200 pearls and counting! Take the Pearls4Peers quiz #2!

Multiple choice (choose 1 answer)
1. Which of the following classes of antibiotics is associated with peripheral neuropathy?
a. Penicillins
b. Cephalosporins
c. Macrolides
d. Quinolones

 

 

2. The best time to test for inherited thrombophilia in a patient with acute deep venous thrombosis is…
a. At least 1 week after stopping anticoagulants and a minimum of 3 months of anticoagulation
b. Just before initiating anticoagulants
c. Once anticoagulation takes full effect
d. Any time, if suspected

 

 

3. All the following is true regarding brain MRI abnormalities following a seizure, except…
a. They are observed following status epilepticus only
b. They are often unilateral
c. They may occasionally be associated with leptomeningeal contrast enhancement
d. Abnormalities may persist for weeks or months

 

 

4. Which of the following is included in the quick SOFA criteria for sepsis?
a. Heart rate
b. Serum lactate
c. Temperature
d. Confusion

 

 

5. All of the following regarding iron replacement and infection is true, except…
a. Many common pathogens such as E.coli and Staphylococcus sp. depend on iron for their growth
b. Association of IV iron replacement and increased risk of infection has not been consistently demonstrated
c. A single randomized-controlled trial of IV iron in patients with active infection failed to show increased infectious complications or mortality with replacement
d. All of the above is true

 

True or false

1. Constipation may precede typical manifestations of Parkinson’s disease by 10 years or more
2. Urine Legionella antigen testing is >90% sensitive in legionnaire’s disease
3. Spontaneous coronary artery dissection should be particularly suspected in males over 50 years of age presenting with acute chest pain
4. Urine dipstick for detection of blood is >90% sensitive in identifying patients with rhabdomyolysis and CK >10,000 U/L
5. Diabetes is an independent risk factor for venous thrombophlebitis

 

 

 

Answer key
Multiple choice questions:1=d; 2=a;3=a;4=d;5=c
True or false questions:1=True; 2,3,4,5=False

 

200 pearls and counting! Take the Pearls4Peers quiz #2!

My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

Night sweats (NS) is a common patient complaint, affecting about a third of hospitalized patients on medical wards1.  Despite its long list of potential causes, direct relationship between the often- cited conditions and NS is usually unclear2, its cause may remain elusive In about a third to half of cases in the primary care setting, and its prognosis, at least in those >65 y of age, does not appear to be unfavorable 2,3.

Selected commonly and less frequently cited conditions associated with NS are listed (Table)2-9.  Although tuberculosis is one of the first conditions we think of when faced with a patient with NS, it should be emphasized that NS is not common in this disease (unless advanced) and is rare among hospitalized patients as a cause of their NS1,9.

In one of the larger study of adult patients seen in primary care setting, 23% reported pure NS and an additional 18% reported night and day sweats5; the prevalence of NS in both men and women was highest in 41-55 y age group. In multivariate analyses, factors associated with pure NS in women were hot flashes and panic attacks; in men, sleep disorders. 

Table. Selected causes of night sweats

Commonly cited Less frequently cited
Neoplastic/hematologic (eg, lymphoma, leukemia, myelofibrosis)

Infections (eg, HIV, tuberculosis, endocarditis)

Endocrine (eg, ovarian failure, hyperthyroidism, orchiectomy, carcinoid tumor, diabetes mellitus [nocturnal hypoglycemia], pheochromocytoma)

Rheumatologic (eg, giant cell arteritis)

Gastroesophageal reflux disease

B-12 deficiency

Pulmonary embolism

Drugs (eg, anti-depressants, SSRIs, donepezil [Aricept], tacatuzumab)

Sleep disturbances (eg, obstructive sleep apnea)

Panic attacks/anxiety disorder

Obesity

Hemachromatosis

Diabetes insipidus

References

  1. Lea MJ, Aber RC, Descriptive epidemiology of night sweats upon admission to a university hospital. South Med J 1985;78:1065-67.
  2. Mold JW, Holtzclaw BJ, McCarthy L. Night sweats: A systematic review of the literature. J Am Board Fam Med 2012; 25-878-893.
  3. Mold JW, Lawler F. The prognostic implications of night sweats in two cohorts of older patients. J Am Board Fam Med 2010;23:97-103.
  4. Mold JW, Holtzclaw BJ. Selective serotonin reuptake inhibitors and night sweats in a primary care population. Drugs-Real World Outcomes 2015;2:29-33.
  5. Mold JW, Mathew MK, Belgore S, et al. Prevalence of night sweats in primary care patients: An OKPRN and TAFP-Net collaborative study. J Fam Pract 2002; 31:452-56.
  6. Feher A, Muhsin SA, Maw AM. Night sweats as a prominent symptom of a patient presenting with pulmonary embolism. Case reports in Pulmonology 2015. http://dx.doi.org/10.1155/2015/841272
  7. Rehman HU. Vitamin B12 deficiency causing night sweats. Scottish Med J 2014;59:e8-11.
  8. Murday HK, Rusli FD, Blandy C, et al. Night sweats: it may be hemochromatosis. Climacteric 2016;19:406-8.
  9. Fred HL. Night sweats. Hosp Pract 1993 (Aug 15):88.
My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?

Great question! “Carotenoderma” refers to the yellow discoloration of the skin caused by increased serum carotenoids1.  Carotenoids are absorbed by passive diffusion from the gastrointestinal tract which are partially metabolized in the intestinal mucosa and liver to vitamin A, and then transported in the plasma into the intercellular lipids of stratum corneum of the skin which has a high affinity for carotene1,2.

The maximal accumulation of carotenoids occurs in areas with an abundance of sweat glands (eg, the palms, soles, nasolabial folds). In the absence of strateum corneum, the sclera is spared!

Of note, there are many causes of carotenoderma besides excessive ingestion of carrots.  Among foods, increased ingestion of tomatoes, tangerines, red palm oil, and squash may also be responsible1,2

Systemic diseases associated with increase in serum carotenoids (possibly related to decreased conversion to vitamin A, hyperlipidemia, or other factors) include hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome, and liver disease.

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References 

  1. Horev L, Ramot Y, Klapholz L. Yellow feet in a patient with breast and thyroid carcinoma, due to oral intake of turmeric. Drug Saf-Case Rep 2015;2:4.https://link.springer.com/article/10.1007/s40800-015-0006-4
  2. Maharshak N, Shapiro J, Trau H. Carotenoderma-a review of the literature. Int J Dermatol 2003;42:178-181. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-4362.2003.01657.x/epdf

 

Contributed by Clara Yang, Medical Student, Harvard Medical School

 

Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?

What is an abnormal post-void residual (PVR) volume?

Although measurement of PVR is a common everyday occurrence in hospitalized patients, the threshold of what constitutes an abnormal value is often poorly defined and not standardized. However, most urologists consider volumes of 50 ml to 100 ml to constitute the lower threshold of abnormal PVR (1).

Large PVRs are associated with urinary tract infections, especially in persons at risk (e.g. diabetes, spinal cord injury), while very large PVRs (>300 ml) may be associated with an increased risk of upper urinary tract dilatation and renal insufficiency.

Chronic urinary retention is often defined as a PVR > 300 ml (2).

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References

1. Kelly CE. Evaluation of voiding dysfunction and measurement of bladder volume. Rev Urol 2004;6 (suppl 1):S32-S37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472847

 

2. Kaplan SA, Wein AJ, Staskin DR, Roehrborn CG, Steers WD. Urinary retention and post-void residual urine in men: separating truth from tradition. J Urology 2008;180:47–54. https://www.ncbi.nlm.nih.gov/pubmed/18485378

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is an abnormal post-void residual (PVR) volume?

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?

Yes!  Although we often associate oral candidiasis with thrush or pseudomembranous white plaques, another common form of oral candidiasis seen in hospitalized patients is “acute atrophic candidiasis” (AAC), also referred to as “antibiotic sore mouth” because of its association with use of broad spectrum antibiotics (1,2). 

Despite the absence of thrush, patients with AAC often have erythematous patches on the palate, buccal mucosa and dorsum of the tongue. Common symptoms include burning sensation in the mouth (especially with carbonated drinks in my experience), dry mouth and taste buds “being off” (2).  

Aside from antibiotics, other predisposing factors for AAC include corticosteroids, HIV disease, uncontrolled diabetes mellitus, iron deficiency anemia, and vitamin B12 deficiency.

So next time you see a hospitalized patient with new onset sore, burning mouth that wasn’t present on admission, think of antibiotic sore mouth!

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References

1. Stoopler ET, Sollecito TP. Oral mucosal diseases. Med Clin N Am 2014;98:1323-1352. https://www.ncbi.nlm.nih.gov/pubmed/25443679

2. Millsop JW, Fazel N. Oral candidiasis. Clin Derm 2016;34:487-94. https://www.ncbi.nlm.nih.gov/pubmed/27343964

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?