3/14 Presby report: polyarthritis

Thanks to Alex for presenting a great case of a middle aged woman with oligo/polyarthritis, ultimately diagnosed with disseminated gonococcus!

Polyarthritis can be a challenging complaint to parse through.

Important questions to ask

  • Timing (acute = <6 weeks)
  • Inflammatory or not (swelling suggests inflammatory)
  • Symmetry
    • This is not necessarily an exact science; a patient with mostly inflamed MCPs and a single DIP on one side and the converse on the other hand would still be considered symmetric
  • Large vs small joints
    • Ex: Lyme often presents with an acute monoarthritis, commonly in the knee; small joints are uncommon
  • History of crystal arthritis
  • Age
    • Older patients are more likely to p/w CPPD/pseudogout
  • Things that predispose to high uric acid
    • CKD
    • EtOH use
  • NSAID responsiveness

On exam, make sure to look for:

  • Joint exam
  • Nodules
  • Tophi (found particularly in the olecranon bursa and in fingertips- they can be very subtle!)
    • Gout tophi tend to be right in the olecranon, whereas rheumatoid nodules tend to be a little distal to the olecranon

Check out this calculator which may help you think about how likely gout is in your patient.

We talked briefly about the ANA.

The ANA is not a standardized test from lab to lab.

  • One lab might be different than another
  • So positivity depends on where it’s being tested, so 1:80 might be considered positive in one place and negative somewhere else
  • In one study, up to 20% of patients have a low level positive ANA
  • Some labs will use an ELISA for the ANA, for which the result will just be a number (not a titer)

The patient was ultimately diagnosed with disseminated gonococcus, with a synovial WBC count of 96000- this is unusual because gonorrhea usually causes a WBC count <50000!

  • Tx: ceftriaxone x 2 weeks + azithromycin
  • Also consider doing a surgical washout of the affected joint, particularly if it’s weight bearing; this may allow the patient to return to weight-bearing status more quickly!

3/12 Presby report: vertigo, MS/NMO

Thanks to Rebecca Wang for presenting a cool case of a middle aged man who presented with dizziness/vertigo and was found to have demyelinating brain lesions, felt to be MS vs NMO.

Differentiating between dizziness and true ‘room spinning’ or vertigo is important. You can categorize the complaint of dizziness into pre-syncope, disequilibrium, lightheadedness and true vertigo (which should be accompanied by the ‘room spinning’ sensation).

Questions to ask when investigating vertigo

  • How long the vertigo has been going on (longer = more concerning for central)
  • Things that provoke the symptoms (changes in head position, head trauma, loud noises)
  • Tinnitus/hearing loss
  • Recent URIs
  • Focal neuro deficits
  • Once vertigo is established, try to differentiate peripheral and central causes.¬† Central causes are often the more acutely concerning because they include mass lesion, stroke, as well as demyelinating conditions, etc
Screen Shot 2018-03-13 at 2.46.22 PM.png

Here’s an excellent table that helps distinguish central vs peripheral vertigo. Note that no one test or feature reliably distinguishes the two.¬†Initial Evaluation of Vertigo, AAFP.

In one study, the presence of vertigo upon waking up in the morning was predictive of a peripheral cause.

Provoking factors may also be helpful in identifying a diagnosis.

  • Symptoms provoked by…
    • positional changes: BPPV
    • recent URI: vestibular neuronitis or labrynthitis
    • migraine triggers: vestibular migraine
    • straining, recent head trauma, loud noises: perilymphatic fistula
Screen Shot 2018-03-12 at 12.19.55 PM.png

The Dix-Hallpike maneuver for positional vertigo is performed by the examiner, who stands at the head of the bed. As the patient is supported and lowered into a position whereby his or her rotated and extended head hangs off the end of the examining table, the examiner observes for nystagmus. In this view, the patient’s head has been rotated to the left and expresses nystagmus with a slow response to the right and a rapid response the left. Repeating the maneuver with the head rotated in the opposite direction would reverse the direction of the nystagmus. A maneuver (with positive indication) will reproduce the patient’s symptoms.

Remember that the Romberg test is generally not a test for cerebellar function but for peripheral neuropathy.

Finally, the HINTS (Head Impuse, Nystagmus, Test of Skew) exam! This test is useful for distinguishing brainstem and cerebellar ischemia from vestibular neuritis or other peripheral causes of vertigo and is most helpful in patients who have had continuous feelings of vertigo or dizziness. It is not useful in patients with momentary position-related transient vertigo (often benign positional vertigo) or those with TIAs who are not dizzy when examined

HINTS was found to have a sensitivity of 96.5% and specificity of 84.4% in identifying central causes of vertigo, which was much better than ABCD2. This is even better than MRI

To summarize: a REASSURING HINTS exam is ALL of the following 1) unidirectional nystagmus 2) no vertical skew 3) abnormal head impulse test (abnormal = nerve problem, not brain problem).

Neuromyelitis optica (NMO)

NMO is a demyelinating disease that primarily targets the optic nerves and spinal cord. 55-85% of brain imaging is normal, although patients can have nonspecific optic nerve enhancement and C/T spine enhancement. Almost all lesions are spinal cord or in cranial nerves.

Hallmark features

  • bilateral or rapidly sequential optic neuritis
  • transverse myelitis (leading to limb weakness, sensory loss, bladder dysfunction)
  • Trunk/leg pain
NMO vs. MS
  • NMO was originally classified as part of MS
  • NMO is now recognized as a separate disease because they do worse than MS patients.¬† NMO is also associated with IgG antibodies to Aquaporin 4, although this is neither necessary nor sufficient for diagnosis
  • NMO shares many features with MS, such as the development of lesions over time and space
  • More acute than MS; progressive decline over several years w/ a higher mortality than MS
  • NMO lesions are almost exclusively brain stem and cranial nerves, and may include transverse myelitis

Differentiating NMO from MS is based on differences with respect to clinical course, pathophys, and response to MS drugs. Some radiographic features that are more suggestive of MS than NMO:

‚Äʬ†Lesions adjacent to lateral ventricle
‚Äʬ†Inferior temporal lobe white matter lesions
‚Äʬ†Ovoid (ie, “Dawson finger”) periventricular lesions
‚Äʬ†U-fiber juxtacortical lesions


Labuguen R. Initial Evaluation of Vertigo. AAFP 2006.


2/26 VA report: pancytopenia, B12 deficiency

Thanks to Ling Wu for presenting an excellent firm report today: a 51 year old Sudanese man with subacute fatigue and weight loss, found to have pancytopenia and Coombs-negative hemolysis and ultimately found to have severe B12 deficiency.

Broadly speaking, pancytopenia results from:

  1. Bone marrow infiltration/replacement: malignancies, infection (TB, fungi), myelofibrosis
  2. Bone marrow aplasia: nutritional deficiencies, infection (HIV, Parvo B19), immune destruction, medications
  3. Cell destruction or sequestration: DIC, TTP, MDS, hypersplenism

Pancytopenia has a huge differential which can be looked up on UpToDate, so I won’t put it here.

How to work up new pancytopenia? Things to consider:

  • CBC w/ differential, BMP, LFTs (look for hemolysis/jaundice)
  • Peripheral blood smear
  • PT/PTT/INR, fibrinogen
  • B12/folate/iron studies
  • Infectious w/u: HIV, HBV/HCV, EBV or CMV as the history dictates, Parvo B19
  • Thorough medical review, consider autoimmune workup

Things like flow cytometry and bone marrow biopsy may need to be considered if the initial workup is unrevealing.

This patient was ultimately diagnosed with B12 deficiency.

Screen Shot 2018-02-26 at 1.51.47 PM.png

Normal mechanisms and defects of B12 absorption. The vitamin B12 (Cbl) released from food protein by peptic action is bound to haptocorrin (HC) in the stomach and travels to the duodenum, where pancreatic proteases digest the HC, releasing Cbl to bind to intrinsic factor (IF). The IF-Cbl complex binds to a specific receptor in the distal ileum (the cubam receptor) and is internalized, eventually released from lysosomes, and transported into the blood. NEJM 2013.


See the NEJM article below for more comprehensive information on causes of B12 deficiency.

Screen Shot 2018-02-26 at 1.44.02 PM.png

Clinical manifestations of B12 deficiency. NEJM 2013.


  • The B12 assay is imperfect: although an extremely low level (<100) is usually associated with clinical deficiency, such low levels are rare
  • Up to 50% of tests have either false positive or false negative values
  • Moral of the story: don’t use the lab’s lower limit of normal to reassure yourself that there’s no B12 deficiency. If they have compatible signs/sx despite a value above the LLN, they may still require supplementation.


  • The body’s daily requirement of B12 is 2.4 őľg
  • Severe deficiency may require injected B12, sometimes lifelong if it is for treatment of pernicious anemia
  • Neither injection nor oral therapy are very efficiently absorbed
  • An increase in the reticulocyte count should be seen in 1 week and correction of megaloblastic anemia in 6-8 weeks


  1. Stabler S. Vitamin B12 deficiency. NEJM 2013.

2/22 VA report: hypocalcemia (mechanisms and management)

Thanks to MK Hannan for giving an outstanding intake report yesterday on a 61 year old alcoholic with a h/o RCC s/p nephrectomy who presented with hypocalcemia.


  • Serum [Ca] is governed by the actions of PTH and Vitamin D on the bones, gut and kidneys
  • Calcium itself regulates its own metabolism via calcium-sensing receptors (CaSR) in the parathyroid gland (inhibits PTH secretion) and kidney (promotes urinary Ca excretion)
  • Serum calcium is transported partly bound to albumin (~45%); small anions such as phosphate and citrate (15%); and partly in the free/ionized state (‘iCal’: 40%)

Acute signs of hypocalcemia

  • Neuromuscular irritability (tetany): paresthesias, muscle twitching, Trousseau/Chvostek’s, bronchospasm, seizures
  • Cardiac: prolonged QT, heart failure (decreased inotropy), hypotension
  • Papilledema

Diagnosis: consider sending off PTH level (most important), BMP, iCal, Vit D level

PTH-related causes of hypocalcemia

  1. PTH absent (ie low PTH): postsurgical, hypo- OR hypermagnesemia (<0.8 or >5), autoimmune parathyroid destruction or Abs to parathyroid CaSR, s/p XRT, infiltrative (very rare)
  2. PTH ‘ineffective’ (ie high PTH): Vit D deficiency or resistance, end-stage CKD (via decreased calcitriol production and hyperphosphatemia), malabsorption (ex: celiac causing Ca malabsorption), pseudohypoparathyroidism
  3. PTH ‘overwhelmed’: osteoblastic metastases (breast, prostate), pancreatitis, sepsis, massive blood transfusions (via citrate), rhabdomyolysis (via increased serum phosphate)

Drugs that can cause hypocalcemia: EDTA, citrate, bisphosphonates, cisplatin, foscarnet (Phos-based Ca chelator)

Management of hypocalcemia

  • Mg repletion (goal >2)
  • Vitamin D repletion (50K units Vit D2 or D3 x 6-8 weeks)
  • Oral calcium w/ goal 1-2g of¬† elemental calcium daily, goal Ca 8-8.5 (low end of nl)
    • Many oral supplements like Ca carbonate contain only 40% elemental Ca; so a 1250mg pill contains ~500mg elemental Ca. Ca citrate is ~20% elemental Ca.
  • Ca gluconate can be given IV in acute situations

1/29 VA report: clots clots clots clots clots clots

Thanks to Malcolm Kearns (not Lil Jon as the title might suggest) for giving an excellent talk on DVTs, related syndromes, and their management.

First, we talked about medications that can cause edema:

Screen Shot 2018-01-31 at 4.00.41 PM.png

Courtesy of Malcolm Kearns

The patient in this case was diagnosed with an SVT. But which veins are considered superficial?

Generally, superficial vein thrombi (SVTs) can be managed conservatively (compression stockings, NSAIDs, hot packs). But there is a role for anticoagulation even with SVTs IF:

  1. The SVT is associated with a DVT
  2. It is located near a junction with a deep vein (saphenofemoral or saphenopopliteal junction)
  3. There is a known or strongly suspected hypercoagulable state (cancer, etc), or the SVT is extensive or recurrent

This patient had repeat imaging that now showed DVTs. It’s important to know that treatment of DVTs can vary depending on where they are:

Screen Shot 2018-01-31 at 4.25.19 PM.png

Other reasons to anticoagulate isolated distal DVTs include:

  • Unprovoked DVT
  • D-dimer >500 ng/ml
  • Inpatient status
  • Immobility
  • Persistent or irreversible risk factors (malignancy etc)
  • Extensive thrombus
  • Symptomatic

We touched on several studies that studied the use of IVC filters for prevention of DVT/PE. Very briefly, the bottom line for some of them:

  • PREPIC (1998)
    • Groups: pts w/ proximal DVT, high risk for PE, placed on UFH vs LMWH w/ or w/o IVC filter
    • All patients were anticoagulated
    • Bottom line: IVC filters significantly reduced PE incidence at 12 days and 8 years BUT they also significantly increased DVT incidence at 2 years and 8 years
  • PREPIC 2 (2015)
    • Group: pts w/ acute PE, high risk for recurrence, placed on A/C alone or A/C + IVC filter
    • Bottom line: IVC filters did not reduce symptomatic PE at 6 months

In general, the take away is that IVC filters are not a panacea and should really be considered in patients in whom a recurrent PE would be catastrophic (likely due to poor cardiopulmonary reserve).

Other interesting takeaways:

  • There is no evidence to suggest that SCDs can mobilize a clot in someone who already has a DVT or SVT
  • There is also no evidence that exercise in someone with a PE can lead to recurrent PE
  • The Choosing Wisely Campaign strongly recommends against doing a hypercoagulability workup in patients with a known cause of DVT. In general, these should be left to the outpatient setting, ideally when patients are off anticoagulation

Ultimately this patient was diagnosed with phlegmasia cerulea dolens, an uncommon condition characterized by extensive and dramatic ileofemoral DVT. The clot can extend into capillaries and prevent blood from leaving the leg, leading to compartment syndrome, hypovolemic shock, and gangrene!

1/31 PPMC Report: Aspiration and PJP Pneumonia

Thank you to Dr. Palevsky and Dr. Gluckman for helping us discuss a really interesting case of an 82 year old gentleman with persistent hypoxia who was ultimately found to have a new diagnosis of HIV presenting with PJP pneumonia.

We discussed techniques for performing a thorough pulmonary exam: (images: https://meded.ucsd.edu/clinicalmed/lung.htm)pcp1

Many of these exam maneuvers use principles of physics to help us determine if the lung tissue is aerated normally, or if there is a process compromising aeration and anatomy. Since sound waves are vibrations, they are transmitted differently through air and solid/liquid media. Thus processes causing consolidation of lung tissue, alveolar filling, or other anatomic/functional pathology will transmit sound waves differently Рleading to different findings on egophony, whispered pectoriloquy, tactile fremitus, and percussion.

Our patient experienced respiratory distress and decompensation following an upper endoscopy procedure. We discussed that his clinical circumstances were concerning for aspiration Рwhich can cause either a pneumonitis (transient inflammation without leading to infection) or a pneumonia (infection). Dr. Palevsky taught us that due to anatomy of the airways branching, aspiration does not always go to the lung bases, and it is important to listen in the central lung fields too.

After a course of treatment for aspiration pneumonia, our patient continued to be hypoxic and tachypneic, so additional workup was pursued and ultimately he was diagnosed with HIV/AIDS and PJP pneumonia. We learned from Dr. Gluckman that 6% of new HIV diagnoses are made in patients older than 80 years, so always think about sending an HIV test on all of your patients, regardless of their age!

PJP is currently classified as a fungus, which is normally cleared by host macrophages and CD4 cells coordinating an immune response – which is why patients with CD 4 < 200 (and other immunocompromised states) are at risk of this infection. Typical symptoms include progressive shortness of breath especially with exertion, fever, and tachypnea, although patients can be asymptomatic. Classic imaging shows bilateral diffuse patchy pulmonary infiltrates. A very elevated beta-D-glucan is supportive of this diagnosis, but the definitive diagnosis requires confirming the presence of PJP in the respiratory secretions or sputum. PJP does not grow in cultures, and obtaining samples can sometimes be difficult and require invasive techniques.

Treatment recommendations depend on severity of disease. Our patient progressed to respiratory failure requiring mechanical ventilation, so he definitely had severe disease! The recommended regimen in that case is high dose trimethoprim-sulfamethoxazole (weight-based) for 21 days, given IV until patient stabilizes. Patients with severe disease should also be treated with steroids. Finally, studies support early initiation of ART in patients presenting with PJP pneumonia.


1/30 PPMC Report: Basics of Dental Medicine for the Internist

Thanks to Dr. Zach Korwin for coming to talk to us about the basics of dental medicine!

We discussed a case of tooth pain presenting to primary care clinic. In order to understand some physical exam maneuvers we can perform to help us localize and diagnose pathology, we learned about dental anatomy: dent1                                                                                                       lonestarsmilesforkids.com

  • Enamel is the hardest layer and is the part on top of the tooth that we can see. This layer is the most difficult for decay to penetrate.
  • Dentin is underneath the enamel; it is a porous and softer material. Once decay reaches dentin, it spreads very quickly. Within the dentin pores are cells that can sense changes in temperature etc and transmit pain — this¬†causes hypersensitivity. Sensitivity toothpastes work by having large molecules clog the pores in the dentin. Interestingly, a narwhal’s tusk is made of dentin!
  • Pulp chamber is a spongy layer inside the tooth that contains vasculature and nerves. Most tooth pain is caused by an insult to the innervated pulp chamber causing inflammation. Since the pulp is contained in a noncompliant tooth, inflammation leads to increased pressure, which is sensed as pain.
  • Periodontal ligament connects the tooth to the surrounding bone. This is also innervated so can also sense pain, which is usually dull pain in the setting of gum disease.

Some additional physical exam maneuvers include:

  • Percussion — should elicit pain on affected tooth, may cause slight discomfort in surrounding teeth
  • Palpation — gums, muscles of mastication, floor of maxillary sinuses
  • Probing — can¬†elicit pain if etiology is periodontal disease
  • Biting — use Q-tip or similar to isolate bite to single tooth at a time
  • Cold test — cold stimulus is applied to teeth individually. A normal response is very transient discomfort. Prolonged and severe discomfort can be seen with pulpitis, and lack of response can be seen if the nerve has been compromised by severe decay/infection.

We discussed the different causes of tooth pain. Some of the possibilities include:dent4Our patient ended up having irreversibly pulpitis. Tooth decay occurs when oral flora (particularly strep mutans) sticks to teeth, sometimes forming biofilms, and produces lactic acid that wears away the teeth. (image: askdoctork.com)dent2

In early stages of tooth decay, the infection has not reached the pulp chamber where the nerves are, so it is usually asymptomatic and can be treated with a filling. If left to progress, the infection can spread through the pulp chamber (causing pain), and ultimately into the bone and form an abscess. Once the pulp is involved, treatment consists of root canal or extraction, and sometimes requires antibiotics aimed at covering anaerobes.

Management of anticoagulation is somewhat provider and patient-dependent. Studies of patients on warfarin have demonstrated that it is safe to continue warfarin for minor dental procedures (such as extraction) if INR is in therapeutic range.

We also discussed indications for antibiotic prophylaxis prior to dental procedures. Notably, uncomplicated joint replacements do not necessitate prophylaxis to prevent prosthetic joint infections. Current guidelines suggest prophylaxis in the following situations: dent3

Finally, we discussed basics of dentures and their complications. Complete dentures (which replace all teeth, as opposed to partial dentures which replace only some missing teeth) can be anchored by implants or can be fit to the ridge of the gums/jaw bone. Without implants or teeth, the bone eventually resorbs. This leads to poorly-fitting dentures, which can cause discomfort and difficulty eating, as well as inducing gag reflex and causing pressure/friction ulcers. Once bone resorption has become severe, treatment options are limited.