Waldman Pain Review Chapters 181-214

Front 1

Give a brief description of workup and empiric treatment of vulvodynia

Back 1

MRI of the pelvis and lumbar spine to rule out malignancy, lumbar radic, abnormality of the plexus, etc. Urinalysis and culture, STD testing including herpes. If all these ruled out, consider COX2 inhibitors, empiric doxycycline 100mg po BID x14 days, TCA or gabapentin, and eventually caudal ESI. Many need psych eval.

Front 2

Describe the symptoms of proctalgia fugax

Back 2

Intermittent pain of the rectum often associated with depression, more common in women. Sometimes made better with insertion of something in the rectum.

Front 3

What is the typical workup for proctalgia fugax?

Back 3

MRI pelvis, colonoscopy, hemeoccult, O and P (not mentioned but I think this would be beneficial). Essentially, rule out neoplastic, infectious, and anatomic pathology. May need psych eval.

Front 4

Differentiate the symptoms of proctodynia and proctalgia fugax

Back 4

proctodynia is dull and constant. Proctalgia fugax is more severe and intermittent.

Front 5

What is thought to be the etiology of proctalgia fugax?

Back 5

It is also known as levator ani syndrome or a disorder of the internal anal sphincter. It is characterized by spasms of the levator ani muscle. There may also be a dysfunction of the pudendal nerve

Front 6

What are some treatments of proctalgia fugax?

Back 6

botox of the levator ani or internal anal sphincter, calcium channel blockers, pudendal nerve block. Hyosciamine (levo-atropine, an antimuscarinic anticholinergic) lozenge under the tongue at night, warm baths, low dose benzodiazepine at night, drotaverine (phosphodiasterase 4 antispasmodic) as a breakthrough.

Front 7

What are common radiographic findings and symptoms of osteitis pubis? What is its typical etiology?

Back 7

Waddling gait, groin pain radiating to the thighs, tenderness over the pubis.

Radiographically, there are erosions and sclerosis of the pubis, particularly around the symphysis.

The typical etiology is hematogenous spread of infection following bladder, inguinal, or prostate surgery.

Front 8

What is the treatment of osteitis pubis?

Back 8

NSAIDs, PT, topicals, local injection

Front 9

What is the innervation of the piriformis muscle?

Back 9

The sacral plexus (nerve to the piriformis, L5-S2)

Front 10

What is the "double crush" syndrome in the context of piriformis syndrome?

Back 10

Concomitant piriformis syndrome and lumbar radiculopathy.

Front 11

What is the one most common cause of chronic hip joint pain?

What are the two second most common causes of chronic hip joint pain?

What are the four lesser common causes of chronic hip joint pain?

Back 11

Osteoarthritis

1) Rheumatoid arthritis

2) Post-traumatic arthritis

1) Lyme disease

2) Villonodular arthritis

3) Collagen vascular diseases (usually a polyarthropathy)

4) Infection

Front 12

What injury and what systemic illness predispose to Baker's cysts?

Back 12

Injury: tear of the medial meniscus or tendinitis of the medial hamstring.

Systemic: rheumatoid arthritis

Front 13

Where is the location of the suprapatellar bursa?

Back 13

Beneath the patella, extending superiorly to the undersurface of the quadriceps

Front 14

What holds the suprapatellar bursa in place?

Back 14

A small portion of the vastus intermedius called the articularis genus muscle.

Front 15

What is the old, colloquial name for prepatellar bursitis?

Back 15

"Housemaid's knee"

Front 16

Describe the locations of the infrapatellar bursae.

Back 16

The superficial infrapatellar bursa sits between the patellar ligament and the subcutaneous tissue.

The deep infrapatellar bursa sits between the patellar ligament and the tibia.

Front 17

If the medial knee has been subjected to trauma, the pes anserine bursa and what other non-bony structure are often injured?

Back 17

the medial collateral ligament.

Front 18

What is the etiology of anterior tarsal tunnel syndrome?

Back 18

Compression of the deep peroneal nerve by the superficial fascia of the ankle.

Front 19

What is the etiology of posterior tarsal tunnel syndrome?

Back 19

Entrapment of the tibial nerve at the flexor retinaculum and the lacunata ligament.

Front 20

Where are the two places along the Achilles tendon where tendonitis is most common?

Back 20

At the site of insertion to the calcaneus and five centimeters proximally, where the tendon is the thinnest.

Front 21

Where are callouses most common with metatarsalgia?

How can you differentiate these from plantar warts?

Back 21

second and third metatarsal heads.

when the callus is trimmed, it should not have thrombosed blood vessels as plantar warts do.

Front 22

How do you distinguish sesmoiditis from metatarsalgia on physical exam?

Back 22

The pain of metatarsalgia is centered over the metatarsal heads and does not move with foot/digit flexion.

Front 23

What is the prevalence of plantar fasciitis between men and women?

Back 23

twice as common in women

Front 24

What is the main difference between CRPS types one and two?

Back 24

Type one has no appreciable nerve damage. Type two does.

Front 25

Describe bone scan findings with CRPS

Back 25

homogenous unilateral hyperperfusion in the affected part at 30 seconds post injection during perfusion phase and at 2 minutes during the blood pool phase. At three hours post injection, there is unilateral periarticular isotope uptake.

Front 26

What is the most common connective tissue disorder?

Back 26

Rheumatoid arthritis

Front 27

List the American College of Rheumatology's classification criteria for RA

Back 27

4/7 must be present. 1-4 must last at least six weeks.

1) Morning stiffness for at least an hour

2) arthritis of 3 or more of the following: PIP, MCP, wrist, elbow, knee, ankle, MTP

3) Arthritis of the wrist, MCP, PIP

4) Symmetric joint involvement

5) rheumatoid nodules. Usually over bony prominences, extensor surfaces, juxta-articular regions

6) Positive RF

7) Radiographic changes including erosions or bony decalcification of the involved joints.

Front 28

Which way do the fingers drift with RA?

Back 28

Ulnar drift

Front 29

What cells make rheumatoid factor?

What does RF bind to?

What types of cells does RF beckon?

Back 29

plasma cells

An IgG (an antibody to an antibody). RF is usually an IgM, but can be any type of the antibody class (IgG, IgM, IgA, IgE, IgD).

T-helpers and macrophages

Front 30

What does the CBC look like with somebody with RA?

Back 30

1) Erythrocytes: mild normocytic, normochromic anemia, with hemoglobin typically above 10 g/dL.

2) There is usually not neutropenia except in Felty syndrome, which is RA with splenomegaly.

3) Mild thrombocytosis

Front 31

What does synovial fluid analysis look like with those with RF?

Back 31

leukocytosis with predominantly PMNs. Decreased viscosity. Increased proteins. No crystals.

Front 32

What are typical early radiographic findings of RA?

Back 32

Ulnar drift, soft tissue changes indicating synovitis, second and third MCP joints.

Front 33

What are the boutonniere and swan neck deformities?

Back 33

Boutonniere deformity: the PIP is flexed and DIP is extended. From the PIP slipping through the extensor tendons like a button.

Swan neck deformity: occurs through a variety of reasons. All tend to have some damage to the PIP volar plate with damage to the insertion of the extensor tendons at the distal phalanx.

Front 34

Distinguish where OA tends to affect first versus RA.

Back 34

OA: first MCP, Heberden's and Bouchard's (DIP, PIP), knee, shoulder spine.

RA: wrist, 2nd or 3rd MCP, PIP (rarely DIP)

Front 35

What disease-modifying drug is becoming first line treatment for RA?

What must be supplemented with this medication?

What labs must be monitored closely?

Back 35

methotrexate. Folic acid. LFTs.

Front 36

What TNF-alpha blocking drugs are now frequently given as stand alones or in combination (sometimes with methotrexate) for RA?

Back 36

entanercept (SQ twice weekly) and infliximab (IV infusion).

Front 37

What is the second most common collagen vascular disease?

Back 37

systemic lupus erythematosis

Front 38

What percentage of people with SLE have polyarthralgias? How destructive do these tend to be in comparison to RA?

Back 38

90%. Less destructive.

Front 39

What is Jaccoud's arthritis? What is the common clinical presentation?

Back 39

Severe arthritis with SLE. These patients tend to present with an acute constellation of symptoms similar to rheumatic fever.

As a reminder, acute rheumatic fever is typically after a streptococcus pyogenes infection and follows the "Jones Criteria", which is:

Joint pain: polyarthralgias

Heart issues: pericarditis and myocarditis

Subcutaneous nodules: over bones or tendons (like rheumatoid nodules)

Erythema marginatum

Syndeham's chorea

Front 40

What is the common cutaneous lesion with SLE?

What is a lesser common variant of an SLE rash? What does this tend to say about the disease/

Back 40

Butterfly/malar rash.

Discoid rash. This indicates that the disease will be milder

Front 41

How frequent is ANA positive with SLE?

Back 41

98%

Front 42

What are two common instances when ANA is falsely positive?

Back 42

syphillis and some drug-induced lupus like states (hydralazine, procainamide, and several beta blockers frequently causes this)

Front 43

What is a less sensitive but more specific lab test for SLE?

Back 43

anti double stranded DNA antibody.

Front 44

What's the deal with CRP with SLE?

Back 44

In contradistinction to RA, they are frequently normal.

However, other studies have shown that hsCRP does have a good correlation with disease severity.

Front 45

In the context of SLE, what should elevated anticardiolipin antibodies alert you to?

Back 45

elevated coagulability.

Front 46

What is the main philosophy of treating mild SLE?

Back 46

Monitor for renal damage and a hypercoagulable state (anticardiolipin). Also monitor for becoming "severe" such as with cardiomegaly, pleural effusions.

Treat with ASA (hypercoagulability) and NSAIDs. The anti-malarials (chloroquine, hydroxychloroquine, etc) may be helpful.

Front 47

What is the main philosophy for treating severe SLE?

Back 47

Look out for system failure. Start prednisone 60 mg/d. Higher dose IV doses may be given as well.

If comorbid renal disease, add cyclophosphamide and azathioprine. Prophylactically anticoagulate.

After the crisis has passed, start on chronic lower dose immunomodulators and monitor anti-DS DNA antibodies for progress.

Front 48

What is the deal with pregnancy and SLE?

Back 48

it is associated with flaring of the symptoms.

Front 49

What is the most common demographic of systemic scleroderma?

Back 49

Women between ages 30 and 50

Front 50

What are common initial features of scleroderma?

Back 50

Sclerodactyly (decreased movement of fingers), Raynaud's phenomenon, esophageal dysmotility.

Front 51

What is the appearance of skin with scleroderma?

Back 51

shiny and atrophic with a swollen, taut appearance. Telangiectasias, hyperpigmentation, and mask-like facies may occur. Subcutaneous calcifications may occur.

Front 52

What organ is typically affected worst with scleroderma?

Back 52

The kidneys, with rapid sclerosis of the small arteries.

Front 53

What percentage of those with scleroderma have elevated ANA?

Back 53

90%

Front 54

How does ANA differ with scleroderma versus CREST syndrome?

Back 54

ANA has an antinuclear pattern with scleroderma and an anti-centromere pattern with CREST syndrome (calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, telangiectasias - a milder disease than systemic sclerosis).

Front 55

What medications are useful for systemic sclerosis?

Back 55

1) Renal manifestations: ACE inhibitors and vasodilators like minoxidil.

2) Musculoskeletal: steroids, NSAIDs

3) CCBs Raynaud's (also vasodilators)

4) Methotrexate and penicillamine to slow the progression of fibrosis.

5) PPIs/H2 blockers for esophageal dismotility.

6) Potential antibiotics for small intestinal bacterial overgrowth.

Front 56

What is the most important part of the workup of polymyositis?

Back 56

Workup for malignancy, as this has a very high comorbidity.

Front 57

What usually precedes polymyositis?

Back 57

a viral infection

Front 58

What type of rash is pathognomonic for dermatomyositis?

Back 58

A heliotrope periorbital rash. Sometimes a generalized maculopapular rash may appear

Front 59

What lab is good to follow for progression of polymyositis?

Back 59

creatine kinase

Front 60

What are the five things to look for in diagnosis polymyositis or dermatomyositis?

Back 60

1) Proximal muscle weakness

2) Elevated CK, oftentimes CRP/ESR

3) Heliotrope rash (dermatomyositis)

4) proximal EMG changes

5) Muscle biopsy

Front 61

What medications should be considered with dermato/polymyositis?

Back 61

Start with corticosteroids like prednisone 60 mg/day, with a taper. Consider methotrexate, cyclosporine, azathioprine, cyclophosphamide.

Front 62

Distinguish polymyalgia rheumatic and polymyositis by EMG findings and weakness.

Back 62

With polymyalgia rheumatica, there is no focal proximal muscle weakness, but rather muscle aches, particularly around the neck/pecs, and pelvis. Also, PMR should have a normal EMG.

Front 63

What is a consistent laboratory finding with polymyalgia rheumatica?

What labs are conspicuously normal in PRM?

Back 63

ESR over 100. CRP is also usually very high.

CK and RA are usually normal.

Front 64

If PMR is diagnosed (and temporal arteritis ruled out - remember 50% comorbidity), what is the treatment?

How useful is following ESR in this?

Back 64

Lower dose corticosteroids, like prednisone 20 mg/day. Following ESR is not helpful as it often remains high.

Front 65

Where is the most common lesion causing "central pain"?

Technically, any lesion from where to where can cause central pain?

Back 65

the ventral posteriolateral thalamus, spinothalamic tract

From the dorsal horns to the cortex

Front 66

Why is fentanyl so strong in comparison to morphine?

Back 66

Very high mu affinity. Full agonist. Most of its potency is because it is very lipophilic, thus easily crossing the blood brain barrier.

Front 67

Distinguish Freud's theory of conversion disorder to the more commonly accepted theory.

Back 67

Freud thought conversion disorder was a subconscious process that occurred as a defense against unacceptable impulses.

Modern thought is that it is a pathological learned behavior that has more to do with secondary gain, social support, etc.

Front 68

Conversion disorder is relatively rare in the U.S. Why does Waldman think this is?

Back 68

Because Freud made it so famous that it is usually immediately recognized.

Front 69

Is conversion disorder intentional?

Back 69

No. That would make it malingering or factitious disorder.

Front 70

What CNS pathology is commonly seen with "la belle indifference"?

Back 70

Right cerebral hemisphere strokes. It is frequently seen in conversion disorder too (not an organic pathology).

Front 71

Describe Munchausen Syndrome

Back 71

going to frequent doctors presenting textbook perfect diseases and life threatening maladies. Often accompanied by self-injury so as to try to validate those complaints. The most notorious is injection of fecal matter in the bloodstream to induce a septic reaction.

Front 72

Regarding primary and secondary gains, what's the main difference between Munchausen syndrome and conversion disorder?

Back 72

Conversion disorder typically has clear primary or secondary gains. Strangely, Munchausen syndrome doesn't. Though Munchausen syndrome is consciously done and conversion disorder is unconsciously done.

Front 73

Give the six degrees of thermal injury

Back 73

1) First degree: erythema and mild pain. Only in the epidermis.

2) Second degree: fluid extravasation and blisters. Papillary layer of the dermis.

3) Third degree: charring of the skin and subcutaneous tissues. Eschar formation. Destruction of pain receptors.

4) Fourth degree burn: the dermis is destroyed and muscle/bone are exposed. No pain.

5) Fifth degree: Muscle has been destroyed.

6) Thermal injury to bone.

Front 74

Give the adult rule of nines for assessing total body surface area.

Back 74

Head 9%

Anterior torso 18%

posterior torso 18%

one lower extremity 18%

one upper extremity 9%

perineum 1%

Front 75

What is the Parkland Formula for fluid replacement in a burn?

Back 75

4 ml x TBSA% x weight in kilograms

Half given during first eight hours and half over the next sixteen.

Fluid given in lactated ringers (LR is superior to NS over the short term as it can is alkalinizing in regards to acidosis associated with acute blood loss - however, it is not good over the long term as it only has a Na of 130 and K of 4).

Front 76

What are the six determinants associated with severity of electrical injury?

Back 76

1) Voltage

2) Amperage type (DC versus AC)

3) Path of current

4) Resistance/conductance of tissue

5) Surface area contact

6) Duration of exposure

Front 77

Which is more dangerous: direct or alternating current? Why?

What is the AC frequency in the US?

Back 77

Alternating current is more dangerous (three times more) because of rapid changes in current flow. This more easily induces tetany, making it impossible for the person to withdrawal the body part. AC also can penetrate the epidermis better than DC.

Levels about 30 mA are associated with tetany of the cardiac muscle.

In the US, the AC frequency is 60 hertz.

Front 78

What is joule heating?

What are the least and most resistive tissues?

Back 78

The more resistant the tissue/substance, the more the electricity is converted to heat.

Nerves are least resistive. Bones are most.

Front 79

Describe the differences in the appearance of the skin with high voltage, low voltage, and lightening electrical injuries.

Back 79

High voltage: deceptively minor skin damage with perhaps a small, leathery entrance/exit area with some hyperemia.

Low voltage: skin and subcutaneous tissue is edematous with dry, shriveled skin around it.

Lightening: "Lichtenberg figure": a christmas tree like burn.

Front 80

Differentiate nociception, pain, and suffering.

Back 80

Nociception: the nervous conduction of pain signals (free nerve endings via A delta and C fibers to the spinothalamic tract, VLP thalamus, etc).

Pain: the conscious, unpleasureable reaction to nociception.

International Association for the Study of Pain (IASP) definition:

"An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage."

Suffering: construct including the global response to not just pain, but fear, disability, etc.

Front 81

What is the female to male incidence of multiple sclerosis?

Back 81

2:1

Front 82

Where do plaques associated with multiple sclerosis tend to aggregate?

Back 82

Periventricular white matter, the basal ganglia, the long tracts of the cord and brainstem, the optic nerves

Front 83

What are the most common presentations of MS?

Back 83

Optic neuritis, transverse myelitis, internuclear opthalmoplegia (medial longitudinal fasciculus lesion), pain/paresthesias.

Front 84

What type of MS do more than 70% of those suffering from it have?

Back 84

The relapsing/remitting form with near complete remission during remissions.

Front 85

What is the most common cause of optic neuritis?

Back 85

MS

Front 86

Besides MS, what is in the differential diagnosis for transverse myelitis?

Back 86

Post infectious etiologies, particularly EBV and Lyme. Of course anything damaging the cord (tumor, infection, aneurysm, etc) may cause it.

Front 87

What is the aphorism regarding fundoscopic exam with acute optic neuritis?

Back 87

"The patient sees nothing (acute vision loss) and the physician sees nothing (normal optic disk early on)."

Front 88

What is the Uhthoff phenomenon?

Back 88

optic neuritis symptoms worse when doing something warm, like eating warm food or taking a hot shower.

Front 89

What is relapsing/remitting MS typically treated with?

Back 89

beta interferon and glatiramer acetate (copaxone)

Front 90

What are the three main theories as to the etiology of "Post Polio Syndrome?"

Back 90

1) Polio is healed and the person has their normal deficits with those deficits that normally occur with aging.

2) A recurrence of dormant polio like shingles with zoster.

3) An enterovirus similar to polio causing an autoimmune reaction

Front 91

What anticholinestherase inhibitor is sometimes used for weakness with polio?

Back 91

Mestinon/pyridostigmine.

Front 92

What percentage of those with Guillain-Barre Syndrome require ventilation?

What tends to be the first symptoms of GBS?

Back 92

30%

tingling in the fingers and toes.

Front 93

What is a common infection prior to GBS?

Back 93

mild respiratory prodrome/virus, typically without fever, 2-4 weeks prior.

Front 94

What physical exam finding is thought to be pathognomonic for GBS (and its absence should cause serious doubt that this is GBS)?

Back 94

arreflexia. Normal or hyperreflexia is almost never seen with GBS.

Front 95

What are the typical three phases of GBS and their durations?

Back 95

1) Evolution: 2 weeks

2) Plateau: one month

3) Recovery: six months

Front 96

What percentage of those with GBS can expect a nearly full recovery?

Back 96

85%

Front 97

Describe the Miller Fischer variant of GBS

Back 97

Descending (not ascending) weakness. Ophthalmolplegia. Ataxia, areflexia.

Front 98

What bacteria have been associated with GBS/AIDP?

Viruses?

Back 98

Campylobacter, borrelia berdorferi, Haemophilus influenzae, Mycoplasma pneumoniae

EBV, CMV, several others

Front 99

What tends to be seen with CSF with AIDP?

Back 99

normal cytology with increasing protein

Front 100

What is frequently seen with MRI with AIDP?

Back 100

Frequently nothing specific. However, often with gadolinium enhancement you can seen hyperintensity along the ventral nerve rootlets.

Front 101

What type of hemoglobin is seen with sickle cell anemia?

Back 101

hemoglobin S

Front 102

What two tissues/organs are most susceptible to sickle cell crises?

Back 102

the long bones and the spleen

Front 103

What is the cause of an aplastic crises with sickle cell anemia?

Back 103

infection with parvovirus b19 causing an acute halt in erythropoeisis.

Front 104

What are three non-analgesic medications that may be beneficial to those with sickle-cell pain?

Back 104

Zinc may help stabilize the erythrocyte membrane.

Hydroxyurea may increase production of fetal hemoglobin.

Oxygen

Front 105

Define dependence in the context of medications and physiology.

Back 105

The physiologic state in which continued intake of a substance is required to maintain homeostasis.

Front 106

Define tolerance in the context of medications and physiology.

Give a less beneficial and a more beneficial example of tolerance.

Back 106

an organism adapts to the effects of the drug over time, with a diminution of one or more of the drug's actions.

Decreasing analgesia from opioids.

Decreased dry mouth from tricyclics.

Front 107

Define addiction in the context of medications and physiology.

Back 107

A disease state characterized by dysfunctional behavior surrounding the use of a substance.

It is the behavior surrounding the acquisition and use/misuse of these drugs that is indicative of addiction.

Front 108

What is the main area of the brain often associated with addiction?

Back 108

The "mesolimbic pathway". This connects the ventral tegmental area (not ventral trigeminal area as stated in Waldman's) adn the nucleus accumbens (main dopamine releasing area in the basal ganglia).

Front 109

What are the three most common theories of addiction?

Back 109

1) Homeostasis theory: disequilibrium between positive reward of drug and negative of withdrawal.

2) Incentive salience theory: sensitization of the dopamine system and dysfunction of modulators cause the patient to seek the drug at the expense of all else.

3) Habit theory: addiction is in part a learned behavior.