EMG chemotherapy, radiation, or resection

prednisone

Antibodies against cancer cells also function against presynaptic calcium channels. With repetitive use these antibodies are overcome.

Affects muscles that are used the least (the proximal muscles)

Acetylcholine receptor antibodies block the function of acetylcholine on nerve contraction.

Muscles you use the most fatigue first (Eyes, Throat) and worsen with repetitive motion.

Neuro [WEAKNESS]

autoimmune disease ascending paralysis

distally moving proximally diarrhea

flu vaccinations

hyporeflexia paresthesia autonomic dysregulation

intubation

LP lots

of proteins very few cells EMG

Nerve Conduction Velocity

IVIG plasmapheresis NEVER

autoimmune etiology myelin demyelinating disease

neurologic symptoms separated by time and space

blurry vision diplopia optic

neuritis MRI periventricular

plaques multiple lesions, corpus callosum relapsing-remitting

LP pleocytosis oligoclonal IgG evoked potentials

chronic management Interferon-B1b acute flares steroids

symptomatic relief

Bethanechol Amitriptyline

Baclofen

History Associated Sxs Repeated Diagnosis Tx Path

Rheumatology [APPROACH TO JOINT PAIN]

Differential Diagnosis

Rheumatology is essentially the diagnosis and management of joint pain. It has quite an extensive differential as it could be the primary complaint or the symptomatology that links all disease.

Unfortunately, many of these diseases have a list of associated symptoms that have be memorized in order to ascertain the correct diagnosis. However, there are some classifications that can help reduce the potential list of diagnoses. The number of joints, pattern, and symmetry of joint pain play a huge role.

Usually monoarticular involvement has to do with a disease of that joint, indicating an absence of systemic involvement. It’s often acute. Polyarticular involvement is associated with systemic disease. Let’s break it down further. In polyarticular disease absence of symmetry means it’s likely degenerative as it reflects the asymmetry of use. If there’s symmetry it indicates autoimmune. Finally, even paying attention to WHICH joint is involved can be useful (RA spares the DIP for example). Besides that, extrarticular manifestations are often unique to a given diagnosis, though crossover does exist. The important thing is that no one finding is sensitive or specific – it’s the combination of symptoms that lets the diagnosis comes to light. Using this algorithm may be useful, but it’s the memorization that excels in rheumatology.

Arthrocentesis

If you see a red, hot, swollen joint, the answer on the test will be Arthrocentesis. The diagnosis can be made without an arthocentesis (history of gout that has a gouty flare), but your reflex should be to tap the joint. In a normal joint there should be a bunch of fluid - that’s it. In degenerative disease it’s the same; the joint is just degraded (neither normal joint or degenerative joint conditions should have prompted a tap). On the other end of the spectrum, a septic joint will be full of pus: white, opaque, LOTS of cells, LOTS of polys. 50,000 is the number to remember. If there are more than 50,000 WBCs it’s septic, regardless.

An inflammatory joint will be somewhere in between; it’ll have some cloudy fluid, some cells, and mostly polys.

The presence of staph tells you septic. If septic and no organism, be cautious of gonorrhea and get a NAAT or chocolate agar culture.

The presence of crystals clues us in on crystal disease.

Inflammatory joint without organisms or crystals means “it’s a rheumatologic disorder” and little else.

Antibodies

Memorize them. There’s no good way other than repetition.

Sorry. They’re mostly non-diagnostic, but they’re another clue.

Bottom line: there isn’t one test, but rather a combination of findings (including serology) that leads to diagnosis.

Single Joint vs Multiple Joints Septic

Crystal, Reactive Osteo, Lupus, Rheumatoid, Scleroderma, Myositis, Seronegatives

Isolated vs Systemic Manifestations Septic

Crystal

Seronegative (IBD)

Lupus (Face, CNS, Renal, Heart, Lung) Rheumatoid (Nodules, Serositis) Reactive (Oral + Genital Ulcer) Degenerative vs Inflammatory

Osteoarthritis Everything Else

Normal NonInflammatory Inflammatory Sepsis

Appearance Clear Clear Yellow, White Opaque

WBC <2 <2 >2, <50 >50

Polys <25% <25% > 50% > 75%

Gram/Cx

Dz None Osteoarthritis Everything

Else

Infectio n WBC is “thousands”

Antibody Interpretation Antibody Interpretation

ANA Sensitive Lupus RO + LA Sjogren’s

Histone Specific

Drug-Induced Lupus CCP Rheumatoid

Arthritis ds-DNA Specific Lupus +

Renal Involvement RF Rheumatoid

Arthritis

Mitochondrial Primary Biliary Cirrhosis Centromere Scleroderma

(CREST)

Indolent Infection Lupus

Rheumatoid Arthritis Seronegative

“Connective Tissue Dz”

acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia.[1] It is associated with detectable antibodies against centromeres (a component of the cell nucleus), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma).

Rheumatology [LUPUS]

Introduction

Lupus is an autoimmune disease mitigated by complement forming complexes. Being autoimmune, it effects women more than men and non-whites more than whites. It is one of the great imitators and can be challenging to make the diagnosis in the early stages.

Presentation (and diagnosis)

There’s no confirmatory step or biopsy that seals the diagnosis of lupus. Instead, the diagnosis is made with 4 of 11 criteria being met. These 11 criteria can be recalled with either the mnemonic MD SOAP BRAIN or via the hideous monster. See both to the right.

The things the patient will care about are going to be the serositis (chest pain), arthritis (with a predilection for the large joints), and the face rashes (malar = butterfly, discoid = disk shaped) or the skin rashes (photosensitivity).

The things that you’ll care about are the cerebritis (encephalopathy, psychosis, obtundation), lupus nephritis (progressive renal failure), and potentially pulmonary hemorrhage.

Certain things just jump out on a test. Libman-Sacks-Endocarditis (LSE) is essentially pathognomonic for Systemic Lupus Erythematosus (SLE). The malar rash that spares the nasolabial fold and early trimester losses are also suspicious for lupus.

Testing (notice this isn’t called “diagnosis”)

There is no confirmatory step. But certain lab tests can be useful.

The CRP (better than ESR) reflects the disease severity. The ANA is the gateway antibody – it is highly sensitive but specific for nothing. If positive, look for other antibodies: particularly the anti-histone (drug-induced lupus), anti-smith (lupus), and ds-DNA (nephritis).

If the patient is in an acute flare (which may appear septic with fever), obtain complement levels. If reduced, it’s likely to be a flare rather than an infection. Unlike some other autoimmune diseases such as Multiple Sclerosis, lupus doesn’t worsen in infection – it may simply be a flare.

Anemia and thrombocytopenia can be seen but are neither sensitive nor specific.

If lupus nephritis is suspected a renal biopsy is required before treatment.