a) arrange pelvic ultrasonography
b) do a urine preganancy test
c) determine serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) concentrations
d) prescribe medroxyprogesterone therapy, 10 mg orally every day for 10 days
e) reassure the patient that this is normal for her age, but she should return in 3 months if her periods do not resume.

View Answer B: Do a urine pregnancy test

7. A 12 year old girl is referred to the clinic by the school nurse for evaluation of scoliosis. Her scoliosis was detected during a routine screening examination at the school and appears mild (curve less than 10 degrees). She is athletic and is otherwise in good health. During the physical examination, particular attention should be given to:

a) arm length
b) blood pressure
c) body weight
d) cardiac examination
e) stage of pubertal development

View Answer E: Stage of pubertal development

The term scoliosis denotes lateral curvature of the spine, which is always associated with some rotation of the involved vertebrae. Scoliosis is classified by its anatomic location, in either the thoracic or lumbar spine, with rare involvement of the cervical spine. The convexity of the curve is designated right or left. Thus, a right thoracic scoliosis would denote a thoracic curve in which the convexity is to the right; this is the most common type of idiopathic curve. Posterior curvature of the spine (kyphosis) is normal in the thoracic area, although excessive curvature may become pathologic. Anterior curvature is called lordosis and is normal in the lumbar and cervical spines. Idiopathic scoliosis generally begins at about 8 or 10 years of age and progresses during growth. In rare instances, infantile scoliosis may be seen in children 2 years of age or less.

Idiopathic scoliosis is about four or five times more common in girls than in boys. The disorder is usually asymptomatic in the adolescent years, but severe curvature may lead to impairment of pulmonary function in later years. It is important to examine the back of any adolescent coming in for a routine physical examination in order to identify scoliosis early. The examination is performed by having the patient bend forward 90 degrees with the hands joined in the midline. An abnormal finding consists of asymmetry of the height of the ribs or paravertebral muscles on one side, indicating rotation of the trunk associated with lateral curvature.

Diseases that may be associated with scoliosis include neurofibromatosis, Marfan's syndrome, cerebral palsy, muscular dystrophy, poliomyelitis, and myelodysplasia. Neurologic examination should be performed in all children with scoliosis to determine whether these disorders are present.

Five to 7% of cases of scoliosis are due to congenital vertebral anomalies such as a hemivertebral or unilateral vertebral bridge. These curves are more rigid than the more common idiopathic curve (see below) and will often increase with growth, especially during adolescence.

Eighty percent of scoliosis is idiopathic. Since 30% of family members are also affected, siblings of an affected child should be examined.

Idiopathic infantile scoliosis, occurring in children 2-4 years of age, is quite uncommon in the United States; it is more common in Great Britain. If the curvature is less than 30 degrees, the prognosis is excellent, as 70% resolve spontaneously. If the curvature is more than 30 degrees, there may be progression, and the prognosis is therefore guarded.

Postural compensation of the spine may lead to lateral curvature from such causes as unequal length of the lower extremities. Sciatic scoliosis may result from pressure on the spinal cord or roots by infectious processes or herniation of the nucleus pulposus; the underlying cause must be sought. The curvature will resolve as the primary problem is treated.

Treatment of scoliosis depends on curve magnitude, skeletal maturity, and risk of progression. Curvatures of less than 20 degrees usually do not require treatment unless they show progression

a) complete blood count
b) determination of bleeding and clotting time
c) examination of bone marrow aspirate
d) hemoglobin electrophoresis
e) serological testing for infectious mononucleosis

View Answer A: complete blood count

I agree with the anonymous poster in the newsgroup that the CBC is to characterize the degree of the patient's anemia (and platelet count) in this case. However, this patient appears to have a platelet disorder rather than hemorragic fever.

Excerpted from the Merk Manual with permission:

Platelet disorder:

Thrombocytopenia may stem from failure of platelet production, splenic sequestration of platelets, increased platelet destruction or utilization, or dilution of platelets. Regardless of cause, severe thrombocytopenia often results in a typical pattern of bleeding: multiple petechiae in the skin, often most evident on the lower legs; scattered small ecchymoses at sites of minor trauma; mucosal bleeding (epistaxis; GI and GU tracts, and vaginal bleeding); and excessive bleeding after surgery. Heavy GI bleeding and bleeding into the CNS may be life-threatening manifestations of thrombocytopenic bleeding. However, thrombocytopenia does not cause massive bleeding into tissues or hemarthroses, such as may occur in bleeding secondary to plasma coagulation factor deficiencies (eg, hemophilia).

A thorough drug history must be taken to rule out exposure to drugs known to cause increased platelet destruction in sensitive patients. About 5% of those receiving heparin may develop thrombocytopenia (see HEPARIN- INDUCED THROMBOCYTOPENIA, below). Thus, it is important to establish whether a patient is receiving heparin. Since this is neither dose- nor route-dependent, it can occur even with the mere use of very low doses as with heparin flushes to keep IV or arterial lines open. Other drugs that less commonly induce thrombocytopenia in sensitive individuals include quinidine, sulfa preparations, oral antidiabetic agents, gold salts, and rifampin. Because patients infected with the human immunodeficiency virus (HIV) may present with an isolated severe thrombocytopenia otherwise indistinguishable clinically from idiopathic thrombocytopenic purpura (ITP, see below), risk factors and history of other symptoms of HIV infection should be elicited. Other important points in a history may be a blood transfusion within 10 days (possible post transfusion purpura), significant alcohol consumption (possible alcohol- induced thrombocytopenia), and symptoms (eg, arthralgia, Raynaud's phenomena, unexplained fever) suggestive of an underlying immunologic disease.

Differential diagnosis: Presence or absence of fever is an important point; it is usually present in thrombocytopenia secondary to infection or active SLE and in thrombotic thrombocytopenic purpura (TTP), but absent in ITP and in drug-related thrombocytopenias. Size of the spleen on physical examination is a second important point. The spleen is not palpably enlarged in most thrombocytopenias caused by increased platelet destruction (eg, ITP, drug- related immune thrombocytopenias, TTP), whereas it will be palpably enlarged in patients with thrombocytopenia secondary to splenic sequestration of platelets, and often in patients with thrombocytopenia secondary to a lymphoma or a myeloproliferative disorder.

Laboratory findings: The peripheral blood cell count is a key examination not only for establishing the presence and severity of thrombocytopenia, but also for detecting clues to its cause. Platelet size should be noted; an increased proportion of large platelets (determined by scanning the blood smear or by measuring mean platelet volume [MPV] with an electronic blood counter) suggests compensatory increased platelet production. It is often found in thrombocytopenias secondary to increased platelet destruction or utilization. Since the bleeding time will be substantially prolonged in severe thrombocytopenia of any cause, it adds no information, but may provide useful information in the patient with a moderate thrombocytopenia (eg, a platelet count of 50,000/uL). A very long bleeding time suggests that the process causing the thrombocytopenia (eg, coating of platelets with antibody) has also impaired the function of circulating platelets. Other screening tests of hemostasis (see above) will be normal unless the thrombocytopenia is associated with another condition affecting hemostasis (eg, liver disease or DIC). Bone marrow aspiration provides the number and appearance of megakaryocytes, and confirmation of the impression gained from the peripheral blood smear of the presence or absence of disease causing marrow failure (eg, leukemia). Measurement of platelet-associated IgG may also be of value in selected patients. Regardless of the history of risk factors for HIV infection, serologic tests should be done with the patient's consent. If a patient receiving heparin becomes thrombocytopenic, a test for heparin-induced platelet aggregation or for heparin-dependent platelet release (of serotonin or ATP) should be carried out.

Treatment of thrombocytopenia varies with its cause and requires rapid identification of the cause and correction if possible (eg, discontinuing heparin in heparin-associated thrombocytopenia, recognizing and treating an infection causing gram-negative endotoxemia, inducing a remission in a patient with acute leukemia). When thrombocytopenia is secondary to decreased production, giving platelet concentrates will usually raise the platelet count for 2 to 3 days. Platelet concentrates should be used prophylactically with discretion, since their effectiveness may be lost with repeated use owing to the development of platelet alloantibodies. If rapid correction of bone marrow failure is not expected, platelet transfusions are often reserved for management of an active bleeding episode. Platelet concentrates should rarely be used prophylactically in patients with thrombocytopenia secondary to increased platelet consumption (eg, in ITP), since they will usually be cleared from the circulation within 1 to several hours. However, if a patient with ITP is experiencing serious mucosal or CNS bleeding (a medical emergency) then high-dose immune globulin is given IV followed by platelet transfusions. The platelet concentrates may be given continuously (1 to 2 u./h) or in larger amounts every few hours (eg, 6 to 8 u. q 4 to 6 h). Platelet concentrates should not be given (unless death from bleeding would otherwise ensue) in 2 thrombocytopenic disorders due to increased platelet consumption: heparin-induced thrombocytopenia and TTP. In these disorders transfused platelets may be incorporated into platelet-fibrin thrombi and thus trigger a serious thrombotic event.

HEMORRHAGIC FEVER WITH RENAL SYNDROME (HFRS)

(Korean Hemorrhagic Fever; Epidemic Nephrosonephritis; Nephropathia Epidemica)

An acute infection caused by species of Hantavirus, transmitted to man from rodents and characterized by renal involvement (nephritis) and hemorrhage.

Etiology and Epidemiology

The genus Hantavirus consists of at least 4 species: Hantaan virus (Korean hemorrhagic fever), Seoul virus (a milder form of Korean hemorrhagic fever), Puumala virus (nephropathia epidemica), and Prospect Hill virus (isolated from meadow voles in Maryland and not associated with human disease). Hantaviruses have been isolated from rodents throughout the world; 42% of Norway rats in Baltimore tested between 1980 and 1986 had antibodies to Hantaan virus. An increasing number of naturally acquired and laboratory- associated infections are being reported in Europe. The virus is present in the urine, feces, and saliva of various rodents, including field and laboratory mice, rats, and voles. Transmission from rodent to rodent is primarily respiratory, with transmission to humans through inhalation of infectious aerosols from rodent excreta. There is no evidence of human-to-human transmission.

Symptoms, Signs, and Laboratory Findings

A milder form of this disease was diagnosed in Scandinavia as nephropathia epidemica and is characterized by sudden onset of high fever, headache, backache, and abdominal pain. On the 3rd or 4th day, conjunctival hemorrhages, palatine petechiae, and a truncal petechial rash may appear. About 20% of patients develop a toxic condition and become mentally obtunded. Oliguria and azotemia develop concomitantly with the hemorrhagic manifestations. Urinalysis reveals proteinuria, hematuria, and pyuria. The rash subsides in about 3 days; the patient develops polyuria and recovers over several weeks.

In the more severe eastern form of HFRS, the clinical course may be divided into 5 phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The incubation period is 7 to 36 days, usually 10 to 25 days. The severity of illness varies considerably; about 65% of cases are mild, while 10 to 15% are severe. The onset is usually abrupt (febrile phase) with chills, fever, backache, abdominal pain, and myalgia. The fever peaks on the 3rd or 4th day. There is a relative bradycardia. One of the most typical early findings is a diffuse reddening of the face, resembling a sunburn. Dermatographism can be demonstrated in > 90% of patients. Petechiae develop on the 3rd to 5th day, initially on the palate, then at pressure areas such as the axillary folds. Conjunctival hemorrhages appear at about the same time. Laboratory findings are unremarkable except for albuminuria, which appears between the 2nd and 5th day. The urinary sediment reveals hematuria and RBC and WBC casts. About the 5th day, shock or hypotension may occur (hypotensive phase); in mild cases, the fall in BP is only transient. At this stage, the Hct increases and marked proteinuria, leukocytosis, and thrombocytopenia develop. About the 8th day, BP returns to normal but oliguria develops (oliguric phase). BUN levels increase rapidly, and hemorrhagic manifestations become more prominent. Diuresis (diuretic phase) occurs about the 11th day, and CNS and pulmonary complications may be seen. The convalescent phase lasts 3 to 6 wk.

Prognosis and Treatment

Overall fatality in HFRS is 6 to 15%. Residual renal dysfunction is uncommon in Korea but may be more common in Europe.

Treatment involves meticulous supportive care. Renal dialysis may be required. Experimental trials suggest that ribavirin IV in dosage regimens similar to those used in Lassa fever may be beneficial.

a) begin a therapeutic trial of aspirin
b) begin a therapeutic trial of ibuprofen
c) determine serum CA-125 concentration
d) do diagnostic laparoscopy
e) do a dilatation and curettage

View Answer B: Begin a therapeutic trial of ibuprofen

From Chris:

Dysmenorrhea, aka "painful menstruation" is the chief complaint of this
17 y/o pt. She experiences a typically
lower abdominal pain consistently on the second day of menstruation, and
apparently at no other interval. The
pain irradiation to the back is probably a "red herring" as nothing else
in the Hx suggest otherwise.
Other remote possibilites on a differential dx of dysmenorrhea
(secondary):
* chronic PID - pt not sexually acive (?)
* intrauterine device
* leiomyomas - pt is too young
* endometriosis - " "
- interestingly enough this pt's menarche was 2 years ago, primary
dysmenorrhea usually presents 2 years after
the onset of menses.
*******************************
An NSAID trial could prove beneficial since the cause for this type of
"painful menst" is thought to be secondary
to Pg-induced myometrial contractions.

Estrogen therapy is an alternative, although beginning Ibuprofen a few
days before the anticipated menses can often help.
******************************
If the pt were older the endometriosis (a known cause of 2ary
dysmenorrhea) would have been given greater consideration, and
particularly if she had a Hx of "infertility."

- CA-125 is often a "false +" in pre-menopausal women !!

a) admit him to the hospital and begin administration of trimethoprim-sulfamethoxazole, intravenously
b) admit him to the hospital and begin administratio nof penicillin and gentamicin, intravenously
c) begin adminstration of erythromycin, orally, and see him again the next day
d) prescribe isoniazin and rifampin, orally
e) recommend aspirin, fluids and rest at home

View Answer A: admit, start on tmp-sulfa IV.

Explanation courtesy of Chris of the Newsgroup.

- A 21 y/o pt with fever, SOB, cough (non-productive ?), and lymphadenopathy initially suggests Infect. Mono, although we are not informed if there is splenomegaly.
- bibasilar rales indicate a pneumonic process, maybe asociated with the other findings. Viral ? EBV ?
- by virtue of the DRExam, we can assume that this patient is a practicing homosexual. Now the differential dx should include R/O Hiv(+), AIDS, and PCP,the latter which could account for the fever, increasing SOB & cough, although the CXR is not typical of the diffuse INTERSTITIAL infiltrates caused by P. carinii.
If you consider AIDS on the list of dx, then the lymphadenopathy could be 2ndary to lymphoma, syphilis etc.
*********************
As far as mgmt is concerned, this pt must be assumed to have PCP and must receive Bactrim. (A)

Questions 11-15

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