Rheumatologic conditions Flashcards

1
Q

Who does CFS primarily affect

A

F>M
average age: 29-35
occurs more frequently among minority populations and those with a lower social-economical status and education level are at a higher risk

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2
Q

what is the pathophysiology of CFS

A

unclear underling pathophysiology - diagnosis of exclusion

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3
Q

what is fatigue

A

described as weakness, tiredness and lethargy

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4
Q

what are the clinically concerning factors of fatigue

A

difficulty initiating activities
difficulty completing activities
memory and concentration difficulties

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5
Q

how is CFS diagnosed

A

with exclusion criteria - there are no objective physical exam findings.

requires 6 months of fatigue and all self reported symptoms

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6
Q

what are we ruling out when trying to determine CFS

A

ruling out medical or psychiatric conditions that might be causing fatigue

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7
Q

what is the treatment of choice for CFS

A

cognitive behavioral therapy and graded exercise

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8
Q

what is cognitive behavioral therapy (CBT)

A

psychotherapy technique aimed at changing throught/behavior

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9
Q

what is Graded exercise therapy (GET)

A

home exercise program to improve conditioning and exercise tolerance

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10
Q

what are alternative treatment options for CFS

A

remaining active, physically and socially.
treat any co-occurring anxiety or affective disorders (common)

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11
Q

what is typically unhelpful in CFS treatment

A

medications

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12
Q

What is the common patient presentation of fibromyalgia

A

affects 3-10% of the population
F>M
average age: 20-50

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13
Q

what is the pathophysiology of Fibromyalgia

A

underling pathophysiology unknown
? abnormal pain perception, ? related to sleep disorder, ? depression, ? viral infectious etiology

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14
Q

what is the typically fibromyalgia presentation

A

MSK pain and impairment in functioning

chronic, achy pain and stiffness that usually involves the neck, shoulder, low back and hips

associated with
fatigue, sleep disturbances, subjective numbness, headache, IBS

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15
Q

How many tigger pints to diagnose fibromyalgia

A

11 of the 18 trigger points PLUS widespread chronic pain

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16
Q

how is fibromyalgia diagnosed

A

symptoms for more than 3 months
there is no specific imaging or lab testing

rule out: amemia, thyroid abnormalities, electrolyte abnormalities

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17
Q

what are the 5 approaches to the treatment of fibromyalgia

A
  1. patient education
  2. non-pharmacologic options
  3. pharmacologic options
  4. treat any co-morbid conditions
  5. identify any available community resouces
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18
Q

what falls under patient education for fibromyalgia treatment

A

treatments can improve the symptoms, disease is not progressive, ID most distressing symptoms, Set treatment expectations (not complete relief of symptoms)

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19
Q

what falls under non-pharmacologic options for the treatment of fibromyalgia

A

mindfullness and meditation, exercise, sleep hygiene

managing their pain and function

20
Q

What are the pharmacologic options for treating fibromyalgia

A

amitriptyline for sleep, fatigue, and chronic pain
gabapentin/pregabalin for pain
muscle relaxants with one of the above for sleep and pain
tramadol and tylenol for pain

21
Q

what pharmacologic aids are unhelpful for fibromyalgia

A

NSAIDs and opioids

22
Q

What is polymyositis

A

chronic muscle inflammation and weakness

typically symmetric and proximal

23
Q

what is the typical patient presentation with polymyositis

A

F>M
average age: 50-60
african americans > caucasians

24
Q

what are patients diagnosed with polymyositis at an increased risk for

A

malignancy

25
Q

what is the typical presentation of polymyositis

A

progressive proximal muscle weakness that usually starts in the LE and moves to UE and neck

NO facial or ocular weakness but may include myocarditis, lung and joint involvement

26
Q

what can polymyositis be coupled with

A

a dermatomyositis - rash that is dusky red in color and commonly involves one or more of the following: face, upper chest, back, neck and shoulders

27
Q

what are other skin findings in dermatomyositis

A

heliotrope rash - periorbital edema and rash over eyelids
Gottron papules - raised violaceous lesions on extensor surfaces of DIP, PIP and MCP joints
Gotton sign - erythematous rash on the extensor surface of fingers, elbows and knees

28
Q

What is the most specific lab test for polymyositis

A

Creatinine kinase (CK) - elevated in all patients

29
Q

What is the gold standard for diagnosis of polymyositis

A

muscle biopsy - endomysial and perivascular inflammation

30
Q

What is the mainstay treatment for polymyositis

A

oral corticosteroids at a high dose (prednisone) and then taper down
if symptoms persist - MTX

hydroxychloroquine for the dermatomyositis rash and avoid the sun

31
Q

What is the patient population for polymyalgia rheumatica

A

disease of older adults - most common rheum disease diagnosed in older adults over 50
F>M
predilection for patients of scandinavian descent

32
Q

what is the pathophysiology of polymyalgia rheumatica

A

a vasculitis - inflammation of the vessel walls that predominately affects the medium sized vessels that is believed to be autoimmune

associated with HLA gene

33
Q

what is the presentation of PMR

A

muscular pain and stiffness that is typically present int he shoulder and pelvic girdle

NO MUSCLE WEAKNESS

often associated with fever, malaise and weight loss in the early presentation

34
Q

How is PMR diagnosed

A

primarily clinical and no imaging is necessary
labs can be supportive with elevated ESR, CPR and most patient have associated anemia

35
Q

how do we treat PMR

A

corticosteroids - low dose - should see affect within 72 hours - if not reconsider diagnosis

36
Q

What is giant cell arterities

A

also known as temporal arteritis
throught to be part of the same disease spectrum as PMR and is also a vasculitis but affects medium AND LARGE vessels

37
Q

What is associated with giant cell arterities

A

unclear association with varicella zoster antigen

38
Q

how does Giant cell arteritis present

A

headache, scalp tenderness, visual disturbances (amaurosis fugax), throat pain, JAW CLAUDICATION and associated fever

39
Q

what is Amaurosis fugax

A

sudden monocular vision loss, partial or complete
CURTAIN COMING DOWN - can lead to blindness

40
Q

What is the presentation of giant cell ateritis

A

temporal artery usually normal to palpation but nodular, enlarged, tender and pulseless

41
Q

what are patients with GCA at greater risk for

A

17x their risk of thoracic aortic aneurysm

42
Q

what is the gold standard for GCA

A

temporal artery biopsy

43
Q

how is GCA treated?

A

corticosteroids are first line (high dose)
but urgent biopsy necessary

if vision loss - IV methypred.

44
Q

What is the difference between Raynauds phenomenon and raynauds disease

A

raynauds phenomenon tends to be more severe and associated with CT diseases, unilateral (asymmetric), quicker progression, skin changes (ulcerations/gangrene), abnormal allens test

Raynauds disease is idiopathic and the more common form, symmetric bilaterally, slower progression, no skin changes, peripheral pulses present, negative allens test

45
Q

What is the progression of Raynauds

A

White, blue, red
Vasospasm - lack of blood flow (white)
lack of arterial flow - cyanosis (blue)
resolution of vasopasm and reprofusion - rebound hyperemia (Pink/red)

46
Q

What is the treatment for raynauds

A

lifestyle modifications
prevention of attacks, avoiding cold exposure, warm clothing, avoid smoking and vasoconstrictive drugs and injuries to your hands