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IM Rotation 2018 > Ortho/Rheum > Flashcards

Ortho/Rheum Flashcards

1
Q

A patient is complaining of widespread muscular pain, fatigue, muscle tenderness, headaches, poor sleep and poor memory problems. The patient states she has felt like this for 6 months. Muscle biopsy reveals “moth-eaten” appearance of the type I muscle fibers. What else is needed for the diagnosis of fibromyalgia?

A

Diffuse pain in 11 out of 18 trigger points > 3 months + widespread pain

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2
Q

A patient is complaining of widespread muscular pain, fatigue, muscle tenderness, headaches, poor sleep and poor memory problems. The patient states she has felt like this for 6 months. Muscle biopsy reveals “moth-eaten” appearance of the type I muscle fibers. What is the management of this patient?

A

Exercise (swimming preferred; has a relaxing effect of water on the muscles)

Medical:
TCAs**
Pregabalin FDA approved** 
Duloxetine (SNRI) 
SSRIs
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3
Q

What is thought to be the etiology of Fibromyalgia?

A

May be an increase in pain perception

Increased Substance P*

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4
Q

How do you diagnose Sjogren’s syndrome?

A

ANA especially AntiSS-A (Ro) & AntiSS-B (La)

+ RF
+Schirmer Test (decreased tear production)

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5
Q

What is Sjogren’s syndrome?

A

An autoimmune disorder that attacks EXOcrine glands*:

Salivary glands –> xerostomia (dry mouth)
Lacrimal glands –> keratoconjunctivitis sicca)
Parotid enlargement*

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6
Q

What is the management of Sjogren’s syndrome?

A

Artificial tears and Pilocarpine for xerostomia

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7
Q

What is the MOA of Pilocarpine?

A

Cholinergic drug that increases lacrimation & salivation

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8
Q

What are the side effects of Pilocarpine?

A

SLUDD-C

Salivation
Lacrimation
Urination
Defecation
Digestion
Constriction
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9
Q

What is the MOA of Cevimeline?

A

Stimulates muscarinic cholinergic receptors

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10
Q

Sjogren’s syndrome patients have an increase incidence of what condition?

A

Increase incidence of non-Hodgkin lymphoma*, interstitial nephritis, and pneumonitis

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11
Q

What type of Sjogren’s syndrome is associated with other autoimmune disorders such as: SLE, RA…etc.?

A

Secondary Sjogren’s syndrome

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12
Q

What type of Sjogren’s syndrome occurs alone?

A

Primary Sjogren’s syndrome

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13
Q

What is the management for Polymyalgia rheumatica?

A

Low dose corticosteroids (10-20 mg/day)

NSAIDS
Methotrexate

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14
Q

A patient is having bilateral proximal joint aching and stiffness, particularly in the morning. The patient says the stiffness lasts greater than 30 min. She states that her pelvic, neck and shoulder girdle. The patient says she does not notice any muscle weakness. How is this condition diagnosed?

A

Clinical dx

Increased ESR
Anemia (normochromic, normocytic)

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15
Q

What condition is Polymyalgia rheumatica related to?

A

Giant Cell Arteritis

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16
Q

What is Polymyalgia rheumatica?

A

Idiopathic inflammatory condition causing synovitis, bursitis, and tenosynovitis leading to pain/stiffness of the PROXIMAL joints (shoulder, hip, neck) in patients >50*

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17
Q

What age group does Polymyalgia rheumatica affect?

A

> 50 years

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18
Q

What is Scleroderma (Systemic sclerosis)?

A

A systemic connective tissue disorder: thickened skin (sclerodactyly) of the lung, heart, kidney, & GI tract

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19
Q

A patient is seen with tight, shiny, thickened skin of the trunk and proximal extremities. Based on this, what is the most likely diagnosis?

A

DIFFUSE cutaneous systemic sclerosis

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20
Q

A 17-year-old patient is seen with tricolor changes of his fingers, toes, ears, nose, and tongue that he states worsens with cold weather or when he is stressed or smoking. During PE you notice his face, neck, distal elbows and knees are also affected. Based on this, what is the most likely diagnosis?

A

Raynaud’s phenomenon

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21
Q

A 17-year-old patient is seen with tricolor changes of his fingers, toes, ears, nose, and tongue that he states worsens with cold weather or when he is stressed or smoking. During PE you notice his face, neck, distal elbows and knees are also affected. What is the best treatment for this patient?

A

Vasodilators:
CCB are TOC*
Prostacyclin

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22
Q

A 17-year-old patient is seen with tricolor changes of his fingers, toes, ears, nose, and tongue that he states worsens with cold weather or when he is stressed or smoking. During PE you notice his face, neck, distal elbows and knees are also affected. You also notice Cutaneous cutis, telangiectactasia, and sclerodactyly (claw hand). Based on this information, what is the best way to diagnose this patient?

A

+ Anti-Centromere Ab* = associated with Limited/Crest dz

  • More specific
  • Better prognosis
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23
Q

A patient is seen with tight, shiny, thickened skin of the trunk and proximal extremities. Based on this, what is the best way to diagnose this patient?

A

+ Anti-Scl-70 Ab = associated with Diffuse & multi-organ involvement

+ ANA (non-specific)

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24
Q

How is Scleroderma (Systemic sclerosis) managed?

A

Acute management: DMARDs or Corticosteroids

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25
Q

What is Systemic Lupus Erythematosus?

A

Chronic systemic, multi-organ autoimmune disorder of connective tissures

Type III HSN (hypersensitivity)

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26
Q

What populations are at higher risk for developing SLE?

A
  1. Young females 9:1
  2. Onset in 20-40s
  3. AA
  4. Hispanic
  5. Native American
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27
Q

What environmental factors contribute to a patient developing SLE?

A
  1. Genetic
  2. Sun exposure
  3. Infections
  4. Hormonal (Estrogen)
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28
Q

What drugs potentiate SLE?

A
  1. Procainamide
  2. Hydralazine
  3. INH
  4. Quinidine
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29
Q

What type of SLE is + for Anti-Histone antibodies?

A

Drug-induced

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30
Q

What is the “triad” of SLE?

A
  1. Joint pain
  2. Fever
  3. Malar “butterfly” rash (spares the nasolabial fold)
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31
Q

What cardiac complications do patients with SLE acquire?

A

Serositis: pericarditis or pleuritis

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32
Q

A patient is seen with annular, erythematous patches on face and scalp that the patient reports heal with scarring. Based on this information, what is the most likely diagnosis?

A

Discoid lupus

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33
Q

What systemic affects does SLE have?

A
  1. CNS
  2. Cardiovascular
  3. Glomerulonephritis
  4. Retinitis
  5. Oral ulcers
  6. Alopecia*
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34
Q

What is the best initial test for SLE?

A

+ Anti-nuclear Ab: ANA

+ RF

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35
Q

Which test is 100% specific for SLE?

A

+ Anti-double-stranded DNA

+ Anti-Smith Ab

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36
Q

A patient is diagnosed with SLE and Anti-phospholipid Ab syndrome. What are they at higher risk for?

A

Arterial & venous thrombosis

37
Q

How do you manage a patient with SLE?

A

Skin:

  1. Sun protection
  2. Lesions = hydroxychloroquine

Arthritis:

  1. NSAIDS
  2. Acetaminophen

+/- Pulse corticosteroids; methotrexate; cyclophosphamide

38
Q

What is Polyarthritis Nodosa (PAN)?

A

Systemic vasculitis of medium/small arteries that leads to necrotizing inflammatory lesions

Type III HSN

39
Q

Which Rheumatologic disorder has an increased association with Hepatitis B?

A

Polyarteritis Nodosa

40
Q

How do you manage Polyarteritis Nodosa?

A

Corticosteroids

41
Q

How do you manage refractory Polyarteritis Nodosa?

A

Corticosteroids

+/- Cyclophosamide

42
Q

How do you manage Polyarteritis Nodosa if the patient is HBV + ?

A

Corticosteroids

+/- Plasmaphoresis

43
Q

A 45 y/o male patient is complaining of fever, myalgia, arthritis, neuropathy and ulcers. On PE, you notice livedo reticularis. Vital signs reveal HTN. Patient denies any dyspnea or chest pain. Biopsy reveals necrotizing inflammatory lesions, but no granulomas. Based on this, what is the most likely diagnosis?

A

Polyarteritis Nodosa

44
Q

A 45 y/o male patient is complaining of fever, myalgia, arthritis, neuropathy and ulcers. On PE, you notice livedo reticularis. Vital signs reveal HTN. Patient denies any dyspnea or chest pain. Biopsy reveals necrotizing inflammatory lesions, but no granulomas. Based on this, what is the best way to diagnose this patient?

A

Tests:

  1. Increased ESR
  2. Angiography/ Renal/ Mesenteric: micro aneurysms with abrupt cut off of small arteries
  3. Classic PAN is ANCA Negative

History:

  1. Age: 45
  2. Gender
45
Q

What is Reactive Arthritis?

A

Autoimmune response to an infection in another part of the body

46
Q

What population does Reactive Arthritis typically affect?

A
  1. 20-40s

2. Males

47
Q

What is the most common etiology of Reactive Arthritis?

A

1-4 weeks post Chlamydia***

Gonorrhea
GI infections: Salmonella, Shigella, Campylobacter, Yersinia

48
Q

What is the triad for the Clinical Manifestation of Reactive Arthritis?

A
  1. Arthritis (asymmetric inflammation; esp lower extremities) “sausage toes/fingers”
  2. Conjunctivitis
  3. Urethritis
49
Q

What is Keratoderma blennorrhagicum?

A

Associated with Reactive Arthritis

= hyperkeratotic lesions on palms/soles

50
Q

A patient with arthritis in his knees and ankles, conjunctivitis and urethritis is suspected of Reactive Arthritis. What is the best way to diagnose this patient?

A
    • HLA-B27
  2. CBC:
    WBC 10-20K
    Increased ESR
    Normochromic anemia
    Increased IgG
  3. Synovial fluid:
    WBC 1-8K cells/m3
    Fluid is bacterial culture negative = Aseptic
51
Q

A patient with arthritis in his knees and ankles, conjunctivitis and urethritis is suspected of Reactive Arthritis. What is the best way to manage this patient?

A

NSAIDS are the mainstay of tx

52
Q

A patient with arthritis in his knees and ankles, conjunctivitis and urethritis is suspected of Reactive Arthritis. What is the best way to manage this patient? The patient is having no response to normal NSAID tx?

A

Methotrexate
Sulfasalazine
Steroids
Anti-TNF agents: Etanercept, Infliximab

53
Q

What is Polymyositis?

A

Idiopathic inflammatory muscle disease of proximal limbs, neck, pharynx

-May affect heart, lungs, and GI

54
Q

How does Clinical Manifestation of Polymyositis?

A

Progressive symmetrical proximal muscle weakness*
Usually painless
Dysphagia
Skin rash
Polyarthritis
Muscle atrophy (difficulty rising from chair/climbing stair, combing hair; problems with overhead movements)

55
Q

A patient is complaining of dysphagia, skin rash, polyarthritis, and difficulty rising from chair and climbing stairs and combing his hair. What is the best way to diagnose this patient’s condition?

A

Increase muscle enzymes (increased aldolase; creatinine kinase)
Increased ESR
Abnormal EMG
+Anti-Jo 1 Ab: myositis specific antibody
+ Anti-ARP Ab
Muscle biopsy: endomysial involvement

56
Q

A patient is complaining of dysphagia, skin rash, polyarthritis, and difficulty rising from chair and climbing stairs and combing his hair. What is the best way to manage this patient?

A

1st line: high dose corticosteroids

+/- Methotrexate
Azathioprine
IV immunoglobulin

57
Q

What is the best initial test to help diagnose RA?

A

+ RF

58
Q

What test is more specific for helping to diagnose RA?

A

+ Anti-cyclic citrullinated peptide antibodies

59
Q

What is RA?

A

Chronic inflammatory disease with persistent SYMMETRIC polyarthritis
bone erosion
cartilage destruction
joint structure loss (due to destruction by pannus)

**T cell mediated

60
Q

What population is at increased risk for RA?

A
  1. Females

2. Smokers

61
Q

What is pannus?

A

granulation tissue that erodes into cartilage and bone

62
Q

How would a patient experiencing the prodrome of RA be feeling?

A 
Systemic sxs: 
Fever
Fatigue 
Weight loss
Anorexia 
Decreased ROM
63
Q

What are Classic RA manifestations?

A
  1. Small joint stiffness: MCP, wrist, PIP, knee, MTP, shoulder, ankle)
  2. Worse with rest
  3. Morning joint stiffness >60 min after initiating movement, improves later in the day
  4. symmetric, swollen, tender “boggy” joint
64
Q

Which of the following are you more likely to see in an RA patient?

A. Heberden’s node + Bouchard’s node
B. Swan neck deformity + Boutonniere deformity

A

B. Swan neck deformity + Boutonniere deformity = RA

A. Heberden’s node + Bouchard’s node = OA

65
Q

Which of the following are you more likely to see in an RA patient?

A. Ulnar deviation at MCP joint
B. PIP Osteophytes
C. Radial deviation at MCP joint
D. DIP Osteophytes

A

A. Ulnar deviation at MCP joint

66
Q

What is a PIP Osteophyte?

A

Bouchard’s node

67
Q

What is the Felty’s syndrome and which Rheumatologic condition is t associated with?

A

Associated with RA

-Rare: Triad of:
1. RA
2. Splenomegaly
3. Decreased WBC/repeated infections
-

68
Q

What is the Caplan syndrome and which Rheumatologic condition is t associated with?

A

Pneumoconiosis + RA

69
Q

What X-ray finding is consistent with RA?

A
  1. Narrowed joint space (Osteopenia/erosions) ***
  2. Subluxation
  3. Deformities
  4. Ulnar deviation of the hand
70
Q

What is the management of an RA patient?

A

PROMPT initiation of DMARDs (Methotrexate)
NSAIDs are 1st line for PAIN control
Steroids are 2nd line if no relief with NSAIDs

71
Q

What is the benefit of treating an RA patient with DMARDs?

A

They reduce permanent joint damage

72
Q

If a patient is having arthritis in > or = to 3 joints for more than 6 weeks; and the patient is complaining of morning stiffness, what is the most likely diagnosis?

A

RA

73
Q

What is OA?

A

Chronic disease due to articular cartilage damage and degeneration

74
Q

What is significant risk factor for OA?

A

Obesity

75
Q

Where does OA most affect the body?

A

Weight bearing joints

  • hips
  • knees
  • cervical/lumbar spine
76
Q

A patient is complaining of evening joint stiffness that gets better with rest. The patient states the pain gets worse throughout the day and with changes in the weather. On PE, you notice hard body joints and no obvious signs of inflammation. X ray findings reveal joint space loss and osteophytes. What is the most likely diagnosis?

A

OA

77
Q

A patient is complaining of evening joint stiffness that gets better with rest. The patient states the pain gets worse throughout the day and with changes in the weather. On PE, you notice hard body joints and no obvious signs of inflammation. X ray findings reveal joint space loss and osteophytes. What is the best way to manage this patient?

A

Acetaminophen preferred initial tx* in elderly with bleeding risk & mild-moderate disease

NSAIDs are more effective

78
Q

What population is at higher risk for Calcium pyrophosphate dehydrate deposition disease?

A
  1. Elderly >60

2. Females

79
Q

What is the acute form of Calcium pyrophosphate dehydrate deposition disease?

A

Acute = Pseudogout (acute arthritis)

red, swollen, tender joint

80
Q

A patient is coming in for an acute flare up of her Calcium pyrophosphate dehydrate deposition disease, what part of the body is most likely affected?

A

Knee

81
Q

A patient is coming in to follow up on her Chondrocalincosis. What would her X ray likely resemble?

A

Cartilage calcification*

Linear radio densities

82
Q

A patient is coming in for a follow up of her chronic Calcium pyrophosphate dehydrate deposition disease, what other rheumatologic condition does this likely resemble?

A

RA / inflammatory arthritis

83
Q

What does OA + Calcium pyrophosphate dehydrate deposition disease resemble?

A

Osteoarthritis

84
Q

A patient is seen with a red, swollen, tender knee. History is indicative of Calcium pyrophosphate dehydrate deposition disease. How would you diagnose this patient?

A

Arthrocentesis: positively birefringent, rhomboid-shaped CPPD crystals (pseudo gout)

85
Q

A patient is seen with a red, swollen, tender knee. History is indicative of Calcium pyrophosphate dehydrate deposition disease. Arthrocentesis reveals positively birefringent, rhomboid-shaped crystals. How do you manage this patient?

A

Pseudo gout: Intra-articular corticosteroids 1st line
NSAIDs
Colchicine (acute or for prophylaxis)

86
Q

A patient is coming in for a follow up of her chronic Calcium pyrophosphate dehydrate deposition disease. Initially, the patient did not have any symptoms, so no treatment was needed. Now, the patient has become symptomatic. PE and Hx are negative for an acute flare up. What do you offer her for her chronic CPPD?

A

Start off with NSAIDs,Colchicine,

and if no response, low dose steroids

87
Q

A patient is coming in for a follow up of her chronic Calcium pyrophosphate dehydrate deposition disease. Initially, the patient has been using NSAIDs and Colchine, but now she states they are not working for her. What do you offer her for her chronic refractory CPPD?

A

Start off with NSAIDs, Colchicine (as the patient did)

and IF NO RESPONSE: low dose steroids

88
Q

A patient has CPPD that is resembling OA. How do you manage this patient?

A

Pseudo-OA: treat like OA (Acetaminophen is preferred 1st line)

IM Rotation 2018 (5 decks)

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