis?

A

CD 8 + T cells

55
Q

What t cells is associated with dermatomyositis?

A

CD4+ T cells