Dysmenorrhea

Dysmenorrhea

Diagnosis and Initial Management of Dysmenorrhea

AMIMI S. OSAYANDE, MD, and SUARNA MEHULIC, MD, University of Texas Southwestern Medical Center, Dallas, Texas Am Fam Physician. 2014 Mar 1;89(5):341-346.

Dysmenorrhea is one of the most common causes of pelvic pain. It negatively affects patients’ quality of life and sometimes results in activity restriction. A history and physical examination, including a pelvic examination in patients who have had vaginal intercourse, may reveal the cause. Primary dysmenorrhea is menstrual pain in the absence of pelvic pathology. Abnormal uterine bleeding, dyspareunia, noncyclic pain, changes in intensity and duration of pain, and abnormal pelvic examination findings suggest underlying pathology (secondary dysmenorrhea) and require further investigation. Transvaginal ultrasonography should be performed if secondary dysmenorrhea is suspected. Endometriosis is the most common cause of secondary dysmenorrhea. Symptoms and signs of adenomyosis include dysmenorrhea, menorrhagia, and a uniformly enlarged uterus. Management options for primary dysmenorrhea include nonsteroidal anti-inflammatory drugs and hormonal contraceptives. Hormonal contraceptives are the first-line treatment for dysmenorrhea caused by endometriosis. Topical heat, exercise, and nutritional supplementation may be beneficial in patients who have dysmenorrhea; however, there is not enough evidence to support the use of yoga, acupuncture, or massage.

Otitis Media

Otitis Media

This editorial illustration was created for a September 2013 cover of American Family Physician. The image summarizes Otitis Media, infection of the middle ear. Although several subtypes of otitis media are distinguished, the term is often used synonymously with acute otitis media. It is very common in childhood. An integral symptom of acute otitis media is ear pain; other possible symptoms include fever, and irritability (in infants). Since an acute otitis media is usually precipitated by an upper respiratory tract infection, there often are accompanying symptoms like cough and nasal discharge.

The common cause of all forms of otitis media is blockage of the Eustachian tube. This is usually due to swelling of the mucous membranes in the nasopharynx, which in turn can be caused by a viral upper respiratory infection or by allergies. Because of the blockage of the Eustachian tube, the air volume in the middle ear is trapped and parts of it are slowly absorbed by the surrounding tissues, leading to a mild vacuum in the middle ear. Eventually the vacuum can reach a point where fluid from the surrounding tissues is sucked in to the middle ear’s cavity (also called tympanic cavity), causing middle ear effusion. This is seen as a progression from a Type A tympanogram to a Type C to a Type B tympanogram.

By reflux or suction of material from the nasopharynx into the normally sterile middle ear space, the fluid may then become infected – usually with bacteria. In rare cases, however, the virus that caused the initial upper respiratory tract infection can itself be identified as the pathogen causing the infection in the middle ear.

Acute otitis media (AOM) is usually developing on the basis of a (viral) upper respiratory infection with blockage of the Eustachian tube and effusion in the middle ear, when the fluid in the middle ear gets additionally infected with bacteria. The most common bacteria found in this case are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

As its typical symptoms overlap with other conditions, clinical history alone is not sufficient to predict whether acute otitis media is present; it has to be complemented by visualization of the tympanic membrane.

To confirm the diagnosis, middle ear effusion and inflammation of the eardrum have to be identified; signs of these are fullness, bulging, cloudiness and redness of the eardrum. Viral otitis may also result in blisters on the external side of the tympanic membrane, which is called bullous myringitis (myringa being Latin for “eardrum”). However, sometimes even examination of the eardrum may not be able to confirm the diagnosis, especially if the canal is small and there is wax in the ear that obscures a clear view of the eardrum. Also, an upset child’s crying can cause the eardrum to look inflamed due to distension of the small blood vessels on it, mimicking the redness associated with otitis media.

Diverticulitis

Diverticulitis

This editorial illustration was created for a May 2013 cover of American Family Physician. The image summarizes Diverticulitis, a common digestive disease which involves the formation of pouches (diverticula) within the bowel wall. This process is known as diverticulosis, and typically occurs within the large intestine, or colon, although it can occasionally occur in the small intestine as well. Diverticulitis results when one of these diverticula becomes inflamed.

Patients often present with the classic triad of left lower quadrant pain, fever, and leukocytosis (an elevation of the white cell count in blood tests). Patients may also complain of nausea or diarrhea; others may be constipated.

Less commonly, an individual with diverticulitis may present with right-sided abdominal pain. This may be due to the less prevalent right-sided diverticula or a very redundant sigmoid colon. Some patients report bleeding from the rectum.
Diverticulitis

The most common symptom of diverticulitis is abdominal pain. The most common sign is tenderness around the left side of the lower abdomen. If infection is the cause, then nausea, vomiting, fever, cramping, and constipation may occur as well. The severity of symptoms depends on the extent of the infection and complications. Diverticulitis may worsen throughout the first day, as it starts as small pains and/or diarrhea, and may slowly turn into vomiting and sharp pains.

Foods such as seeds, nuts, and corn were, in the past, thought by many health care professionals to possibly aggravate diverticulitis. However, recent studies have found no evidence that suggests the avoidance of nuts and seeds prevents the progression of diverticulosis to an acute case of diverticulitis. Not only has this research shown that they do not appear to be aggravating the diverticulitis, but it appears that a higher intake of nuts and corn could in fact help to avoid diverticulitis in male adults. Most cases of simple, uncomplicated diverticulitis respond to conservative therapy with bowel rest and antibiotics. Despite being recommended by several guidelines, the use of antibiotics in mild cases of uncomplicated diverticulitis is supported with only “sparse and of low quality” evidence, with no evidence supporting their routine use. However, recurring acute attacks or complications, such as peritonitis, abscess, or fistula may require surgery, either immediately or on an elective basis.

People may be placed on a low residue diet. This low-fiber diet gives the colon adequate time to heal without needing to be overworked. Later, patients are placed on a high-fiber diet.

“Hands Free” Femoral Retraction

“Hands Free” Femoral Retraction

The illustration posted in this example was created for the April 2013 issue of Orthopaedics feature and peer-reviewed article, Technical Trick: Simple, No-Hands Retraction for Lateral Approach to the Proximal Femur.

A simple technique is described that allows the orthopaedic surgeon to perform no-hands retraction during the lateral approach to the proximal femur during fixation of an intertrochanteric fracture with a sliding hip screw. All instruments remain sterile and within 6 inches of the surgical wound. Use of this technique is particularly useful in the event that a surgeon is operating with only one surgical assistant who may not be able to provide adequate assistance with retraction while concurrently preparing surgical instruments.

MenoDepression

MenoDepression

The illustration depicted was created for the April 2013 26(4) issue of JAAPA feature article, Treatment options for major depression during the menopausal (Bobbie Posmontier, PhD, CNM, PMHNP-BC).
Compared to men, women experience 1.7 times the prevalence of depression, largely because of fluctuations in reproductive hormones. Even without a prior history of depression, vulnerability to depressive symptoms may be especially increased during the menopausal transition as a result of greater sensitivity to the extreme fluctuating levels of estrogen, other hormonal influences, and single nucleotide polymorphisms that are unique to women. PAs need to understand the varying presentations for women with depression, a major health burden and component of the National Commission on Certification of Physician Assistants Blueprint, and to appreciate the nuances of treatment if underlying hormonal fluctuations are driving symptoms. Emerging science is redefining the initial treatment approaches, and traditional therapies for major depression may be inadequate to control the symptom burden of patients with menopausal depression. The purpose of this article is to aid PAs in understanding the hormonal and genetic influences as well as the symptoms of menopausal transition that overlap with symptoms of major depression and to discuss effective assessment and multidisciplinary management of major depression during perimenopause.

The Philadelphia Chromosome

The Philadelphia Chromosome

This illustration was created for JAAPA, February 2013 • 26(2).

The Philadelphia chromosome is formed when a piece of chromosome 9 exchanges places with a piece of chromosome 22, resulting in a balanced translocation t(9;22)(q34;q11) and the formation of an abnormal fusion gene BCR-ABL1.

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm. The American Cancer Society estimated that in 2012, the number of newly diagnosed CML cases would be 5,430, with 610 deaths.1 The discovery of the tyrosine kinase inhibitor (TKI) imatinib has revolutionized the treatment and prognosis of CML, making imperative early recognition of CML. Timely diagnosis will ensure that patients receive early treatment, significantly improving their prognosis.

CML is caused by a cytogenetic abnormality that is thought to be acquired and involves a balanced translocation between chromosome 9 and chromosome 22. The BCR gene on chromosome 22 fuses with the ABL1 gene on chromosome 9, resulting in the abnormal fusion gene BCR-ABL1 located on chromosome 22 (Figure 1). The fusion gene produces a protein with tyrosine kinase activity that causes cells to proliferate. The resultant abnormal chromosome 22 [t(9;22)(q34;q11)] is also known as the Philadelphia (Ph) chromosome. It is identified in 95% of patients with CML and can be detected in all myeloid cells, including granulocytes, erythrocytes, monocytes, and B lymphocytes

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