CM Flashcards
(224 cards)
polymyalgia rheumatica (PMR)
who is it common in? what are the lab tests like? what is commonly associated with this disease? what do you use to treat this disease? how soon can people come off it?
>50, northern european ancestry 2:1 females
abrupt onset of intense morning stiffness of neck, shoulders and hip girdle but muscle strength is normal, fatigure and anorexia also common
elevated ESR >50 mm/hr and CRP
15% can get great cell arteritis/temporal arteritis
low dose steroids 10-20 mg only drug that works, looks to normalize the CRP and ESR
usually self limiting 65% taper of steroids 1 year, 85% in 2 years
what can people develop from Polymyalgia rheumatica (PMR) and what percent of people does this happen in?
giant cell arthritis/temporal areritis
15%
what should you do if the ESR and the CRP values for polymyalgia rheumatica (PMR) don’t normalize with steroid use?
rethink the diagnosis
Giant cell arteritis (GCA)
what age group is this common in and what other disease does this commonly present with? the release of which things cause this? 6 presentations? what can this damage? tests? treatments?
[giant head]
>50, often seen with PMR
involves the medium/large blood vessels of the head and neck including those that supply the optic nerve, involves release of IL1 and IL6
inflammatory cells get into the adventia of the temporal and other arteries and plug the flow
1. scalp tenderness
2. temporal headaches
3. jaw claudication
4. sudden loss of vision
5. bounding or absent temporal pulses
- rare subclavian bruits
higher ESR and CRP than PMR, anemia
high dose steroids 60mg, slowly tabler off 1-2 years, some require low dose chronically <10 mg
what are the four complications that can come from giant cell arteritis?
blindness
scalp necrosis
lingual infarction
aortic dissection/aneurysm
what are the four major complications seen with long term use of high dose steroids?
osteoporosis
cataracts
increased BS
weight gain
Granulomatosis with polyangitis (GWP)

what causes it? what are the 6 presentations? what do you worry about the most? what tests are important for this? what is the treatment and the new drug? where are these patients? what 3 systems do you worry about the most?
potentially fatal, involves small vessels, forms necrotizing granulomas in the upper airways, lungs, and kidneys, multisystem is key, very sick so in the hospital
the antineutrophil cytoplasmic antibodies C-ANCA attack the neutrophil and cause vascular injury and necrosis,
- eyes
- skin (palpable purpura)
- Upper airway ( ottis media, sinusitis, epitaxis, subglottic stenosis)
- kidney (nephrotic syndrome/failure)
- lung (hemmorage, lung failure)
- cardiac (pericarditis)
labs: elevated CRP, ESR, thrombocytosis, creatine, hematuria, casts, and proteinuria (all elevated)
treatment:
- High-dose steroids with cyclophosphamide
- methotrexate (chemo) or azathioprine (transplant drug)
- rituximab=anti CD20 drug targets B cells
what is the survival rate for giant cell arteritis after the invention of immunosuppressants?
90%
polyarteritis nodosa (PAN)
what causes this and what illness is it typically associated with? what are 6 possible presentations on the body? what are four complications we worry about? what is the treatment? what is the special test we do to diagnose this?
[no do web, need a plan B]
50s-60s, medium blood vessels, high adominal involvement, associated with HEP B
abdominal pain due to mesenteric ischemia, pain associated with meal consumption
myalgia
hypertension
skin: livdeo reticularis (lace like rash), palpable purpura, fingertip ulcerations, subcutantous nodules on palms
testicular pain
labs: increased ESR, CRP, increased transaminadases, decreased albumin, HEP B, proteinuria/hematuria without casts
mesenteric/renal angiography where you see beading instead of smooth tubes
treatment:
- high dose steroids with cyclophosphamide
- mexotrexate or azathioprine
- treat Hep B with antiviral acyclovir
- plasma exchange to remove immune complexes
see bowel perforation, renal failure, stroke to HTN, foot/wrist drop since complexes wipe out nerve
ESR inflammation test
what two things effect it? what other 3 factors will it increase in? How long does it take to see result?
sedimentation rate, rate at which RBC fall in a standarized tube in 1 hour
influenced by fibrinogen and immunoglobulins
increases with : age, women, adipose tissue
can take days to increase or decrease
high sed rate means falls faster
CRP inflammation test
synthesized by the liver in response to inflammation or infectious state, rises and falls quickly
what does it mean if the ESR and CRP are both elevated?
infection, inflammation, trauma, cancer
ESR is ELEVATED, CRP is NORMAL
what does this mean? 4 examples?
conditions with elevated immunoglobulins
SLE
myoloma
liver disease
sjogrens
rheumatoid factor test
what is this most commonly seen in? what 4 other diseases can produce a postivite test? what is important to keep in mind when doing this test?
IgM that is directed against IgG that is present in 80% of patients with RA
also seen in: Hep C, Sjogrens, TB, cryoclobulinemia
***may have a low positive result***so must use in relation to clinical picture
anti-CCP antibody
antibody against citrulline-containing peptides
more specific for RA than rheumatoid factor? (95%)
Antinuclear antibody (ANA)
who is it likely to produce a false positive in? percentage? Name 6 patterns
IgG against nuclear antigens
produces titer and pattern with immunofluoresence
higher the titer more clinical significance
false positives in 10-20% of females
diffuse/homogenous
periphreal
speckled
nucleolar
centromere
SCL-70
diffuse homogenous ANA pattern seen in…..
1
SLE
periphreal ANA pattern seen in …..
1
SLE
Speckled ANA patter seen in….
2
SLE, Sjogrens
nucleolar ANA pattern seen in…
1
scheloderma systemic disease
Centromere ANA pattern seen in…
1
CREST syndrome
SCL-70 ANA pattern seen in….
1
schleroderma systemic disease
Antineutrophil cytoplasmic antibody (ANCA)
what are the two types and what do they test for?
autoantibodies that recognize proteins in the neutrophil, associated with vasculitis
P-ANCA- myeloperoxidases (MPO), microscoptic polyangitis
C-ANCA- proteinase 3 (PR3), granulomatosis
fibromyalgia

what is it? how long do you need to have it? what are the requirements? what are the 4 presentations? what are the 4 important things you need to rule out? what testing is ok? which arent? what should you NOT treat with? what are 4 potential medical treatments?
central pain syndrome, pain threshold disorder >3 months 6:1 females
increased activity in somatosensory cortex, posterior insula, and thalamus
allodynia (percieved pain when non, hugging), hyperplasia (aplified pain perception)
aggrevated by stress, lack of sleep, activity
- widespread muskulo pain
- sleep disturbance
- no objective physical findings
-
11/18 trigger points
* important to test deep tendon reflexes and sensation*
testing proceed with caution: NEED TO RULE OUT CELIAC DISEASE, IBS, VIT D DEF, HYPOTHYROIDISM
DO NOT ORDER RA/ANA
can order thyroid, electrolytes, vit D, ESR/CRP, Hep C, CPK
Don’t treat with: NSAIDS, narcotics
Treat with: Tricylic antipressants (help sleep), selective serotonin reuptake inhibitors (SSRIs), dual acting, lyrica neurontin but SO many side effects





















































































