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Rheumatology > MKSAP 19 > Flashcards

MKSAP 19 Flashcards

1
Q

6 most important lytic bone lesions?

A

Thyroid cancers.
Lymphoma (NHL)
Melanoma.
Multiple myeloma.
Renal cancer.
Sarcoidosis.

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2
Q

most important blastic bone lesion?

A

Prostate cancer

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3
Q

2 most important, lytic/blastic bone lesions?

A

Lung cancer.
Breast cancer.

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4
Q

Bone symptoms of Sjogren’s Syndrome

A

Non-erosive arthritis

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5
Q

Skin symptoms of Sjogren

A

Non-nodular rash

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6
Q

most common cause of kidney disease in patients with long-standing poorly controlled (not taking biologic therapy), inflammatory diseases, like ankylosing, spondylitis or rheumatoid arthritis?

A

AA amyloidosis-Renal amyloidosis, presenting as proteinuria

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7
Q

When to suspect AA amyloidosis in AS?

A

Men, pt with peripheral joint disease and with h/o uveitis

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8
Q

Urinalysis findings of Renal Amyloidosis vs Analgesic nephropathy

A

Isolated proteinuria vs pyuria/proteinuria and hematuria

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9
Q

2 main kidney diseases in AS (separate from secondary to NSAID use)

A

AA amyloidosis ( UA- isolated proteinuria), improves with aggressive AS treatment
IgA nephropathy ( UA- hematuria and proteinuria), unaffected by aggressive treatment of AS.

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10
Q

Interstitial nephritis clinical presentation?

A

Fever, rash, eosinophilia/eosinophiluria (not sensitive or specific).
Most common UA findings- Pyuria, WBC casts.
Other important findings- rise in creatinine, hematuria, proteinuria.

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11
Q

Which caution to exercise while prescribing Methotrexate in females?

A

Contraceptives should be given in females of child bearing age as Mtx is aw pregnancy loss and fetal abnormalities.

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12
Q

3 main TNFi

A

Abatacept, Tofacitinib and Rituximab

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13
Q

Mycophenolate mofetil moa

A

Reversible inhibitor is Inosine Monophosphate Dehydrogenase, affects lymphocyte stimulation and proliferation.

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14
Q

Prosthetic joint infections classification based on duration and most common causative agent?

A

Early onset (<3 months)- Staph Aureus
Delayed onset (3-12 months) - CONS (Staph epidermidis)
Late onset (>12 months)- Staph Aureus

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15
Q

Risk factors for Prosthetic joint infection with Pseudomonas Aeruginosa

A

H/o GI or GU infection or Immunosuppression.

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16
Q

Mainstay of treatment in SLE and why?

A

HCQ, reduces disease associated damage, prevent disease flares, and improve kidney and overall survival.
It also reduces risk of thrombosis, liver disease and MI and improve lipid profiles.

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17
Q

Classify SLE based on severity

A

Mild- no organ involvement.
Severe- organ involvement like nephritis, CNS disease.

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18
Q

Glucocorticoid indications and usage in SLE

A

Used in acute disease.
After disease stabilizes, taper to lowest effective dose, not more than 7.5 mg/d within 4-6 months, discontinue early if possible.
Azathioprine or MTX is recommended if patients with mild disease have refractory symptoms.

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19
Q

Important aspects of Management of SLE besides pharmacotherapy

A

Sun protection, vaccinations and LSM

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20
Q

Pharmacotherapy for severe SLE

A

Mycophenolate or cyclophosphamide, in addition to glucocorticoids and HCQ.

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21
Q

Bone and soft tissue changes in chronic gouty arthritis

A

soft tissue swelling, tophus, and well-defined erosions that have sclerotic borders and overhanging margins.

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22
Q

Considerations before pharmacotherapeutic management of an acute flare of gout

A

CKD (for Colchicine)
Bleeding risk / anticoagulation (Indomethacin)
Hyperglycemia (Prednisone)

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23
Q

Criteria for initiating Urate lowering therapy for patients with Gout

A

Gout with any of the following indications:
One or more subcutaneous tophi
Evidence of radiographic damage (any modality) attributable to gout
Frequent flares ( 2 or more annually)

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24
Q

Serum urate target with Urate Lowering Therapy

A

6

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25
Q

Can you initiate Urate lowering therapy during Acute Flare of gout?

A

Yes as it improves future adherence, but only if the pt is also being adequately treated for acute flare.

It does NOT treat acute flare, if administered alone, can prolong flare duration.

When initiating allopurinol, patients should continue taking anti-inflammatory flare prophylaxis for at least 3 to 6 months because urate lowering therapy Transiently raises the frequency of flare occurrence.

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26
Q

3 most Important considerations for using Colchicine in acute gout?

A

Most effective within first 24 hours of the episode.
CKD
GI toxicity causes dose limitations

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27
Q

Colchicine Dosage in acute gout

A

In absence of CKD,
First dose- 1.2 mg
One hour later- single 0.6 mg dose, then
0.6 mg daily

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28
Q

Treatment approach to acute gout- pharmacotherapy and non pharmacological

A

Drug options- Colchicine, NSAIDs, Predni based on pt comorbidities. Optional urate lowering therapy.

Non-pharmacological - Topical ice.

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29
Q

Indications of kidney biopsy in SLE

A

Glomerular Hematuria
Cellular Casts
Spot UPCR > 500
Unexplained decrease in eGFR

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30
Q

First line therapy for Ank Spond

A

NSAIDs + Physical Therapy

If an NSAID is started early in the course of AS (<3 yrs), 35% patients will enter remission compared to 12-15% of those starting it later.

Unlike other rheumatologic diseases, NSAID has disease modifying effect in AS.

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31
Q

Second and 3rd line treatment for Ank Spond

A

2nd line-
TNFi- Etanercept
IL-17i - Secukinumab or Ixekizumab

3rd line (only if TNFi and IL-17i are contraindicated)-
JKi (Janus Kinase inhibitors)- Tofacitinib and Upadacitinib

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32
Q

Drugs more useful in Peripheral Joint disease rather than axial

A

Nonbiologic agents like- MTx and Sulfasalazine

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33
Q

What cancer to monitor for in Sjogren?

A

Lymphoma, most commonly- Mucosa associated lymphoid tissue lymphomas

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34
Q

6 Risk factors for Lymphoma in Sjogren

A

Parotid gland enlargement
Depressed C4
Elevated Rheumatoid Factor
Elevated Anti-Ro/SSA and anti-La/SSB
Monoclonal gammopathy
Cryoglobulinemic Vasculitis

35
Q

Primary vs Secondary Sjogren

A

Primary occurs in isolation
Secondary occurs in setting of other rheumatologic diseases, most commonly- RA and SLE

36
Q

Antibodies that can be seen in Drug Induced Lupus

A

Antihistone (Non specific)

ANCA ( especially P-ANCA) and F-actin- seen with Minocycline

ANA may be transiently positive but *typical autoantibodies of SLE are absent.

37
Q

Drug induced lupus vs SLE (Idiopathic)

A

DLE is milder, characterized by more skin (acne) and Joint symptoms (could be similar other inflammatory arthritis like RA with symmetrical peripheral joint involvement) (No organ damage- urinalysis is normal.

DLE may have transient ANA positive but lack typical autoantibodies to SLE

38
Q

2 features that should trigger SLE in your head in a patient with arthralgia, regardless of gender?

A

TCP and abnormal urinalysis ( possible kidney disease)

39
Q

First line treatment for mucocutaneous ulcerations in Behcet

A

Colchicine,
followed by Apremilast

40
Q

Apremilast indication in Behcet

A

Apremilast is a reasonable alternative to Colchicine as a glucocorticoid sparing agent for recurrent oral ulcers in Behcet syndrome. Either in addition or as an alternative.

41
Q

Autoinflammatory syndromes (FMF) pathophysiology

A

Monogenic disease, gene mutation causing activation of inflammasomes and expression of proinflammatory mediators like IL-1beta for FMF

42
Q

5 clinical subtypes of Psoriatic Arthritis

A

Symmetric Polyarthritis
asymmetric oligoarthritis
distal interphalangeal predominant disease
Spondyloarthritis
Arthritis Mutilans

43
Q

Criteria for diagnosis of Behcet Disease

A

International Criteria for Behcet Disease scoring system

44
Q

Pathognomic feature of Behcet Disease

A

Pathergy

45
Q

Clinical diagnostic features for FMF?

A

Multiple recurring episodes of fever, abdominal pain, rash and arthritis.
Other symptom can be- serositis (including Pericarditis)

46
Q

How to diagnose FMF

A

Clinical symptoms, definitively confirmed by genetic testing- MEFV gene mutation

47
Q

Criteria for diagnosing Psoriatic Arthritis (PsA)

A

CASPAR (Classification Criteria for Psoriatic Arthritis)

48
Q

Pathognomic feature of Spondyloarthropathy like PsA

A

Dactylitis

49
Q

Which tissue to use to Dx GPA?

A

Kidney

50
Q

Standard treatment regimen for GPA?

A

High dose oral glucocorticoids plus rituximab (preferred)
IV pulse glucocorticoids
Cyclophosphamide

51
Q

Features of an inflammatory pain?

A

Night pain, morning stiffness and pain that improves with activity.

52
Q

Evaluation of an inflammatory low back pain ( spondyloarthritis)

A
  1. Compelling clinical picture
  2. Pain radiograph of SI joint (may be normal for 1 to 2 yrs after symptoms develop)
  3. HLA-B27 (positive test in background of compelling clinical picture, confirms the dx)
  4. MRI of pelvis for SI inflammation (more sensitive than CT to detect SI inflammation) (If HLA is negative or in a patient with inflammatory LB ache and positive HLA but no other features of spondyloarthritis)
53
Q

Reason for ANA as the initial test in evaluation of a suspected Rheumatologic Disease?

A

ANA is very sensitive but low specificity ( If ANA is negative, then further subserology testing is typically negative). Therefore if ANA is negative, then serology testing is not indicated.

If ANA is positive, then specific subserologies are indicated on the basis of clinical scenario.

54
Q

Anti DS DNA vs Anti Smith antibodies for SLE?

A

Anti DS DNA (95 % specific, 50-60% sensitive), found in more severe disease, especially KIDNEY DISEASE. Levels follow disease activity and useful to MONITOR drug therapy.

Anti Smith- Most specific (99%) for SLE, low sensitivity. Levels do not correlate with disease activity.

55
Q

3 FDA approved medications for Fibromyalgia

A

Pregabalin (starting 50/75 nightly titrating upto 225 BID)
Duloxetine
Milnacipran

56
Q

What is DISH?

A

Diffuse idiopathic skeletal hyperostosis-
Noninflammatory condition, can occasionally have elevated inflammatory markers, causes calcification and ossification of spinal ligaments (esp Anterior Longitudinal Ligament) and entheses ( tendon and ligament attached to bone), causing pain stiffness and reduced ROM.
Imaging shows flowing linear calcification and ossification along anterolateral aspects of vertebral bodies.

More common in Men > 45, most involve thoracic spine.

It does NOT affect SI joint.

57
Q

Chronic back pain and stiffness, DISH vs AS (Ank Spond)?

A

DISH- Men, > 45, SPARES SI (Prominently involves thoracic spine)
AS- < 45, SI involvement

58
Q

Most effective LSM in reducing patients’ risk of developing RA?

A

Smoking cessation.
A dose dependent relationship exists between smoking and development of Seropositive RA.
Smoking causes lung inflammation which activates enzymes such as peptidylarginine deiminase which deaminates arginine to form citrullinated peptides. These are presented as antigens by a shared epitope coded by HLA-D allele, leading to production of anti-CCP antibodies that could initiate inflammation by fixing complement in tissues.

59
Q

Dx
Photosensitive distribution of dermatomyositis rash on the face. Heliotrope rash over eyelids. Gottron papules on the elbows and knees. With normal CK and no muscle symptoms.

A

Amyopathic Dermatomyositis:
Patients never develop muscle involvement, can be diagnosed with skin biopsy confirmation of Dermatomyositis in the setting of atleast 6 months without muscle involvement.

60
Q

Photosensitive rash of dermatomyositis vs SLE?

A

Both can have similar facial rash and skin biopsy findings.
SLE does not have Heliotrope rash or Gottron papules on hands, elbows and knees.

61
Q

Differentials of Malar Rash?

A

SLE- Photosensitive, lacks heliotrope and gottron.
Dermatomyositis- Photosensitive, characteristic Heliotrope rash and Gottron papule
Rosacea- would not cause skin changes on extremities.

62
Q

What to suspect in patients with Ank Spond who develop abdominal pain, diarrhea or change in bowel habits?

A

IBD- Crohn and UC occur with similar frequency.
Occurs early in the course of disease, by 10 yrs of AS, the risk of IBD has returned to general population level.

63
Q

Diagnostic criteria for IBS

A

Recurrent abdominal pain at least 1 day a week for 3 months, along with atleast 2/3 of :
Pain related to Defecation
Change in stool frequency
Change in stool consistency

64
Q

Lyme arthritis presentation and diagnosis?

A

LA is a late stage manifestation of lyme ds. Monoarticular, mostly knee.
Suspect in pt with intreated or incompletely treated Lyme.

Dx : All pt with LA should have positive results on ELISA and Western Blot confirmatory serologies.
A second enzyme immunoassay can be used as a confirmatory test.

Borrelia DNA can be detected by PCR in synovial fluid, but this test offers no advantage to Serologic testing.

65
Q

Treatment of Lyme Arthritis?

A

28 days Doxycycline.
28 days of amoxicillin is an alternative first line therapy.

For pts whose arthritis improves but does not completely resolve, a second 28 day course of the same antibiotic can be prescribed.

66
Q

Treatment of persitent arthritis ( after 2x 28 days courses of Doxy) ?

A

Suggests Reactive Arthritis.
Rheumatologist referral. Tx with HCQ or MTx.

67
Q

Diagnostic feature of CPP crystal arthritis on plain XR?

A

Chondrocalcinosis (thin white line that tracks below the surface layer of cartilage, representing CPP deposition within cartilage)

68
Q

Acute Gout vs CPP crystal arthritis

A

Gout typical joint involvement : knee with current or prior joint involvement of first MTP, forefeet, ankles and fingers.
Acute episode lasts : 1-2 weeks.
Crystals: Negatively Birefringent and needle shaped.

CPP typical: Knee or wrist
Acute episode lasts more than 2 weeks.
Crystals: Positively birefringent and rhomboid.

69
Q

When to consider TNFi or IL-17i in AS patients?

A

After failure of trial of atleast 2 NSAIDs for 2-4 weeks, or if intolerant to NSAIDs.

70
Q

Name 3 TNFi?

A

Etanercept (a fusion protein)
Adalimumab and Infliximab (monoclonal antibodies).

Selection depend on comorbidities, such as Uveitis or IBD, where monoclonal antibodies would be more appropriate.

71
Q

2 IL-17i?

A

Secukinumab
Ixekizumab

72
Q

2 Janus Kinase inhibitors?

A

Tofacitinib
Upadacitinib

73
Q

First, second, third and fourth line agents for AS?

A
  1. NSAIDs
  2. TNFi (after failure of NSAIDs) ( fusion protein vs monoclonal antibodies based on pt comorbidities)
  3. IL-17i ( alternative to TNFi or when TNFi are contraindicated after failure of NSAIDs)
  4. Janus Kinase inhibitors (only after TNFi or IL-17i have failed or are contraindicated)
74
Q

Drug selection based on axial vs peripheral disease?

A

Non biologic disease modifying agents such as MTx or Sulfasalazine have no efficacy in axial disease and limited efficacy in peripheral disease.

Treatment with Sulfasalazine is recommended primarily for pts with prominent peripheral arthritis and few or no axial symptoms and in these pts, it may be more effective than MTx.

75
Q

DOC for Scleroderma Renal Crisis?

A

Captopril (IV ACEi that can be rapidly titrated due to short half life)

BB may exacerbate Raynaud phenomenon and therefore be avoided in patients with Systemic Sclerosis.

76
Q

Which type of Scleroderma is associated with Renal Crisis?

A

Can occur in both Diffuse or Limited but more common in Diffuse disease.

77
Q

Risk factors for scleroderma renal crisis ?

A

Recent onset systemic sclerosis (<4 yrs)
Diffuse skin disease
Presence of anti- RNA polymerase III antibodies
Recent use of glucocorticoids

78
Q

Which type of antibodies in Systemic Sclerosis are aw increased risk of Scleroderma Renal Crisis?

A

Anti-RNA polymerase III antibodies

79
Q

Clinical presentation of SRC (Scleroderma Renal Crisis)?

A

Similar to HTN emergency: headache, encephalopathy, retinopathy, AKI and HF.

Labs: Anemia, TCP, proteinuria, evidence of MAHA- schistocytes on PBS.

80
Q

Disease modifying agents for SRC (Scleroderma Renal Crisis)

A

ACEi, regardless of serum creatinine levels.

Patient may need temporary dialysis, and kidney functions may improve during therapy for upto 24 months after presentation.

81
Q

Role of prophylactic ACEi to prevent SRC?

A

Prophylactic use of ACEi does NOT prevent SRC and may lead to poorer renal outcomes.

82
Q

BB are DOC In which types of HTN emergencies?

A

Eclampsia/Preeclampsia
ACS
Aortic dissection

83
Q

Glucocorticoid sparing agent of choice in GCA?

A

Tocilizumab ( can be administered during glucocorticoid tapering or as monotherapy following discontinuation of glucocorticoids)

Cyclophosphamide (used mainly in GPA), MTx, infliximab- not useful.

84
Q

Generally acceptable indications for a Glucocorticoid sparing agent?

A
  • Presence of comorbid diseases that are negatively affected by Glucocorticoids.
  • Development of glucocorticoid related adverse effects.
  • Prolonged need for treatment.

Rheumatology (1 decks)

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