Rheumatology w/Dr. Endo Flashcards

1
Q

`Normal ESR:

Elevation means?

A

ERYTHROCYTE SEDIMENTATION RATE =Rate at which RBCs settle out of soln in one hr

-In the presence of inflammation, serum [fibrinogen] increases making blood stickier and causing “Rouleaux” stacking, which clumps RBCs together and causes them to fall out of solution FASTER.

Thus stickier blood sediments FASTER than blood from a pt with no inflammation.

NML ESR INCREASES WITH AGE, Females nrmly higher:

ESR mm/hr = (Age + 10 if female ) / 2

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2
Q

Normal CRP?

Elevation means?

A

1

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3
Q

Ankylosing Spondylitis

A

Inflammation and fusing of the Axial Skelleton (Head, spine, ribs, sternum, ossicles, hyoid) though the disease is systemic. Sacroiliac inflammation often present

Onset 20-30 usually genetic

Dull low back pain and stiffness wakes pts in the early am. Progresses to loss of spinal ROM.

MRI + Xray show fusing of the spine and ribs

TNF-Alpha and IL1 are out of line

Hearing and vision complications possible. 40% have anterior eye chamber inflammation.

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4
Q

Max Tylenol/ day

Antidote?

A

3,000 mg daily max

Antidote is MUCOMYST (Acetadote)

W/I 4-8 hrs or up to 10 hrs after overdose

IV preferred, diluted in 5% Dextrose

Oral Available

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5
Q

Rheumatoid Factor / RF

A

RF is essentially an autoantibody to IgG

Found in Rheumatoid Arthritis but not at all stages, so it is possible to have RA but have a Negative RF. In that case, more studies would be ordered such as CCP (cyclic citrullinated peptide)

RF and IgG form immune complexes that are responsible for some of the symptoms of Rheumatoid Arthritis.

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6
Q

CCP/ Cyclic Citrullinated Peptide Antibody

A

CCP’s presence is + for inflammation

When + with RF, the dx is very likely RA and a severe, quickly progressing form thereof.

When + where RF is -, a milder form of RA or early RA is likely

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7
Q

Giant Cell Arteritis, what do you know about it?

Sxs
Greatest Risk
Dx
Rx

A

f

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8
Q

ADD SYNCOPE to your cardiac ROS

A

k

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9
Q

Methotrexate

For ?
Risky Effects?
How to manage Effects?

A

s

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10
Q

Bisphosphenates

  • How to take?’
  • Risks?
A

s

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11
Q

Steroid Side Effects/Risks?

A
    • Osteoporosis
    • Wt Gain d/t Lipid and Glucose Derangement
    • Striae
    • Aggression + Mood Issues
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12
Q

Anti Nuclear Antibody (ANA)

A
ANAs are AutoAntibodies.  
-- Present normally in small amounts
-- High ANA indicates Autoimmune dz or drug cause
    -Lupus
    -RA
    -
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13
Q

Osteoarthritis vs Rheumatoid

A

OSTEO

RHEUMO

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14
Q

Doxy for Rosacea? Why?

A

We don’t know. It just works and has been used since the 50s.

Its low dose Doxy (40mg/day: 30 immediate 10 extended release) is a tried and true Rosacea remedy, albeit with systemic effect especially on the gut.

All Tetras decrease inflammation by suppressing neutrophil migration and chemotaxis

Dr. Mead prefers not to use the Doxy and instead to use IVERMECTIN an oral anti parasitic agent more commonly used against SCABIES. The theory is that it works because Rosacea may be caused by tiny MITES in the pilosebacious glands. There is an Ivermectin 1% creme in the works.

For just reducing the redness of rosacea, we can turn to topicals made with alpha receptor agonists such as are found in eye drops (Brimonidine Tartrate) and nasal decongestant (Oxymetazoline).

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15
Q

Lupus Screen Test and what to do if it’s positive:

A

Screen is Anti Nuclear Antibody Test (ANA). 98%
of Lupus Pts will test (+) for ANAs. So will
up to 10 % of people in general. Likewise
Rheumatoid Arthritis and Scleroderma also
create ANAs. Additionally, this has a
50% false (+) rate so… if its negative, likely no
Lupus (or scleroderm or RA…) If it’s positive,
Though, TEST On…

                     -ANA PANEL is the next test, to ID 
                     which autoantibodies are present:

                           --Anti-double-stranded DNA- (+) in 30%
                                     of Lupus only in 1% gen pop.  
                                     High in Lupus Kidney Involvement
                           --Anti-Smith - The Sm antibody is 
                                      really exclusive to Lupus Pts.  It's 
                                      only present in 30% of them but it
                                      isn't found in the general popular.
                           --ATnti-U1RNP-Not specific to lupus; they        
                                    do mean there is a rheumatic 
                                    conditions : RA, systemic sclerosis, 
                                    Sjogren’s syndrome, polymyositis.
                           --Anti-Ro/SSA- This one can be (+) in 
                                    15% of the general population but
                                    most often in Cutaneous or 
                                    Neonatal Lupus and Sjogrens.  
                                    Neonatal Lupus causes congenital
                                    heart block so pregnant Lupus Pts
                                    get tested for these antibodies
                           --Anti-Histone - usually Drug Induced 
                                    Lupus but sometimes systemic
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16
Q

Tocilizumab/ Actemra

A

MAB targets Interleukine 6

Also used in combination with Methotrexate and other DMARDS

RA: Mild to Moderate

17
Q

Interleukine 6 (IL6)

A

Pro-Inflammatory Cytokine secreted by T-Cells and Macrophages AND…. Osteoblasts when they are triggering Osteoclast differentiation.

IL-6 stimulates the inflammatory and auto-immune processes in many diseases such as diabetes,[22] atherosclerosis,[23] depression,[24] Alzheimer’s Disease,[25] systemic lupus erythematosus,[26] multiple myeloma,[27] prostate cancer,[28] Behçet’s disease,[29] and rheumatoid arthritis.[30

18
Q

HUMIRA/ Adalimumab

A

targets TNF-Alpha

RA
Psoritic Arthritis and Plaque Psoriasis
Crohns
Juvenile Arthritis
Ulcerative Colitis
Anklyosing Spondyliits
19
Q

Xeljanz / TofactiNib

A

Tyrosine Kinase Inhibitor

Oral RA med

NIBs are

20
Q

Enbrel/ Etanercept

A

TNF Inhibitor

RA, 
Juv Arth, 
Psoritic Arth, 
Plaque Psoriasis
Ankylosing Spondylitis

Acts as decoy TNF Receptor and thereby hijacks TNF activity

TNF is secreted by Lymphocytes and Macrophages. It attracts WBCs namely Neutrophils to the site and kicks off the Inflammation cascade.

21
Q

Orencia/ Abatacept

A

Blocks T-Cells from being activated by Antigen Presenting Cells

22
Q

ReFlex Sympathetic Dystrophy’s aka Complex Regional Pain Syndromes I and II- what do you know about this

A

Reflex Sympathetic Dystrophy (fondly RSD) is the old name for Complex Regional Dystrophy.

RSD was a catch all for sympathetic dysfunction, usually in a limb, that did nor arise from DIRECT nerve damage.

Causalgia was the name for sympathetic dysfunction directly CAUSED by trauma to the nerve.

Sympathetic dysfunction presents as pain to the touch but also strange areas of no sweating and areas of vasodilation (Hot and Red) or constriction (Blue/White and cold).

Now we call it Complex Regional Pain Syndrome or CRPS
CRPS type I is without direct nerve trauma
CRPS type II results from direct nerve trauma

Meds for this are Gabapentin, Hydocodone and NSAIDS

23
Q

Nabumetone / Relafen

A

NSAID

Non-Acidic Cox 2 Blocker. It has lower risk of GI ulcer, Kidney damage and even lower risk of heart failure than did Celebrex (Celecoxib) the famously removed then reinstated COX-2 blocker.

24
Q

Mycophenolate

A

Anti-proliferative derived from fungus, hence “Myco”

Interferes in purine (guanine) synthesis and thereby slows down B + T cell proliferation. Literally suppresses immune cell production and thereby decreases all immune activity

25
Q

Azathiopine / Azasan/ Imuran

A

A full on Purine Synthesis inhibitor, blocks both Guanine and Adenine (whereas Orencia/Abatacept only blocks Guanine)

a STEROID SPARING agent, you use this (or Orencia/Abatacept) to suppress the immune system when trying to taper someone off steroids.

Thus preventing DNA synthesis and reducing cell proliferation IN GENERAL but especially in rapidly proliferating cells like blood cells. It reduces proliferation of B and T cells and that’s how it works to suppress the immune system but is suppresses ALL rapid cellular proliferation and so ANEMIA is likely as is FATIGUE

26
Q

Helper T Cells ( or Th cells) importance?

A

Helper T cells regulate and even suppress the activity of T-Cells.

If they are too active, T-Cells are overactive and autoimmune disorders arise.

If they are under active, as they are during immune suppressive treatments, then the body is susceptible to infection because the T-Cells are to some extent inactivated.

There are two main categories of Helper T Cells: Th1 and Th2.
- Th1 helper-Ts mainly activate Macrophages to phagocytize bacteria and protozoa. If Th1 cells are overactive, Type 1 Diabetes may result.

 -Th2 helper-Ts mainly activate eosinophils, basophils, and mast cells as well as B cells to attack extracellular PARASITES like helminths. It Th2 is over activated, allergies, asthma and atopic dermatitis result
27
Q

The symptom CONSTELLATION of Rheumatic Disorders

A
Uveitis
Inflammatory Bowel Disorders
      Crohns
      Ulcerative Colitis
      Enteritis (small bowel inflame)
Joint pain
Skin (plaque psoriasis)
Aortitis (rare, inflamm of the aorta)
28
Q

Compare Methotrexate to TNF-Alpha inhibitors like Enbrel and Humira as to time to effect and sxs reduction and halting disease progress in RA and Psoriasis

A

Methotrexate is the standby at around 10-12 mg/week. It is slow to reach effectiveness (8-12 weeks). It does relieve symptoms and it does slow the progression of RA and Psoriasis

29
Q

What the heck IS lupus anyway?

A

An Autoimmune disorder wherein the immune system attacks CONNECTIVE TISSUE.

CONNECTIVE TISSUE? Tendon, ligament, skin, cornea, cartilage, bone, blood vessels, gut, and intervertebral disc.. Also the scaffolding for organs, esp Liver and Bone Marrow.

Lupus patients are GENETICALLY SUSCEPTIBLE. This doesn’t mean they are genetically predestined to suffer actual Lupus but it does mean they are vulnerable to developing it in response to some sort of environmental or systemic trigger like an infection but this remains unclear.

Since Lupus involves developing autoantibodies and nuclear proteins are not usually out and about, when a Lupus Pt’s antibodies get a look at nuclear proteins from normal cell break down, they make more, lots more antibodies to those NUCLEAR proteins than would the average person. Thus the main Lupus Blood screen is for elevated antinuclear antibodies:
-Anti-Nuclear Antibody Screen (ANA). This one is NOT specific to Lupus, even 10% of well people make these. ALL Lupus patients have them though. So this is the first screen. If it’s positive, you must TEST ON…

ANA PANEL is the next test, to ID
which autoantibodies are present:

                           --Anti-double-stranded DNA- (+) in 30%
                                     of Lupus only in 1% gen pop.  
                                     High in Lupus Kidney Involvement
                           --Anti-Smith - The Sm antibody is 
                                      really exclusive to Lupus Pts.  It's 
                                      only present in 30% of them but it
                                      isn't found in the general popular.
                           --ATnti-U1RNP-Not specific to lupus; they        
                                    do mean there is a rheumatic 
                                    conditions : RA, systemic sclerosis, 
                                    Sjogren’s syndrome, polymyositis.
                           --Anti-Ro/SSA- This one can be (+) in 
                                    15% of the general population but
                                    most often in Cutaneous or 
                                    Neonatal Lupus and Sjogrens.  
                                    Neonatal Lupus causes congenital
                                    heart block so pregnant Lupus Pts
                                    get tested for these antibodies
                           --Anti-Histone - usually Drug Induced 
                                    Lupus but sometimes systemic
30
Q

Most common cancer in Rheumatoid Arthritics

A

Malignant Lymphoma

Makes sense. We’re suppressing the immune system so nobody is checking B-Cells at the gate to ensure they’re not whacked out.

Lymphoma is cancer of the lymph system, typically nodes.

Malignant simply refers to the ability of the cancer cells to metastasize. It’s more of a staging adjective than anything.

31
Q

Enthesopathy

A

Any disorder involving the attachment of a tendon or ligament to bone.

Enthesis = the site of attachment

Enthesitis= inflammation at the site of attachment

Tendonitis (obviously)
Adhesive Capsulitis of the Shouder
Plantar Fascitis
Bone Spurs
Tennis Elbow...
32
Q

MCP

A

MetaCarpoPhalangeal Joint

the “knuckle”

RA damages it such that fingers ulnar deviate

33
Q

PIP

A

Proximal InterPhalangeal Joint

Flexion makes a claw

RA also affects these joints classically

34
Q

DIP

A

Distal InterPhalangeal Joint

Not usually involved in RA unless PIP and MCP are both already involved.

If it’s just the PIPs think Osteoarthritis.

35
Q

Spondilitis=

Akylosis=

Ankylosing Spondylitis=

A

Spondilitis is inflammation of the spine

Ankylosis is fusing of the vertebrae

Fused spine caused by inflammation. This is an autoimmune condition and the inflammation is caused by autoimmune antibodies BUT…. Ankylosing Spondylitis is RH (-) meaning it is NOT technically Rheumatoid.

Instead HLA-B27 will be positive in Ankylosing Spondylitis. HLA-B27 is a protein on the membranes of Antigen Presenting Cells. 90% of AS patients are HLA-B27 positive but not everyone who is HLA-B27 positive gets AS…. thus additional genes must be involved in addition to the one that precipitates the presence of HLA-B27. Still, that’s the only one we have identified so that’s the one we look for

Diagnosing AS involves proving:
-That you are seronegative for RA factor
-That your sacrum and spine show fusing (on Xray)
-That you have INFLAMMATION (CRP likely high)
-That you are HLA-B27 positive (though 10% are negative)
-That you are ANA Negative (therefore its not Lupus…)
-That you have one of the non-spinal manifestations of
AS, essentially other signs of AutoImmune Disease:
-Uveitis/Iritis
-Crohns/Ulcerative Colitis
-Psoritic Arthritis/Psoriasis
-Enthesopathies - Disorder of tendon/ligament
attachment to bone, Most Commonly:
–Achilles Tendonitis
–Plantar Fascitis
–Adhesive Capsulitis of the shoulder