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Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses.
Afterward, acromegaly develops. The term "acromegaly," meaning extremity
enlargement, seriously understates the manifestations. The hands enlarge and a
doughy, moist handshake is characteristic. The fingers widen, causing patients to
enlarge their rings. Carpal tunnel syndrome is common. The feet also grow, particularly
in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat
size increases. The mandible becomes more prominent, causing prognathism and
malocclusion. Tooth spacing widens. Macroglossia occurs, as does hypertrophy of
pharyngeal and laryngeal tissue; this causes a deep, coarse voice and sometimes
makes intubation difficult. Obstructive sleep apnea may occur. A goiter may be noted.
Hypertension (50%) and cardiomegaly are common. At diagnosis, about 10% of
acromegalic patients have overt heart failure, with a dilated left ventricle and a
reduced ejection fraction. Weight gain is typical, particularly of muscle and bone.
Insulin resistance is usually present and frequently causes diabetes mellitus (30%).
Arthralgias and degenerative arthritis occur. Overgrowth of vertebral bone can cause
spinal stenosis. Colon polyps are common, especially in patients with skin papillomas.
The skin may also manifest hyperhidrosis, thickening, cystic acne, and areas of
acanthosis nigricans. GH-secreting pituitary tumors usually cause some degree of
hypogonadism, either by cosecretion of prolactin or by direct pressure upon normal
pituitary tissue. Decreased libido and impotence are common, as are irregular menses
or amenorrhea. Secondary hypothyroidism sometimes occurs; hypoadrenalism is
unusual. Headaches are frequent. Temporal hemianopia may occur as a result of the
optic chiasm being impinged by a suprasellar growth of the tumor. Endoscopic
transnasal, transsphenoidal pituitary microsurgery removes the adenoma while
preserving anterior pituitary function in most patients. Surgical remission is achieved in
about 70% of patients followed over 3 years. GH levels fall immediately; diaphoresis
and carpal tunnel syndrome often improve within a day after surgery. Transsphenoidal
surgery is usually well tolerated, but complications occur in about 10% of patients,
including infection, cerebrospinal fluid leak, and hypopituitarism. Hyponatremia can
occur 4-13 days postoperatively and is manifested by nausea, vomiting, headache,
malaise, or seizure. It is prudent to monitor serum sodium levels postoperatively.
Dietary salt supplements for 2 weeks postoperatively may prevent this complication.
Patients who fail to have a clinical or biochemical remission after surgery are treated
with a dopamine agonist (eg, cabergoline), octreotide, pegvisomant, or a combination
of these medications. Cabergoline may be used first, since it is an oral medication.
Cabergoline therapy is most successful for tumors that secrete both prolactin (PRL) and
GH, but can also be effective for patients with normal serum PRL levels. Therapy with
cabergoline will shrink one-third of such tumors by more than 50%. Cabergoline is
administered orally, starting with 0.25 mg twice weekly. If the patient tolerates
cabergoline, the dosage may be increased gradually, based upon serum GH and IGF-I
levels; the maximum dosage is 1 mg orally twice weekly. Side effects of cabergoline
include nausea, fatigue, constipation, abdominal pain, and dizziness. Cabergoline is
expensive. Somatostatin analogs may be used to treat patients who have persistent
acromegaly despite pituitary surgery. Octreotide and lanreotide are somatostatin
a) Paraseptal
b) Irregular
c) Panlobulillar
d) Centrolobulillar
e) Parahiliar
frecuente que la forma panacinar y representa el 95% de los casos. Los productos del
tabaco y el carbón tienen un papel predominante en la génesis de este tipo de
enfisema.
a) Cultivo de exudado
b) Pruebas de sensibilidad
c) Microscopia de esputo
d) Tele de tórax
e) Examen clínico
a) Broncografía contrastada
b) Broncoscopía directa
c) Gammagrafía de perfusión pulmonar
d) Tele de tórax en posición supina
e) Espirometría computarizada
De las opciones presentadas la que parece “mas verdadera es la opción C”, enseguida
se cita una breve referencia.
Pulmonary arteriography remains the reference standard for the diagnosis of
pulmonary thromboembolism. An intraluminal filling defect in more than one projection
establishes a definitive diagnosis. Secondary findings highly suggestive of pulmonary
thromboembolism include abrupt arterial cutoff, asymmetry of blood flow¾especially
segmental oligemia¾or a prolonged arterial phase with slow filling. Pulmonary
arteriography was performed in 755 patients in the PIOPED study. A definitive diagnosis
was established in 97%; in 3% the studies were nondiagnostic. Four patients (0.8%)
with negative arteriograms subsequently had pulmonary thromboemboli at autopsy.
Serial arteriography has demonstrated minimal resolution of thrombus prior to day 7
following presentation. Thus, negative arteriography within 7 days of presentation
excludes the diagnosis. Pulmonary arteriography is a safe but invasive procedure with
well-defined morbidity and mortality data. Minor complications occur in approximately
5% of patients. Most are allergic contrast reactions, transient renal dysfunction, or
related to percutaneous catheter insertion; cardiac perforation and arrhythmias are
reported but rare. Among the PIOPED patients who underwent arteriography, there
were five deaths (0.7%) directly related to the procedure. Pulmonary hypertension is
thought to increase the risk of serious complications, though a study of patients with
average pulmonary arterial pressures of 74/34 mm Hg developed no major
complications or deaths associated with pulmonary arteriography. The appropriate role
of pulmonary arteriography in the diagnosis of pulmonary thromboembolism remains a
subject of active debate. There is wide agreement that arteriography is indicated in
several specific situations: in patients with nondiagnostic V/Q scans, intermediate or
high clinical pretest probability of pulmonary thromboembolism, and negative
noninvasive leg studies; in any patient in whom the diagnosis is in doubt when there is
a high clinical pretest probability of pulmonary thromboembolism; and when the
diagnosis of pulmonary thromboembolism must be established with certainty, as when
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a) Hemoptisis
b) Tos
c) Síncope
d) Disnea
e) Dolor torácico pleurítico
a) Fiebre
b) Flebitis
c) Cianosis
d) Taquipnea
e) Taquicardia
a) Micrognatia
b) Prognatismo
c) Disminución del tamaño de los senos paranasales
d) Hipotelorismo
e) Microglosia
Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses.
Afterward, acromegaly develops. The term "acromegaly," meaning extremity
enlargement, seriously understates the manifestations. The hands enlarge and a
doughy, moist handshake is characteristic. The fingers widen, causing patients to
enlarge their rings. Carpal tunnel syndrome is common. The feet also grow, particularly
in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat
size increases. The mandible becomes more prominent, causing prognathism
and malocclusion. Tooth spacing widens. Macroglossia occurs, as does
hypertrophy of pharyngeal and laryngeal tissue; this causes a deep, coarse voice and
sometimes makes intubation difficult. Obstructive sleep apnea may occur. A goiter may
be noted. Hypertension (50%) and cardiomegaly are common. At diagnosis, about 10%
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of acromegalic patients have overt heart failure, with a dilated left ventricle and a
reduced ejection fraction. Weight gain is typical, particularly of muscle and bone.
Insulin resistance is usually present and frequently causes diabetes mellitus (30%).
Arthralgias and degenerative arthritis occur. Overgrowth of vertebral bone can cause
spinal stenosis. Colon polyps are common, especially in patients with skin papillomas.
The skin may also manifest hyperhidrosis, thickening, cystic acne, and areas of
acanthosis nigricans. GH-secreting pituitary tumors usually cause some degree of
hypogonadism, either by cosecretion of prolactin or by direct pressure upon normal
pituitary tissue. Decreased libido and impotence are common, as are irregular menses
or amenorrhea. Secondary hypothyroidism sometimes occurs; hypoadrenalism is
unusual. Headaches are frequent. Temporal hemianopia may occur as a result of the
optic chiasm being impinged by a suprasellar growth of the tumor.
a) Hipermenorrea
b) Menorragia
c) Oligomenorrea
d) Metrorragia
e) Amenorrea
a) Deficiencia de vitamina B 12
b) Rasgo de talasemia alfa
c) Deficiencia de hierro
d) Esferocitosis hereditaria
e) Hemoglobinuria nocturna paroxística
a) Ferritina sérica
b) Cuenta de reticulocitos
c) Hierro sérico
d) Porcentaje de saturación de transferrina
e) Reservas de hierro de la medula ósea
Iron deficiency is the most common cause of anemia worldwide. Iron is necessary for
the formation of heme and other enzymes. Total body iron ranges between 2 and 4 g:
approximately 50 mg/kg in men and 35 mg/kg in women. Most (70-95%) of the iron is
present in hemoglobin in circulating red blood cells. One milliliter of packed red blood
cells (not whole blood) contains approximately 1 mg of iron. In men, red blood cell
volume is approximately 30 mL/kg. A 70-kg man will therefore have approximately
2100 mL of packed red blood cells and consequently 2100 mg of iron in his circulating
blood. In women, the red cell volume is about 27 mL/kg; a 50-kg woman will thus have
1350 mg of iron circulating in her red blood cells. Only 200-400 mg of iron is present in
myoglobin and nonheme enzymes. Aside from circulating red blood cells, the major
location of iron in the body is the storage pool, as ferritin or as hemosiderin and in
macrophages. The range for storage iron is wide (0.5-2 g); approximately 25% of
women in the United States have none. The average American diet contains 10-15 mg
of iron per day. About 10% of this amount is absorbed. Absorption occurs in the
stomach, duodenum, and upper jejunum. Dietary iron present as heme is efficiently
absorbed (10-20%) but nonheme iron less so (1-5%), largely because of interference by
phosphates, tannins, and other food constituents. Small amounts of
iron¾approximately 1 mg/d¾are normally lost though exfoliation of skin and mucosal
cells. There is no physiologic mechanism for increasing normal body iron losses.
Menstrual blood loss in women plays a major role in iron metabolism. The average
monthly menstrual blood loss is approximately 50 mL, or about 0.7 mg/d. However,
menstrual blood loss may be five times the average. To maintain adequate iron stores,
women with heavy menstrual losses must absorb 3-4 mg of iron from the diet each
day. This strains the upper limit of what may reasonably be absorbed, and women with
menorrhagia of this degree will almost always become iron deficient without iron
supplementation. In general, iron metabolism is balanced between absorption of 1
mg/d and loss of 1 mg/d. Pregnancy may also upset the iron balance, since
requirements increase to 2-5 mg of iron per day during pregnancy and lactation.
Normal dietary iron cannot supply these requirements, and medicinal iron is needed
during pregnancy and lactation. Repeated pregnancy (especially with breast-feeding)
may cause iron deficiency if increased requirements are not met with supplemental
medicinal iron. Decreased iron absorption can on very rare occasions cause iron
deficiency and usually occurs after gastric surgery, though concomitant bleeding is
frequent. By far the most important cause of iron deficiency anemia is blood loss,
especially gastrointestinal blood loss. Chronic aspirin use may cause it even without a
documented structural lesion. Iron deficiency demands a search for a source of
gastrointestinal bleeding if other sites of blood loss (menorrhagia, other uterine
bleeding, and repeated blood donations) are excluded. Chronic hemoglobinuria may
lead to iron deficiency since iron is lost in the urine; traumatic hemolysis due to a
prosthetic cardiac valve and other causes of intravascular hemolysis (eg, paroxysmal
nocturnal hemoglobinuria) should also be considered. As a rule, the only symptoms of
iron deficiency anemia are those of the anemia itself (easy fatigability, tachycardia,
palpitations and tachypnea on exertion). Severe deficiency causes skin and mucosal
changes, including a smooth tongue, brittle nails, and cheilosis. Dysphagia because of
the formation of esophageal webs (Plummer-Vinson syndrome) also occurs. Many iron-
deficient patients develop pica, craving for specific foods (ice chips, etc) often not rich
in iron. Iron deficiency develops in stages. The first is depletion of iron stores. At this
point, there is anemia and no change in red blood cell size. The serum ferritin will
become abnormally low. A ferritin value less than 30 mcg/L is a highly reliable indicator
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of iron deficiency. The serum total iron-binding capacity (TIBC) rises. Bone marrow
biopsy for evaluation of iron stores is now rarely performed because of intraobserver
variation in its interpretation. After iron stores have been depleted, red blood cell
formation will continue with deficient supplies of iron. Serum iron values decline to less
than 30 mcg/dL and transferrin saturation to less than 15%. In the early stages, the
MCV remains normal. Subsequently, the MCV falls and the blood smear shows
hypochromic microcytic cells. With further progression, anisocytosis (variations in red
blood cell size) and poikilocytosis (variation in shape of red cells) develop. Severe iron
deficiency will produce a bizarre peripheral blood smear, with severely hypochromic
cells, target cells, hypochromic pencil-shaped cells, and occasionally small numbers of
nucleated red blood cells. The platelet count is commonly increased. Other causes of
microcytic anemia include anemia of chronic disease, thalassemia, and sideroblastic
anemia. Anemia of chronic disease is characterized by normal or increased iron stores
in the bone marrow and a normal or elevated ferritin level; the serum iron is low, often
drastically so, and the TIBC is either normal or low. Thalassemia produces a greater
degree of microcytosis for any given level of anemia than does iron deficiency. Red
blood cell morphology on the peripheral smear is abnormal earlier in the course of
thalassemia.
a) Talasemia alfa
b) Rasgo trepanocitico
c) Talasemia beta
d) Esferocitosis hereditaria
e) Persistencia hereditaria de hemoglobina fetal
a) Reticulocitosis
b) Consumo de alcohol
c) Deficiencia de folato
d) Deficiencia de vitamina B 12
e) Enfermedad hepática
Folic acid is the term commonly used for pteroylmonoglutamic acid. In its reduced form
of tetrahydrofolate, it serves as an important mediator of many reactions involving
one-carbon transfers. Important reactions include the conversion of homocysteine to
methionine and of deoxyuridylate to thymidylate, an important step in DNA synthesis.
Folic acid is present in most fruits and vegetables (especially citrus fruits and green
leafy vegetables) and daily requirements of 50-100 mcg/d are usually met in the diet.
Total body stores of folate are approximately 5000 mcg, enough to supply
requirements for 2-3 months. By far the most common cause of folate deficiency is
inadequate dietary intake. Alcoholics, anorectic patients, persons who do not eat
fresh fruits and vegetables, and those who overcook their food are candidates for folate
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deficiency. Reduced folate absorption is rarely seen, since absorption occurs from the
entire gastrointestinal tract. However, drugs such as phenytoin, trimethoprim-
sulfamethoxazole, or sulfasalazine may interfere with folate absorption. Folic acid
requirements are increased in pregnancy, hemolytic anemia, and exfoliative skin
disease, and in these cases the increased requirements (five to ten times normal) may
not be met by a normal diet. Patients with increased folate requirements should
receive supplementation with 1 mg/d of folic acid.
a) Leucemia promielocítica
b) Linfoma de linfocitos pequeños
c) Leucemia mieloide crónica
d) Leucemia mieloblástica M2
e) Linfoma de Burkitt
a) Artritis reumatoide
b) Enfermedad de Raynaud
c) Vasculitis
d) Lupus eritematosos sistémico
e) Sífilis secundaria
a) Insuficiencia mitral
b) Estenosis mitral
c) Insuficiencia aórtica
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d) Estenosis aórtica
e) Estenosis tricúspidea
No single specific clinical manifestation or specific laboratory test unequivocally
establishes the diagnosis of rheumatic fever.
Carditis: This important finding in acute rheumatic fever is a pancarditis that involves
the pericardium, epicardium, myocardium, and endocardium. Carditis is the only
residual of acute rheumatic fever that results in chronic changes. Common
manifestations include evidence of valvular insufficiency, most frequently affecting the
mitral valve, but the mitral and the aortic valve may be affected. Isolated involvement
of the aortic valve is rare. Tricuspid valve or pulmonary valve involvement is unusual.
Valvular insufficiency is present in the acute state of the disease. Later, in
the chronic stage, scarring of the valve with either typical "fish-mouth"
abnormality or even calcified valve tissue may lead to stenosis. A combination
of insufficiency and stenosis is often found. Carditis occurs in 40-80% of patients with
rheumatic fever. In the recent outbreaks in the United States, more than 80% of
patients in one of the large series had evidence of carditis. Other manifestations of
carditis include pericarditis, pericardial effusion, and arrhythmias (usually first-degree
heart block, but third-degree or complete heart block may occur). The carditis of
rheumatic fever may be mild or very severe, leading to intractable heart failure; rarely,
surgical intervention, even in the acute stage of the disease, may be necessary if
medical management cannot control the heart failure. These patients usually have
myocardial involvement and significant valvular insufficiency.
Polyarthritis: This is the most confusing of the major criteria and probably leads to
more diagnostic errors than any of the other manifestations. The arthritis of acute
rheumatic fever is exquisitely tender. It is not uncommon for children with this form of
arthritis to refuse to allow even bed sheets or clothing to cover an affected joint. The
joints are red, warm, and swollen. The arthritis is migratory and affects several
different joints: the elbows, knees, ankles, and wrists. It rarely occurs in the fingers,
toes, or spine. It need not be symmetric. Effusions may be present. If the joint is
aspirated, a leukocytosis is usually found; polymorphonuclear leukocytes are the cells
found most frequently. However, there are no specific laboratory findings in the
synovial fluid. The arthritis does not result in chronic joint disease. After anti-
inflammatory therapy is begun, the arthritis may disappear in 12-24 hr. Untreated, it
may persist for a week or more. In many patients with early arthritis of rheumatic
fever, because of treatment with anti-inflammatory drugs, the classic migratory
polyarthritis does not develop, confusing the diagnosis.
Chorea: Sydenham chorea, a unique part of the rheumatic fever syndrome, occurs
much later than other manifestations. These choreoathetoid movements may begin
very subtly. The latent period following streptococcal pharyngitis may be as long as
several months, and the movements are often very difficult to detect at the onset.
However, careful questioning of parents and teachers usually reveals evidence of
increased clumsiness. One of the best signs of this in school-aged children is a marked
deterioration in their handwriting. Emotional lability is a frequent finding. Sydenham
chorea may affect all four extremities or may be unilateral. Although at one time it
could be seen in as many as one half of patients with acute rheumatic fever, more
recent evidence suggests that it occurs, at least in the United States, in 10% or fewer
cases. Sydenham chorea frequently is the only symptom of rheumatic fever. It usually
disappears within weeks to months. It may return, but this has become a rare
occurrence.
Erythema Marginatum: This unique rash seen in patients with rheumatic fever is
another of the major manifestations that can be very difficult to diagnose. It occurs
very infrequently, and therefore few clinicians have had extensive experience in
recognizing it. Although early in the disease it may be manifested as nonspecific pink
macules that are usually seen over the trunk, later in its fully developed form,
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blanching occurs in the middle of the lesions, sometimes with fusing of the borders,
resulting in a serpiginous-looking lesion. This rash can be made worse with application
of heat, but characteristically it is evanescent. The rash does not itch. It often occurs in
patients with chronic carditis. The rash of erythema marginatum can be mistaken for
the rash seen with Lyme disease.
Subcutaneous Nodules: These lesions occur infrequently and are most commonly
observed in patients with severe carditis. These pea-sized nodules are firm and
nontender, and there is no inflammation. They are characteristically seen on the
extensor surfaces of the joints, such as the knees and elbows, and over the spine.
Minor Manifestations: The minor manifestations are much less specific but may be
necessary to confirm a diagnosis of rheumatic fever. They include the clinical findings
of fever and arthralgia. Arthralgia is present if a patient feels discomfort in a joint in the
absence of objective findings (e.g., pain, redness, warmth) on physical examination.
Fever, usually a temperature no higher than 101-102°F, may be present. High
temperature of 103-104°F requires careful re-evaluation and consideration of other
diagnoses.
The major complication of acute rheumatic fever is the development of
rheumatic valvular heart disease. None of the other manifestations results in a
chronic disease. The mitral valve is most frequently involved, but the aortic and
tricuspid valves also may be affected. The tricuspid valve usually becomes involved
only in patients who have significant mitral or aortic disease resulting in pulmonary
hypertension.
a) Thompson
b) Ranson
c) Reiter
d) Jones
e) Child
a) Degenerativa
b) Proliferativa
c) Congénita
d) Inmunológica
e) Tóxica
and brain; and an abnormal immune response by the human host. The search for the
correct hypothesis has been severely hampered by the fact that there is no adequate
animal model. The most popular hypotheses are those that postulate an abnormal
immune response by the human host to some still undefined component of group A
streptococci. The resulting antibodies might then cause the immunologic damage
leading to clinical manifestations. The latent period, usually 1-3 wk between the onset
of the actual group A streptococcal infection and the onset of symptoms of acute
rheumatic fever, lends support to an immunologic mechanism of tissue damage.
Although the specific antigen or antigens responsible for inciting such an immune
response have still to be identified, several possibilities exist. Group A Streptococcus is
a complex microorganism producing a large number of somatic and extracellular
antigens that evoke brisk immune responses. This theory is further supported by the
observation that different humans appear to respond quantitatively differently to
streptococcal antigens. For example, in vitro studies with human lymphocytes show
that individuals can be divided into high and low responders to streptococcal blastogen
A, an extracellular product of the organism. This finding is compatible with the clinical
and epidemiologic observations that not all people appear to be susceptible to
developing rheumatic fever. The possibility of an abnormal immune response is also
based on cross reactivity between group A streptococci M protein and human tissue.
The M protein is the virulence factor that is responsible for the organism's ability to
resist phagocytosis. In addition, after infections with group A streptococci, type-specific
immunity is conferred against the specific M protein type. The group A streptococcal M
protein shares certain amino acid sequences with some human tissues, and this has
been proposed as a possible source of cross reactivity between the organism and its
human host, leading to the abnormal immune response. One of the two classes of M
protein correlates with serotypes of group A streptococci that are frequently isolated
from patients with acute rheumatic fever. In patients with Sydenham chorea, common
antibodies to antigens are found in the group A streptococcal cell membrane and the
caudate nucleus of the brain. This observation further supports the concept of an
abnormal autoimmune mechanism for the central nervous system manifestations of
rheumatic fever and Sydenham chorea. An understanding of the pathogenesis of
rheumatic fever must encompass the differences in human susceptibility to the
development of acute rheumatic fever, including an unusual incidence of rheumatic
fever and rheumatic heart disease among members of certain family groups. In regard
to this genetic influence, a specific alloantigen is present on the surface of non-T
lymphocytes in 70-90% of rheumatic individuals, but fewer than 30% of "control"
nonrheumatic individuals have the marker. The marker is more common in families in
which there is an index case of rheumatic fever than in nonaffected members of
"control" families. Although humans may have genetic differences in rheumatic
susceptibility, the exact mechanism remains unknown. It is unlikely that the recent
outbreaks of acute rheumatic fever in the United States are caused by an increasingly
susceptible population based only on genetics. It is most likely that the pathogenetic
mechanism for the development of rheumatic fever after upper respiratory tract
infection with group A beta-hemolytic streptococci involves a combination of specific
characteristics of the organism and some yet incompletely defined genetic
predisposition in the human host.
a) Atenolol
b) Metoprolol
c) Betaxolol
d) Propanolol
e) Acebutolol
a) Biopsia excisional
b) Biopsia incisional
c) Aspiración con aguja para citología
d) Estudio de captación de yodo radioactivo
e) Examen de tiroides con ultrasonido
1020.- Virus conocidos como agentes etiológicos del carcinoma del cuello
uterino:
Aunque es por todos conocido que la infección por VPH tipo 16 y 18 es característica de
lesiones precancerosas para cérvix y vulva, también esta documentado que la
infección por VHS tienen un rasgo de recurrencia del 65% que se relaciona con una
mayor incidencia de cáncer de cérvix, y que además facilita el contagio por VIH.
Ceftriaxona
Gentamicina
Trimetropin/Sulfametoxasol
Colimicina
Furazolidona
a) 9 meses
b) 12 meses
c) 15 meses
d) Previo al ingreso a la escuela (preescolar)
e) Inició de la adolescencia
a) Isoniazida
b) Rifampicina
c) Fenobarbital
d) Trimetoprim-sulfametoxazol
e) Difenilhidantoina
a) Hipotalamo
b) Núcleos amigdalinos
c) Hipocampo
d) Lóbulo frontal
e) Núcleo anterior
La causa más común de muerte en las primeras 48 hrs posteriores a un infarto agudo
del miocardio es la fibrilación ventricular (FV). Entre otras causas se mencionan la
rotura cardiaca, bombeo insuficiente debido a infarto masivo, complicaciones
mecánicas agudas como la rotura del tabique ventricular o regurgitación mitral aguda
y choque cardiogénico.
a) Anafilaxia
b) Citotoxicidad por anticuerpos
c) Deposito de complejos inmunes
d) Hipersensibilidad retardada
e) Daño tisular mediado por células
genes, and HLA class III genes encoding C´2 and C´4). The relevant HLA DR/DQ genes
increase risk for SLE by approximately twofold if one susceptibility haplotype is present
and by four- to sixfold if two or more are present. Some proteins important in clearing
apoptotic cells play a role in genetic susceptibility; for example, homozygous
deficiencies of early components of complement Clq, C´2, and C´4 and certain alleles
of mannose-binding ligand increase the risk for SLE. Clq deficiency confers the highest
genetic risk known but is rare. There are at least five chromosomal regions
independent of HLA that contain susceptibility genes. Within one of these regions on
chromosome 1 are alleles encoding Fc? receptors that bind subsets of IgG (IgG1, -2, or
-3): African Americans inheriting one allele of Fc?RIIA have a receptor that binds the Ig
in immune complexes weakly; those persons have increased risk for lupus nephritis.
Caucasians and Asians in some populations with alleles of Fc?RIIIA that bind Ig weakly
are predisposed to SLE. A region on chromosome 16 contains genes that predispose to
SLE, rheumatoid arthritis, psoriasis, and Crohn's disease, suggesting the presence of
"autoimmunity genes" that, when interacting with other genes, predispose to different
autoimmune diseases. Thus, SLE is modified by multiple susceptibility genes, some of
which interact. There are likely to be protective gene alleles as well. These gene
combinations influence immune responses to the external and internal environment;
when such responses are too high and/or too prolonged, autoimmunity results. Female
gender is permissive for SLE; females of many mammalian species make higher
antibody responses than males. Women exposed to estrogen-containing oral
contraceptives or hormone replacement have an increased risk of developing SLE
(approximately twofold). Estradiol binds to receptors on T and B lymphocytes,
increasing activation and survival of those cells, thus favoring prolonged immune
responses. Several environmental stimuli may influence SLE1. Exposure to ultraviolet
light causes SLE flares in approximately 70% of patients, possibly by increasing
apoptosis in keratinocytes and other cells or by altering DNA and intracellular proteins
to make them antigenic. It is likely that various infections that stimulate immune
responses (antibodies and activated T lymphocytes) that cross-react with self or
responses that, as they mature, develop the ability to recognize self can promote
autoimmune responses that lead to SLE. The observation that children and adults with
SLE are more likely to be infected by Epstein-Barr Virus (EBV) than age-, gender-, and
ethnically matched controls without SLE is intriguing, because EBV activates B
lymphocytes and also contains amino acid sequences that mimic sequences on human
spliceosomes — a common autoantibody specificity in people with SLE. Thus, interplay
between genetic susceptibility, gender, and environmental stimuli may result in
autoimmunity. For maximal production of harmful autoantibodies, B cells require help
from T cells, and those functions of T and B cells are normally downregulated by
several mechanisms. In murine SLE models, many downregulating networks are
abnormal, including generation of multiple types of regulatory and natural killer T cells
and of humoral idiotypic downregulating networks. In SLE, biopsies of affected skin
show deposition of Ig at the dermal-epidermal junction (DEJ), injury to basal
keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around
blood vessels and dermal appendages. Clinically unaffected skin may also show Ig
deposition at the DEJ. In renal biopsies, the pattern of injury is important in diagnosis
and in selecting the best therapy. The World Health Organization (WHO) has classified
lupus nephritis as grade I (no histologic changes), II (proliferative changes confined to
the mesangium), III (proliferative changes in tufts of 10 to 50% of glomeruli; higher
proportions of glomeruli affected suggest worse prognosis), IV [diffuse proliferative
glomerulonephritis (DPGN) affecting >50% of glomeruli], V (predominantly
membranous changes with various degrees of proliferation), and VI (end stage, scarred
glomeruli). In addition, pathologists report the extent of inflammatory (potentially
reversible) and chronic (irreversible scarring in glomeruli, renal tubules, and blood
vessels) changes. In general, treatment for lupus nephritis is not recommended in
patients with class I or II disease or with extensive irreversible changes. In contrast,
a) AINEs
b) Alopurinol y glucocorticoides
c) Colchicina y AINEs
d) Pirazona y alopurinol
e) Cirugía para extracción de tofos
Monosodium urate (MSU) gout is a metabolic disease most often affecting middle-aged
to elderly men and postmenopausal women. It is typically associated with an increased
uric acid pool, hyperuricemia, episodic acute and chronic arthritis, and deposition of
MSU crystals in connective tissue tophi and kidneys. Acute arthritis is the most
frequent early clinical manifestation of MSU gout. Usually, only one joint is affected
initially, but polyarticular acute gout is also seen in male hypertensive patients with
ethanol abuse as well as in postmenopausal women. The metatarsophalangeal joint of
the first toe is often involved, but tarsal joints, ankles, and knees are also commonly
affected. In elderly patients, finger joints may be inflamed. Inflamed Heberden's or
Bouchard's nodes may be a first manifestation of gouty arthritis. The first episode of
acute gouty arthritis frequently begins at night with dramatic joint pain and swelling.
Joints rapidly become warm, red, and tender, and the clinical appearance often mimics
a cellulitis. Early attacks tend to subside spontaneously within 3 to 10 days, and most
of the patients do not have residual symptoms until the next episode. Several events
may precipitate acute gouty arthritis: dietary excess, trauma, surgery, excessive
ethanol ingestion, adrenocorticotropic hormone (ACTH) and glucocorticoid withdrawal,
hypouricemic therapy, and serious medical illnesses such as myocardial infarction and
stroke. After many acute mono- or oligoarticular attacks, a proportion of gouty patients
may present with a chronic nonsymmetric synovitis, causing potential confusion with
rheumatoid arthritis. Less commonly, chronic gouty arthritis will be the only
manifestation and, more rarely, the disease will manifest as inflamed or noninflamed
periarticular tophaceous deposits in the absence of chronic synovitis. Women represent
only 5 to 17% of all patients with gout. Premenopausal gout is a rare occurrence and
accounts for only about 17% of all women with gout; it is seen mostly in individuals
with a strong family history of gout. A few kindreds of precocious gout in young
females caused by decreased renal urate clearance and renal insufficiency have been
described. Most women with gouty arthritis are postmenopausal and elderly, have
arterial hypertension causing mild renal insufficiency, and are usually receiving
diuretics. Also, most of these patients have underlying degenerative joint disease, and
inflamed tophaceous deposits may be seen on Heberden's and Bouchard's nodes. The
mainstay of treatment during an acute attack is the administration of an anti-
inflammatory drug such as colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs),
or glucocorticoids depending on the age of the patient and comorbid conditions. Both
colchicine and NSAIDs may be quite toxic in the elderly, particularly in the presence of
renal insufficiency and gastrointestinal disorders. In elderly patients, one may favor the
use of intraarticular glucocorticoid injections for attacks involving one or two larger
joints or ice pack applications along with lower oral doses of colchicine for gouty
synovitis affecting small joints. Colchicine given orally is a traditional and effective
treatment, if used early in the attack, in at least 85% of patients. One tablet (0.6 mg) is
given every hour until relief of symptoms or gastrointestinal toxicity occurs, or a total
of four to eight tablets may be given in accordance with the age of the patient. The
drug must be stopped promptly at the first sign of loose stools, and symptomatic
treatment must be given for the diarrhea. Intravenous colchicine is sometimes used
and can reduce, though not eliminate, the gastrointestinal side effects. Intravenous
colchicine is most reliable for pre- or postoperative prophylaxis in 1- to 2-mg doses
when patients cannot take medications orally. Life-threatening colchicine toxicity and
sudden death have been described with the administration of >4 mg/d intravenously.
The intravenous dose for acute gouty arthritis is 1 to 2 mg given slowly through an
established venous line over 10 min in a soluset, and two additional doses of 1 mg
each may be given at 6-h intervals, but the total dose should never exceed 4 mg.
NSAIDs are affective in ~90% of patients, and the resolution of signs and symptoms
usually occurs in 5 to 7 days. The most effective drugs are those with a short half-life
and include indomethacin, 25 to 50 mg tid, ibuprofen, 800 mg tid, or diclofenac, 50 mg
tid. Cyclooxigenase-2 highly selective inhibitors are probably equally effective but with
less short-term gastrointestinal toxicity. Oral glucocorticoids such as prednisone, 30 to
50 mg/d as the initial dose and tapered over 5 to 7 days, a single intravenous dose of
methylprednisolone, 7 mg of betametasone, or 20 to 40 mg of intraarticular
triamcinolone acetonide have been equally effective. ACTH2 as an intramuscular
injection of 40 to 80 IU in a single dose or every 12 h for 1 to 2 days is effective in
patients with acute polyarticular refractory gout or with a contraindication for using
colchicine or NSAIDs. Attempts to normalize serum uric acid to <300 umol/L (5.0
mg/dL) to prevent recurrent gouty attacks and eliminate tophaceous deposits entail a
commitment to long-term hypouricemic regimens and medications that generally are
required for life. Hypouricemic therapy should be considered when the hyperuricemia
cannot be corrected by simple means (control of body weight, low-purine diet, increase
in liquid ingestion, limitation of ethanol intake, and avoidance of diuretic use). The
decision to initiate hypouricemic therapy is usually made taking into consideration the
number of acute attacks, family history of gout, presence of MSU1 tophaceous
deposits, uric acid excretion >800 mg per 24 hours, presence of uric acid stones, and
risk for acute uric acid nephropathy during chemotherapy for myeloproliferative
disorders. Uricosuric agents, such as probenecid, can be used in patients with good
renal function who underexcrete uric acid, with <600 mg in a 24-hour urine sample.
Urine volume must be maintained by ingestion of 1500 mL of water every day.
Probenecid can be started at a dosage of 200 mg twice daily and increased gradually
a) Litiasis urinaria
b) Infección de vías urinarias
c) Pielonefritis enfisematosa
d) Cistitis
e) Prostatitis
a) Ácido úrico
b) Pirofosfato de calcio
c) Hidroxiapatita
d) Estruvita
e) Fosfato de calcio
a) Poliartritis infecciosa
b) Fiebre reumática
c) Osteoartritis
d) Artritis reumática
e) Artropatía por deposito de cristales
least 20% of disability in patients with RA, greater than the 14% attributable to
articular signs and symptoms. In another study, helplessness had a direct effect on
disease activity.
a) Crisis de Stoke-Adams
b) Embolia cerebral
c) Hemorragia cerebral intraparenquimatosa
d) Trombosis cerebral
e) Hemorragia subaracnoidea
1034.- Segundo enunciado: La causa más probable del cuadro clínico actual
del paciente es:
a) Warfarina
b) Plasma fresco congelado
c) Heparina
d) Marcapaso temporal
e) Atropina
Intracardiac thrombi, which complicate many types of heart disease, are important
because of their potential to embolize. Those in the left atrium and ventricle may
embolize to the systemic circulation and are a significant cause of stroke. Acute
anticoagulation can be a temporary bridge to chronic anticoagulation in selected
clinical settings. Acute anticoagulation can be achieved with either unfractionated
heparin or low-molecular-weight heparin. The purpose of replacing diseased native
heart valves is primarily to improve hemodynamics and hence functional status and
long-term survival. The first prosthetic valves were mechanical, and although the
hemodynamic status improved following implantation, thromboembolic complications
occurred and caused such disastrous complications as stroke. Initially it was unclear
whether thromboembolism was caused by the introduction of a foreign body into the
circulation or by the underlying pathology. Thromboembolic risk continues well after
endothelialization of the sewing ring has occurred, suggesting that the mechanical
prosthesis or underlying cardiac abnormality is the cause. Whatever the mechanism, it
is apparent that these complications can be reduced with anticoagulation. Because a
mechanical prosthesis necessitates life-long anticoagulation, it is important to evaluate
patients for hemorrhagic risk prior to valve surgery. For women of child-bearing age, an
important consideration is the type of valve (mechanical or biologic) to be implanted
because of the risks of anticoagulation with pregnancy. When using anticoagulation to
reduce the thromboembolic complications associated with prosthetic valves, however,
it is important to recognize that no antithrombotic regimen guarantees a
thromboembolus-free course or a hemorrhage-free valve implant.
a) Carbamacepina y penicilina
b) Ceftriaxona y fenobarbital
c) Gluconato de calcio y sulfato de magnesio
d) Ceftriaxona y sulfato de magnesio
e) Sulfato de magnesio y fenobarbital
a) Parasitaria
b) Febril
c) Micotica
d) Bacteriana
e) Viral
a) Fenobarbital
b) Furosemida
c) Dexametasona
d) Fenitoina
e) Solución glucosada hipertonica
diagnosed; (2) a more rapid form, in which symptoms and signs of meningitis progress
over the course of 1 or 2 days; and (3) a fulminant form, with rapid deterioration and
shock early in the course of illness. Host and bacterial factors influence the type of
presentation. Recognizing the infant or child with meningitis or other invasive bacterial
infection among the large numbers of children with febrile illnesses due to viral or
uncomplicated bacterial infections of the upper respiratory tract requires expertise as
well as careful observation and examination. The differential diagnosis in children with
fever and alteration in CNS function includes other infections, such as viral meningitis,
encephalitis, brain abscess, and subdural or epidural abscess; Lyme disease; rickettsial
or Mycoplasma infections, and leptospirosis. Initial empirical therapy using cefotaxime
or ceftriaxone plus vancomycin (60 mg/kg/day divided q6h) is prudent for children and
infants 1 month and older. Limited clinical data preclude recommendations regarding
rifampin combined with a cephalosporin. In the Hib vaccine era, ampicillin plus
chloramphenicol is not an optimal combination for initial therapy because of its
probable inadequacy against resistant pneumococcal strains. Once an organism has
been identified and the antimicrobial susceptibility pattern is known, antibiotic therapy
can be simplified or modified. Penicillin G can be used to complete therapy for
pneumococcal or meningococcal meningitis due to susceptible organisms. Cefotaxime
or ceftriaxone is continued for penicillin-resistant pneumococci that are susceptible to
these two agents (MIC =0.5 µg/mL). Although many patients with isolates requiring an
MIC of 1.0 µg/mL for third-generation cephalosporins have been treated successfully,
this fact should not be relied on. It is prudent to repeat the CSF examination after 24 to
48 hours of therapy in patients with pneumococcal infection to document a sterile
culture and negative Gram stain. If results of the second CSF culture or Gram stain is
positive, or a pneumococcal isolate requires an MIC of 1.0 µg/mL or greater for
extended-spectrum cephalosporins, vancomycin (if not previously begun) with or
without rifampin should be added.[33] Rifampin should be added if the patient is
already receiving vancomycin. Vancomycin penetration into CSF during meningitis may
be unpredictable, and thus, peak serum levels should be in the upper therapeutic
range (35 to 40 µg/mL). Chloramphenicol is an option for treatment of bacterial
meningitis caused by ampicillin-resistant Hib or in the child with a history of
anaphylaxis or respiratory distress associated with penicillin or other ß-lactam
antibiotics. Because the pharmacokinetics of chloramphenicol is variable, serum
concentrations should be monitored to ensure that safe and effective levels are
achieved.[34] Ideal peak values are 15 to 30 µg/mL at 60 to 120 minutes after the
infusion is complete. Levels exceeding 30 µg/mL are associated with bone marrow
suppression; levels greater than 50 to 80 µg/mL have been related to ”gray baby“
syndrome (which is not confined to infants) and impaired myocardial contractility.
Chloramphenicol is best avoided in children with septic shock. Additionally, several
drugs affect the metabolism of chloramphenicol: Concurrent administration of
phenobarbital and rifampin lowers the chloramphenicol metabolism, whereas
administration of phenytoin raises it. Other potentially useful antimicrobial agents for
the treatment of bacterial meningitis are cefepime and meropenem, both of which
have been shown to be equivalent to third-generation cephalosporins in treatment of
children infected with common meningeal pathogens. The efficacy of these antibiotics
against ß-lactam–resistant pneumococci has not been defined, although it appears not
to be superior to that of cefotaxime or ceftriaxone. The use of imipenem-cilastatin is
not recommended in children with CNS infection because of potential epileptogenic
activity of imipenem in the pediatric population. Because of the increasing rate of
isolation of multiple-drug-resistant pneumococci worldwide, there is an urgent need to
develop antibiotics with different mechanisms of action against these strains.
Accordingly, new fluoroquinolones are currently undergoing clinical evaluation in
children with bacterial meningitis. Modulating the host response to infection may be
beneficial in decreasing some sequelae of meningitis. Prospective studies have shown
that dexamethasone therapy initiated just before or concurrently with the first dose of
Síndrome producido por una lesión del simpático cervical en cualquier punto de su
recorrido; se manifiesta como miosis, ptosis y enoftalmos en el ojo del lado afecto.
a) Anfotericina B
b) Vancomicina
c) Fluconazol
d) Miconazol
e) Ketoconazol
a) 5 a 15 años
b) 20 a 40 años
c) 40 a 50 años
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d) Mayores de 50 años
e) Lactantes menores
Erythema nodosum is an uncommon reaction pattern seen mainly on the anterior tibial
areas of the legs. It appears as erythematous nodules in successive crops and is
preceded by fever, malaise, and arthralgia. Bilateral red, tender, rather well-
circumscribed nodules are seen mainly on the pretibial surface of the legs but also on
the arms and the body. Later, the flat lesions may become raised, confluent, and
purpuric. Only a few lesions develop at one time. Careful clinical and laboratory
examination is necessary to determine the cause of this toxic reaction pattern. The
following tests should be performed: complete blood cell count, erythrocyte
sedimentation rate, urinalysis, serologic test for syphilis, chest roentgenogram, and
specific skin tests, as indicated. The causes of erythema nodosum are streptococcal
infection (rheumatic fever, pharyngitis, scarlet fever, arthritis), fungal infection
(coccidioidomycosis, trichophyton infection), pregnancy, sarcoidosis, lymphogranuloma
venereum, syphilis, chancroid, drugs (contraceptive pills, sulfonamides, iodides,
bromides), and, rarely, tuberculosis. The disorder occurs predominantly in
adolescent girls and young women.
a) Neumonía intraventricular
b) Meningitis
c) Infarto cerebral
d) Hidrocefalia
e) Absceso cerebral
The etiologic agents responsible for septicemia vary according to age and immunologic
status of the patient and the place of microbial acquisition (i.e., community or hospital
setting). In the 1980s and early 1990s, before the widespread implementation of
intrapartum chemoprophylaxis, group B streptococcus (GBS) was the predominant
etiologic agent of neonatal septicemia in the United States. Escherichia coli,
enterococcus, Listeria monocytogenes, non–group D a-hemolytic streptococcus, and
nontypable Haemophilus influenzae are other microorganisms responsible for sepsis
neonatorum. Early-onset neonatal septicemia can have a fulminant course and high
case-fatality rate. GBS and Listeria strains can also cause late-onset septicemia and
meningitis. Nosocomially acquired infection, which appears between the fourth
postnatal day and the time of hospital discharge, can be caused by a variety of
organisms, including coagulase-negative staphylococci, Staphylococcus aureus, gram-
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negative enteric or environmental bacilli, and Candida spp. Herpes simplex virus,
enteroviruses (coxsackievirus and echovirus), and adenovirus must be considered in
the differential diagnosis of a “septic” neonate if (1) no improvement is observed after
initiation of antibiotic therapy and (2) bacterial cultures are sterile. Infants in the
community are exposed to pathogens as maternal protection wanes. Thus, they can
have septicemia due to H. influenzae type b (Hib; in areas where immunization with the
conjugate vaccine is not routine), Streptococcus pneumoniae, and Neisseria
meningitidis. Septicemia in infants younger than 3 months can be caused by either
neonatal or non-neonatal pathogens. Additionally, S. aureus and Salmonella spp. cause
invasive disease. Occasionally, viruses such as respiratory syncytial virus,
enteroviruses, and adenovirus can cause clinical findings indistinguishable from those
in bacterial infection. Sepsis not associated with an obvious site of infection is less
common in patients without underlying disorders who are older than 5 years of age.
Meningococcemia can occur in this age group, and acute disseminated group A
streptococcal and staphylococcal infection can occur in otherwise healthy children.
Patients with S. aureus septicemia usually have primary or secondary foci of infection
in the lung, bone, joint, heart, or brain. Children with invasive streptococcal infection
may or may not have primary soft tissue infection or pharyngitis; secondary sites of
infection are common. Rocky Mountain spotted fever is another important diagnosis to
consider in a child with sepsis syndrome and a rash that is maculopapular, petechial, or
both. Ehrlichiosis also can cause SIRS with or without rash. In infants and children with
nosocomial infection and in patients with primary or secondary immunodeficiency, a
broad array of common and uncommon bacteria cause sepsis. Certain conditions can
predispose children to septicemia caused by specific pathogens: Asplenia or sickle cell
disease can predispose to septicemia due to S. pneumoniae or Salmonella septicemia;
nephrotic syndrome to S. pneumoniae septicemia or peritonitis; and human
immunodeficiency virus (HIV) infection to S. pneumoniae, Hib, S. aureus, or
Pseudomonas aeruginosa septicemia. Viridans streptococci have been increasingly
recognized as common etiologic agents of severe sepsis syndrome in neutropenic
patients, particularly those treated with high doses of cytarabine. Cytomegalovirus
infection must be considered in the immunocompromised host with a clinical sepsis
syndrome. Septicemia caused by most organisms has a typical clinical course,
progressing from fever and acute inflammation to shock and multiorgan dysfunction
syndrome (MODS), with attendant physiologic derangements. Progression can be
insidious (e.g., coagulase-negative staphylococcal infection or typhoid fever) or
fulminant (e.g., meningococcemia, streptococcal or staphylococcal toxic shock).
Early-onset bacterial infections appear most commonly on day 1 of life, and the
majority of cases appear at less than 12 hours. Respiratory distress due to pneumonia
is the most common presenting sign. Other features include unexplained low Apgar
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scores without fetal distress, poor perfusion, and hypotension. Late-onset bacterial
infection (at more than 5 days of age) presents in a more subtle manner, with poor
feeding, lethargy, hypotonia, temperature instability, altered perfusion, new or
increased oxygen requirement, and apnea. Late-onset bacterial sepsis is more
often associated with meningitis or other localized infections. Low total white
counts, absolute neutropenia (< 1000/mL), and elevated ratios of immature to mature
neutrophils are suggestive of neonatal bacterial infection. Thrombocytopenia is also a
common feature. Other laboratory signs are hypoglycemia or hyperglycemia with no
change in glucose administration, unexplained metabolic acidosis, and elevated C
reactive protein. In early-onset bacterial infection, pneumonia is invariably present;
chest x-ray films show infiltrates, but these infiltrates cannot be distinguished from
those resulting from other causes of neonatal lung disease. Definitive diagnosis is
made by positive cultures from blood, CSF, and the like. Early-onset infection is most
often caused by group B b-hemolytic streptococci (GBS) and gram-negative enteric
pathogens (most commonly E coli). Another organism to consider is Haemophilus
influenzae. Late-onset sepsis is caused by coagulase-negative staphylococci (most
common in infants with indwelling central venous lines), Staphylococcus aureus, GBS,
Enterococcus, Pseudomonas, and other gram-negative organisms.
a) Avitaminosis B
b) Escorbuto
c) Avitaminosis A
d) Raquitismo
e) Pelagra
a) Retinoides
b) Calciferol
c) Ácido Ascórbico
d) Vitaminas del complejo B
e) Niacina
primary dietary source is vitamin D–fortified milk and formulas. Egg yolk and fatty fish
contain some vitamin D. Vitamin D absorption depends on normal fat absorption.
Absorbed vitamin D is transported to the liver in chylomicrons. Vitamins D2 and D3
undergo 25-hydroxylation in the liver and then 1a-hydroxylation in kidney proximal
tubules to yield 25-hydroxycholecalciferol (calcifediol) and calcitriol, respectively. PTH
activates the 1a-hydroxylase enzyme in the kidney. Calcifediol is the major circulating
form of vitamin D. Calcitriol is the biologically active form of vitamin D. Calcitriol
stimulates the intestinal absorption of calcium and phosphate, the renal reabsorption of
filtered calcium, and the mobilization of calcium and phosphorus from bone. Vitamin D
deficiency results from lack of adequate sunlight coupled with a low dietary intake. An
infant requires only 30 minutes per week of total body sun exposure or 2 hours per
week of head exposure to maintain adequate vitamin D status. The young breast-fed
infant can acquire sufficient vitamin D from human milk if the mother's vitamin D
status is optimal. Otherwise, a vitamin D supplement is required to avoid risk of rickets.
In the United States, cow's milk and infant formulas are routinely supplemented with
vitamin D. Nutritional rickets may occur in older infants and children who are not
exposed to the sun or whose skin is deeply pigmented and who do not drink vitamin D
fortified milk. Vitamin D deficiency also occurs in fat malabsorption syndromes,
including small intestinal disease, cholestasis, and lymphatic obstruction. Use of P-450–
stimulating drugs may decrease hydroxylated vitamin D, which can also be decreased
by hepatic and renal disease and by inborn errors of metabolism. End-organ
unresponsiveness to calcitriol may also occur. The clinical effects of vitamin D
deficiency are osteomalacia (adults) or rickets (children), in which there is an
accumulation in bone of osteoid (matrix) with reduced calcification. Cartilage fails to
mature and calcify. The effects include craniotabes, rachitic rosary, pigeon breast,
bowed legs, delayed eruption of teeth and enamel defects, Harrison groove, scoliosis,
kyphosis, dwarfism, painful bones, fractures, anorexia, and weakness. X-ray findings
include cupping, fraying, and flaring of metaphyses; the loss of sharp definition
of bone trabeculae accounts for the general decrease in skeletal radiodensity. The
diagnosis is supported by characteristic radiologic abnormalities of the skeleton, low
serum phosphorus levels, high serum alkaline phosphatase levels, and high PTH levels.
The diagnosis can be confirmed by a low level of serum calcifediol. Rickets is treated
with 1600–5000 IU/d of vitamin D3 (1 IU = 0.25 µg). If this is poorly absorbed,
calcifediol, 2 µg/kg/d, or calcitriol, 0.05–0.2 µg/kg/d, is given. Renal osteodystrophy is
treated with calcitriol.
a) Anticuerpos anti-acetilcolina
b) Anticuerpos antigliadina
c) Anticuerpos antinucleares
d) Anticuerpos anti-centromero
e) Anticuerpos anti-VHC
Primary biliary cirrhosis (PBC) is an autoimmune liver disease that generally affects
middle-aged women and is the most common chronic cholestatic liver disease in adults
in the United States. PBC is characterized by ongoing inflammatory destruction of the
interlobular and septal bile ducts that leads to chronic cholestasis and biliary cirrhosis,
with consequent complications such as portal hypertension and liver failure. Evidence
for an immunologic cause of PBC includes immunohistochemical data showing the
presence of activated T cells in areas of bile duct destruction, the presence of highly
specific autoantibodies reactive with antigens on the surface of biliary epithelial cells,
and the association of PBC with other disorders thought to be autoimmune in nature.
PBC may be discovered incidentally on routine blood testing but also can present with
pruritus or fatigue. The diagnosis should be considered in the setting of elevated serum
alkaline phosphatase, cholesterol, and immunoglobulin M (IgM) levels. The presence
of antimitochondrial antibody in serum is highly characteristic of the disease.
Ursodeoxycholic acid (UDCA) is the only medication of proven benefit for patients with
PBC; liver transplantation represents a life extending alternative for patients who have
end-stage PBC. It also is important to recognize and treat the complications of chronic
cholestasis, such as osteopenic bone disease, fat-soluble vitamin deficiency,
hypercholesterolemia, and steatorrhea. Survival models are used in determining the
prognosis of the disease as well as the timing of liver transplantation. AMAs have been
shown to be directed against the E2 component of the pyruvate dehydrogenase
complex (PDC-E2), the E2 unit of the branched-chain 2-oxo-acid dehydrogenase
complex (BCOADC-E2), and the E2 subunit of the 2-oxo-glutarate dehydrogenase
complex (OGDC-E2), as well as the E1 subunit of PDC and protein X. These enzymes all
are located on the inner mitochondrial membranes. At least one of these components
usually reacts with AMA in patients with PBC. The most frequent antigen against which
AMAs are directed is PDC-E2; PDC-E2 reacting antibodies are present in more than 90%
of PBC patients. AMAs are not the only PBC-specific autoantibodies. Antibodies
against the nuclear pore protein gp210, a transmembrane glycoprotein, are found
in 25% of patients who have AMA-positive PBC and in up to 50% of those who have
AMA-negative PBC. Their specificity for PBC when detected by immunoblotting is above
99%, and they seem to have prognostic importance. Antibodies against p62, a nuclear
pore glycoprotein, are found in about 25% of patients with PBC and are highly specific
for PBC. Anti-p62 antibodies and anti-gp210 antibodies appear to be mutually exclusive
in PBC patients. AMAs are present in serum in approximately 90% to 95% of patients
with PBC. The M2 antibody, which is directed against the pyruvate dehydrogenase
complex of the inner mitochondrial membrane, has a sensitivity rate of 98% and
specificity rate of 96% for the diagnosis of PBC. Other autoantibodies found in patients
with PBC are rheumatoid factor (70%), antismooth muscle antibody (66%), antithyroid
(antimicrosomal, antithyroglobulin) antibody (41%), and antinuclear antibody
(35%).
a) Choque eléctrico
b) Haloperidol
c) Diazepam
d) Paroxetina
e) Fenitoina
An acutely agitated or psychotic patient can be calmed in a very short period of time.
For several years various protocols for rapid neuroleptization were promulgated;
however, it was never demonstrated that rapid relief of acute psychosis led to shorter
hospitalizations or that it was in the best interests of the patient to use this treatment.
A common practice in the United States is to administer high-potency
dopamine receptor antagonist (haloperidol), intramuscularly if necessary and
a benzodiazepine concurrently. This allows for a lower dose of the antipsychotic,
and a decreased likelihood of extrapyramidal adverse effects. Although there are as yet
no controlled studies regarding the use of the newer seroton-dopamine antagonists or
anticonvulsants in emergency room settings, their efficacy and relative lack of
extrapyramidal symptoms make them potentially useful alternatives.
Los antipsicóticos típicos tienen como mecanismo de acción el bloquear el receptor
post-sinaptico D2 de la dopamina. Sus usos cliniclos incluyen: tratamiento de la
esquizofrenia, psicósis asociada a otra enfermedad mental, tratamiento de síntomas
positivos (ej, alucinaciones, delusiones, thought broadcasting, etc).
a) Carcinoma basocelular
b) Epitelioma espinocelular
c) Enfermedad de Bowen
d) Carcinoma espinoso
e) Melanoma
Basal cell carcinoma is the most common malignancy of the skin. Fortunately, a basal
cell epithelioma or carcinoma is almost never a metastasizing tumor, and the cure rate
can be close to 100% if these lesions are treated early and adequately. There are four
clinical types of basal cell carcinoma: (1) noduloulcerative, (2) pigmented, (3) fibrosing
(sclerosing, morphea-like), and (4) superficial. The noduloulcerative basal cell
carcinoma is the most common type. It begins as a small waxy nodule that enlarges
slowly over the years. A central depression usually forms that eventually progresses
into an ulcer surrounded by a pearly or waxy border. The surface of the nodular
component has a few telangiectatic vessels, which are highly characteristic. The
pigmented type is similar to the noduloulcerative form, with the addition of brown or
black pigmentation. The fibrosing type is extremely slow growing, is usually seen on
the face, and consists of a whitish, scarred plaque with an ill-defined border, which
rarely becomes ulcerated. This type is difficult to treat. The superficial form may be
single or multiple, is usually seen on the back and the chest, and is characterized by
slowly enlarging red, scaly areas that, on careful examination, reveal a nodular border
with telangiectatic vessels. A healed atrophic center may be present. Ulceration is
superficial when it develops.
a) Cretinismo
b) Escorbuto
c) Beriberi
d) Raquitismo
e) Osteogénesis imperfecta
1053.- El germen que con mayor frecuencia produce infeccion de las vias
urinarias en los pacientes diabeticos es:
a) Escherichia coli
b) Staphylococcus aureus
c) Staphylococcus epidermidis
d) Proteus mirabilis
e) Pseudomona aeruginosa
Individuals with DM have a greater frequency and severity of infection. The reasons for
this include incompletely defined abnormalities in cell-mediated immunity and
phagocyte function associated with hyperglycemia, as well as diminished
vascularization. Hyperglycemia aids the colonization and growth of a variety of
organisms (Candida and other fungal species). Many common infections are more
frequent and severe in the diabetic population, whereas several rare infections are
seen almost exclusively in the diabetic population. Examples of this latter category
includes rhinocerebral mucormycosis, emphysematous infections of the gall bladder
and urinary tract, and "malignant" or invasive otitis externa. Invasive otitis externa is
usually secondary to P. aeruginosa infection in the soft tissue surrounding the external
auditory canal, usually begins with pain and discharge, and may rapidly progress to
osteomyelitis and meningitis. These infections should be sought, in particular, in
patients presenting with hyperglycemic hyperosmolar state. Pneumonia, urinary tract
infections, and skin and soft tissue infections are all more common in the diabetic
population. In general, the organisms that cause pulmonary infections are similar to
those found in the nondiabetic population; however, gram-negative organisms, S.
aureus, and Mycobacterium tuberculosis are more frequent pathogens. Urinary tract
infections (either lower tract or pyelonephritis) are the result of common
bacterial agents such as Escherichia coli, though several yeast species
(Candida and Torulopsis glabrata) are commonly observed. Complications of
urinary tract infections include emphysematous pyelonephritis and emphysematous
cystitis. Bacteriuria occurs frequently in individuals with diabetic cystopathy.
Susceptibility to furunculosis, superficial candidal infections, and vulvovaginitis are
increased. Poor glycemic control is a common denominator in individuals with these
infections. Diabetic individuals have an increased rate of colonization of S. aureus in
the skin folds and nares. Diabetic patients also have a greater risk of postoperative
wound infections. Strict glycemic control reduces postoperative infections in diabetic
individuals undergoing coronary artery bypass grafting and should be the goal in all
diabetic patients with an infection.
1054.- Recien nacido prematuro con peso de 1,250 gramos y apgar de 6-7,
inicio a los pocos minutos de vida con quejido respiratorio, taquipnea, tiros
intercostales bajos, retraccion xifoidea, aleteo nasal y acrocianosis. El
diagnostico más probable es:
a) Neumonía in utero
b) Aspiración de meconio
c) Mala adaptación pulmonar
d) Enfermedad de la membrana hialina
e) Taquipnea transitoria del recien nacido
The respiratory distress syndrome (RDS) is the most common cause of death among
premature infants. It is caused by immaturity of the lungs and occurs in approximately
70% of infants weighing less than 1,500 g, but in less than 1% of those whose birth
weight is over 2,500 g. Males, infants of diabetic mothers, infants delivered by
cesarean section, and infants born to a mother who has had a previous child with RDS
have a particularly high incidence of this disorder. Asphyxia during labor or delivery
also seems to predispose the neonate to RDS. Conditions that may lessen the risk of
RDS include prolonged rupture of membranes, maternal drug addiction, and
intrauterine growth retardation. The primary abnormality in RDS appears to be
deficient synthesis or release of pulmonary surfactant. This material lines the alveoli of
the mature lung and lowers the surface tension required to keep the alveolus open
during expiration. When surfactant is deficient, diffuse alveolar atelectasis ensues,
resulting in pulmonary insufficiency. Surfactant production is normally very low in utero
until the third trimester of pregnancy; it then increases gradually until 33–36 weeks'
gestation, when there is an abrupt rise to near-term levels. Respiratory distress often
develops in infants born prior to this “surge” and does not improve until surfactant
production “turns on” at 48–72 hours after birth. Those who die during the acute stage
of respiratory insufficiency have profound, generalized atelectasis on autopsy. Often,
an eosinophilic material composed of fibrin, hemoglobin products, and cellular debris
coats the terminal bronchioles; this is the classically described “hyaline membrane,”
but it is not present in all cases, nor is it specific for RDS. Respiratory distress
syndrome produces characteristic clinical and radiographic findings. Tachypnea, nasal
flaring, and retractions are usually present within the first hour of life and are often
noted at birth. As the infant becomes progressively distressed, cyanosis is evident, and
an expiratory grunt or cry is audible. Auscultation reveals poor breath sounds
throughout the chest, often with fine, scattered crackles. The chest roentgenogram
shows a diffuse granular opacification of the lung fields, with prominent air
bronchograms; the heart border and diaphragms are often obscured. Blood gas
analysis demonstrates hypoxemia and, in severe cases, hypercapnia and acidosis.
Signs and symptoms usually worsen through the first 3 days of life, after which
improvement and recovery are the rule, unless complications such as patent ductus
arteriosus (PDA) or bronchopulmonary dysplasia have developed.
a) Neurastenia
b) Hipertiroidismo
c) Miastenia gravis
d) Botulismo
e) Oftalmoplejia progresiva externa
a) Haemophilus influenzae
b) Chalmydia trachomatis
c) Staphylococcus aureus
d) Candida albicans
e) Streptococcus pneumoniae
(palpable purpura). Petechial lesions may occur, but most hemorrhages are slightly
larger. The rash usually begins on the lower extremities and buttocks, but the entire
body may be involved. New lesions can continue to appear for 2–4 weeks.
Approximately two thirds of patients develop migratory polyarthralgias or polyarthritis,
primarily of the ankles and knees. Edema of the hands, feet, scalp, and periorbital
regions may occur. Abdominal colic—due to hemorrhage and edema primarily of the
small intestine—occurs in about 50% of those affected. Between 25% and 50% of those
affected develop renal involvement, with hematuria, proteinuria, or nephrotic
syndrome. Some children develop hypertension. Hematuria alone is never the
presenting complaint for Henoch-Schönlein purpura but usually manifests in the second
to third week of illness. Renal involvement occurs more commonly in males than in
females and in older patients than in younger ones. Testicular torsion may occur.
Neurologic symptoms are possible. Generally, treatment is unwarranted. Corticosteroid
therapy may provide symptomatic relief for severe gastrointestinal or joint
manifestations but does not alter skin or renal manifestations. Aspirin is useful for the
pain associated with arthritis. If culture for group A b-hemolytic streptococci is positive
or if the ASO titer is elevated, penicillin should be given in full doses for 10 days.
The active transport of Ca2+ and PO43- from the intestine is increased by a metabolite
of vitamin D. The term "vitamin D" is used to refer to a group of closely related sterols
produced by the action of ultraviolet light on certain provitamins. Vitamin D3, which
is also called cholecalciferol, is produced in the skin of mammals from 7-
dehydrocholesterol by the action of sunlight. The reaction involves the rapid
formation of previtamin D3, which is then converted more slowly to vitamin D3
(cholecalciferol). In the liver, vitamin D3 is converted to 25-hydroxycholecalciferol
(calcidiol, 25-OHD3). The 25-hydroxycholecalciferol is converted in the cells of the
proximal tubules of the kidneys to the more active metabolite 1,25-
dihydroxycholecalciferol, which is also called calcitriol or 1,25-(OH)2D3. Vitamin D
deficiency causes defective calcification of bone matrix and the disease called rickets
in children and osteomalacia in adults. The full-blown condition in children is
characterized by weakness and bowing of weight-bearing bones, dental defects, and
hypocalcemia. In adults, the condition is less obvious. It used to be most commonly due
to inadequate exposure to the sun in smoggy cities, but now it is more commonly due
to inadequate intake of the provitamins on which the sun acts in the skin.
a) Adenocarcinoma
b) Carcinoma indiferenciado
c) Linfoma
d) Leiomiosarcoma
e) Carcinoma anaplasico
a) Fibrilación ventricular
b) Fibrilación auricular con respuesta ventricular rápida
c) Hipertensión arterial
d) Insuficiencia cardiaca
e) Taquicardia ventricular
Sinus tachycardia at rest and during sleep as well as during exercise is the
most consistent rhythm disturbance in patients with thyrotoxicosis. About
5% to 10% of patients have atrial fibrillation; most are elderly, but it can occur in
young adults. The ventricular rate in atrial fibrillation is often rapid as a result
of the increased rate of conduction of the electrical impulses through the
atrioventricular node. Most patients with atrial fibrillation have the arrhythmia for
less than 4 to 8 weeks before the diagnosis of thyrotoxicosis is made. In the absence of
evidence for chronicity, most patients spontaneously revert to sinus rhythm within 8 to
12 weeks after antithyroid treatment is begun. Spontaneous reversion to sinus rhythm
after treatment of the thyrotoxicosis is less common in elderly patients with chronic
atrial fibrillation or patients who have underlying coronary or other heart disease or
anatomic abnormalities of the mitral valve or left atrium. The development of
persistent atrial fibrillation poses the potential for systemic embolization and stroke.
The risk of embolism seems small and is limited largely to older patients with
coexistent heart disease. The value of anticoagulation is controversial; it is discussed in
more detail later. Atrial flutter and other supraventricular tachyarrhythmias (including
a) Renal
b) Cardiaca
c) Hepatica
d) Pulmonar
e) Intestinal
a) Anilina
b) Morfina
c) Dextrometorfan
d) Cianuro
e) Fenotiazidas
El azul de metileno es una sustancia cristalina verde-azulada que se utiliza como tinte
histológico e indicador de laboratorio. También se emplea en el tratamiento de la
intoxicación por cianuro y en la metahemoglobinemia.
1066.- Caso clinico seriado: Una paciente de 22 años, gesta 1, que cursa con
embarazo de 37 semanas de evolución, presenta perdida del conocimiento
posterior a crisis convulsivas tonicoclonicas, presion arterial de 170/120
mmHg, frecuencia cardiaca de 100 por minuto, reflejos osteoteninosos
aumentads, frecuencia cardiaca fetal de 130 por minuto y edema importante
en los miembros inferiores, no se aprecian signos de trabajo de parto ni
modificaciones cervicales. Primer enunciado: El diagnostico más probable es:
a) Eclampsia
b) Preeclampsia severa
c) Crisis epilepticas tipo gran mal
d) Crisis hipertensiva
e) Hipertension inducida por el embarazo
Eclampsia occurs in 0.2–0.5% of all deliveries, with occurrence being influenced by the
same factors as in preeclampsia. In rare instances, eclampsia develops before 20
weeks' gestation. About 75% of eclamptic seizures occur before delivery. About 50% of
postpartum eclamptic seizures occur in the first 48 hours after delivery, but they may
a) Síndrome nefritico
b) Asma
c) Hepatitis B
d) Artritis séptica
e) Meningitis viral
a) Tubulo proximal
b) Membrana glomerular
c) Asa de Henle
d) Tubulo contorneado distal
e) Tubulo colector
Los principales sitios de acción de la aldosterona son el túbulo distal y la región cortical
de los colectores, donde promueve la reabsorción de sodio. La aldosterona se elabora
en la zona glomerulosa de la corteza suprarrenal. Es el mineralocorticoide más potente
producido en esta glandula. La tasa de secreción de aldosterona es cien veces inferior
a la del cortisol y su aclaramiento plasmático mucho más rápido.
El túbulo contorneado proximal resorbe alrededor del 70% del agua filtrada utilizando
como impulsor la fuerza osmótica transtubular, generada por la absorción de solutos.
Cuando el equilibrio de sodio corporal es el adecuado, la reabsorción de sodio y agua
aumenta en paralelo.
a) Metronidazol
b) Ornidazol
c) Pamoato de pirantel
d) Piperacina
e) Pirimetamina
a) Arritmia sinusal
b) Extrasistoles ventriculares
c) Bloqueo auriculoventricular
d) Fibrilación auricular
e) Taquicardia sinusal
Glycosides of digitalis, which have been used in the treatment of heart failure for more
than 200 years, are the most frequently used inotropic agents and the only oral
positive inotropic preparation approved for treatment of heart failure. Digitalis
glycosides, of which digoxin if the agent most commonly used, relieve symptoms by
improving cardiac performance through increased myocardial contractility, improved
LV function, and increased cardiac output and renal perfusion. Neurohumoral
modulating actions have also been reported. Several studies suggest that treatment
with digitalis decreases plasma renin activity, attenuates sympathetic drive, reduces
plasma norepinephrine levels, and improves baroreceptor sensitivity. These effects are
seen as playing an important role in treating heart failure. The beneficial effect of
digitalis glycosides in patients with heart failure complicated by the
occurrence of atrial fibrillation has been well documented and is generally
well accepted by most clinicians. The results of several studies indicate that in
patients with heart failure, digitalis does exert sustained beneficial hemodynamic
effects accompanied by improvement in both clinical status and exercise tolerance.
(Those who did not benefit from treatment with digitalis had milder degrees of heart
failure or evidence of primarily diastolic dysfunction.) Because some evidence suggests
that use of digitalis in suspected or confirmed MI may be associated with adverse
outcome, it is appropriate to consider alternatives to treatment with digoxin for
patients with MI and heart failure.
a) Directa negativa
b) Directa positiva
c) Indirecta positiva
d) Indirecta negativa
e) Directa e indirecta positivas
sintetizado por la madre atraviesa la placenta, se une a los hematíes fetales e induce
su hemólisis. Clínicamente el feto puede estar ligera o gravemente afecto, según la
cantidad de anticuerpo y la capacidad de la eritropoyesis fetal para compensar la
hemólisis. Si la hemólisis puede ser compensada por el feto, este llegará a término sin
grandes problemas, dado que el exceso de bilirrubina es metabolizado por la madre. Si
la hemólisis es muy grave, el feto sufrirá anemia severa, insuficiencia cardiaca y puede
morir intraútero con grandes edemas; es el denominado hydrops fetalis. El
diagnóstico anteparto puede establecerse mediante la prueba de Coombs,
indirecta en la madre, y con espectofotometría del líquido amniótico, que
proporciona información sobre el grado de afectación fetal. El tratamiento
consistirá en transfusiones intraútero, exanguinotransfusión o fototerapia, según la
afectación fetal. Recientemente se han empleado con éxito las inmunoglobulinas
intravenosas.
a) Volumen corriente
b) Volumen residual
c) Capacidad residual funcional
d) Capacidad vital
e) Capacidad pulmonar total
a) Furosemida
b) Diazepam
c) Espironolactona
d) Lactulosa
e) Eritromicina
Bacterial infections of the CNS may present acutely (symptoms evolving rapidly over 1–
24 hours), subacutely (symptoms evolving over 1–7 days), or chronically (symptoms
evolving over more than 1 week). Diffuse bacterial infections involve the
leptomeninges, superficial cortical structures, and blood vessels. Although the term
“meningitis” is used to describe these infections, it should not be forgotten that the
brain parenchyma is also inflamed and that blood vessel walls may be infiltrated by
inflammatory cells that result in endothelial cell injury, vessel stenosis, and secondary
ischemia and infarction. While awaiting the results of diagnostic tests, the physician
should start broad-spectrum antibiotic coverage as noted below. After specific
organisms are identified, antibiotic therapy can be tailored based on antibiotic
sensitivity patterns. Bacterial meningitis in children under age 3 months is treated
initially with cefotaxime (or ceftriaxone if the child is over age 1 month) and ampicillin;
the latter agent is used to treat Listeria and enterococci infections, which rarely affect
older children. Children over age 3 months are given ceftriaxone, cefotaxime, or
ampicillin plus chloramphenicol. If Streptococcus pneumoniae cannot be ruled out by
the initial Gram stain, vancomycin or rifampin are added until cultures are reported,
because penicillin-resistant pneumococci are common in the United States. Therapy
may be narrowed when organism sensitivity allows. Duration of therapy is 7 days for
meningococcal infections, 10 days for H influenzae or pneumococcal infection, and 14–
21 days for other organisms. Slow clinical response or the occurrence of complications
may prolong the need for therapy. Although therapy for 7 days has proved successful
in many children with H influenzae infection, it cannot be recommended without further
study if steroids are also used. Neuroimaging with CT and MRI scans may be helpful in
demonstrating the presence of brain abscess, meningeal inflammation, or secondary
problems such as venous and arterial infarctions, hemorrhages, and subdural effusions
when these are expected. In addition, these procedures may identify sinus or other
focal infections in the head or neck region that are related to the CNS infection. CT
scanning may demonstrate bony abnormalities, such as basilar fractures. EEGs may be
helpful in the assessment of patients who have had seizures at the time of
presentation. The changes are often nonspecific and characterized by generalized
slowing. In some instances, such as herpes simplex virus infection, focal
electronegative activity may be seen early in the course and may be one of the earliest
laboratory abnormalities to suggest the diagnosis. EEGs may also show focal slowing
over regions of abscesses. Unusual but characteristic electroencephalographic patterns
are seen in some patients with subacute sclerosing panencephalitis.
Pediatric urinary tract infection (UTI) may involve the urethra, bladder, or kidney.
Outside the clinical setting of systemic perinatal infection or prematurity, UTIs in
infants raise the possibility of urinary tract abnormalities. Boys less than 3 months of
age are more susceptible than girls. During the first year of life, circumcised males are
more likely to experience UTI due to a urinary tract abnormality than are females and
uncircumcised males. Older boys with a first infection should also be examined for
urinary tract abnormalities. A more conservative, watchful approach may be taken with
older girls, especially if they are sexually active or have poor personal hygiene and no
clinical features that arouse suspicion of significant urinary tract disease (eg, enuresis
or short stature). At least 8% of girls and 2% of boys will have a UTI in childhood. It is
particularly important to detect these infections in young children, since many children
less than 5 years of age with febrile UTIs have pyelonephritis. In this age group, the
infection commonly leads to renal scarring, especially in those less than a year of age.
Focal renal scarring may be a risk factor for hypertension and renal disease later in life.
The most common organisms causing UTI are E coli (> 80%), Klebsiella, Proteus
(increaed in males), enterococcus, all normal fecal flora, and, infrequently,
Staphylococcus. In the absence of bacteremia, enteric organisms are presumed to gain
access to the urinary tract via the urethra. The likelihood of infection is increased
with abnormalities of the urinary tract, poor perineal hygiene or infection,
sexual activity, instrumentation, or dysfunctional voiding. Normal voiding
serves to safeguard against bacterial contamination of the urethra
developing into infection. Newborns may exhibit fever or hypothermia, poor
feeding, jaundice, failure to thrive, or sepsis. Infants may have unexplained fever,
irritability, or foul-smelling urine. Preschool children may have abdominal pain,
vomiting, strong-smelling urine, fever, enuresis, or frequency, dysuria, or urgency.
School-age children are often afebrile, but usually have the classic signs of UTI, such as
enuresis, frequency, dysuria, and urgency. Costovertebral angle tenderness may be
elicited in cases of pyelonephritis. It is very rare for children with bacterial UTI to
present with hemorrhagic cystitis, which is more common with viral infections. Urinary
tract infection is the most common occult bacterial cause of unexplained fever in
infants less than 2 years of age. Sick children should be treated presumptively when
the laboratory findings are suggestive. Initial therapy should be based on prior
antibiotic use, location of the infection (eg, kidney, bladder), and the organism and its
drug sensitivities. Uncomplicated urethritis or cystitis can be treated with a single oral
antibiotic that the patient has not used recently. Amoxacillin, trimethoprim-
sulfamethoxazole (TMP-SMX), or a later generation cephalosporin can be used as initial
therapy. Choice of antibiotic should also take into account community bacterial
resistance patterns. TMP-SMX has generally yielded higher cure rates when compared
with amoxacillin. TMP-SMX and cephalosporins are not active against enterococcus.
Enterococcus might be suspected when a Gram stain is performed. Duration of therapy
should be 7 to 10 days. Short course, high dose therapy should not be used in children.
The choice of antibiotic should be reviewed when culture and sensitivity results are
available. In toxic, dehydrated children who cannot receive oral therapy, especially if
there is suspected pyelonephritis, hospitalization should be considered. Many of these
children will be bacteremic (~5% of children less than 2 years of age). A non-toxic,
older child with suspected pyelonephritis need not be admitted to the hospital (as long
as compliance is not in question), but antibiotic coverage should be broad (ampicillin or
cephalosporin plus gentamicin) until the bacteria's sensitivity to antibiotics is known.
Antibiotic dosage must be adjusted for patients with associated acute or chronic renal
failure. If the organism is sensitive to the antibiotic chosen and the child improves
within 2 days, no test of cure is needed. If symptoms persist, bacterial sensitivity
should be checked, the child reexamined, and a repeat urine culture obtained.
Persistent symptoms and bacteriuria indicate one of the following: 1) wrong choice of
antibiotic; 2) development of bacterial resistance; 3) superinfection with a different
organism; or 4) a significant anatomic abnormality in the urinary tract.
a) Policitemia
b) Plaquetopenia
c) Leucopenia
d) Hiperleucocitosis
e) Enfermedad hemorragica del recién nacido
Los lactantes con un riesgo especial de padecer policitemia son los lactantes PEG a
término y postérmino, los niños de madres diabéticas, los lactantes con pinzamiento
tardío del cordón y los que presentan hipertiroidismo neonatal, síndrome
adrenogenital, trisomía 21, síndrome de transfusión gemelar (receptor) y síndrome de
Beckwith-Wiedemann. En algunos lactantes, la policitemia puede reflejar una
compensación por pedíodos prolongados de hipoxia feral debida a insuficiencia
placentaria; estos lactantes tienen niveles de eritropoyetina más altos en el
nacimiento.
1080.- Caso clinico seriado: Hombre de 32 años, desde hace tres meses
presenta debilidad muscular; se fatiga facilmente y hace algunos días noto la
aparicion de manchas hiperpigmentadas en las rodillas, el cuello y en las
areas expuestas al sol. Sus examenes de laboratorio muestran: sodio 123
mEq/l y potasio 5.3 mEq/l. Primer enunciado: el diagnostico probable es:
a) Hipercortisolismo
b) Feocromocitoma
c) Insuficiencia suprarrenal
d) Aldosteronismo primario
e) Hipotiroidismo
a) Determinación de TSH
b) Determinación de ácido vanilmandelico
c) Determinación de cortisol en el plasma
d) Determinación de renina
e) Prueba de dexametasona
weekly. Once the crisis has passed, the patient must be investigated to assess the
degree of permanent adrenal insufficiency and to establish the cause if possible.
The cause of postnatal pyloric circular muscle hypertrophy leading to gastric outlet
obstruction is not known. The incidence is 1–8:1000 births, with a 4:1 male
predominance and a positive family history present in 13% of patients. Recent studies
suggest that erythromycin therapy may be associated with development of pyloric
stenosis in infants under 30 days. Vomiting usually begins between ages 2 and 4 weeks
and rapidly becomes projectile after every feeding; it starts at birth in about 10% of
cases. Onset of symptoms may be delayed in premature infants. The vomitus is rarely
bilious but may be blood-streaked. The infant is hungry and nurses avidly.
Constipation, dehydration, weight loss, fretfulness, and finally apathy occur. The upper
abdomen may be distended after feeding, and prominent gastric peristaltic waves from
left to right may be seen. An olive-sized mass can be felt on deep palpation in the right
upper abdomen, especially after the child has vomited. Hypochloremic alkalosis with
potassium depletion occurs. Hemoconcentration is reflected by elevated hemoglobin
and hematocrit values. Elevated unconjugated bilirubin occurs in 2–5% of cases.
a) Endoscopia
b) Serie esofagogastroduodenal
c) Radiografía simple de abdomen
d) Colon por enema
e) Ultrasonido
a) Funduplicatura de Nissen
b) Piloromiotomia
c) Resección intestinal
d) Colostomia
e) Gastrostomia
Pyloromyotomy is the treatment of choice and consists of incision down to the mucosa
along the pyloric length. The procedure can be performed laparoscopically. Prior to
a) Ciprofloxacino
b) Rifampicina
c) Tetraciclina
d) Tetraciclina + estreptomicina
e) TMP-SMX
Brucellosis (also called undulant fever, Mediterranean fever, Malta fever) is an infection
that causes abortion in domestic animals. It is caused by one of six species of Brucella
coccobacilli. It may occasionally be transmitted to humans, in whom the disease could
be acute or chronic with ongoing fever and constitutional symptoms without localized
findings. After a 2- to 8-week incubation period, affected patients present with a
spectrum of disease that varies from an asymptomatic form to a severe illness with
bacteremia. Affected patients typically present with fever, sweats, headaches, malaise,
and weight loss. If undiagnosed, these symptoms may persist for months to a year.
When symptoms last for more than 12 months without any localization, the disease is
classified as chronic. Physical examination, though normal in most cases, may reveal
bilateral diffuse lymphadenopathy, splenomegaly, and hepatomegaly in 20%-30% of
patients. In the localized form, the infection may affect virtually any organ system. The
osteoarticular, gastrointestinal, genitourinary, and cardiovascular are among the more
common affected systems. These forms have signs and symptoms related to the
affected organ system. An infectious discitis with adjacent vertebral bony osteomyelitis
typically in the lumbar area, is the most common manifestation of localized
osteoarticular disease. Sacroilitis is also characteristic of the musculoskeletal form of
the infection. Infective endocarditis occurs in < 2% of brucellosis cases. Patients with
chronic brucellosis may have long periods of no symptoms followed by the intermittent
recurrence of fever, chills, myalgias, and nonspecific symptoms. This form of relapsing
brucellosis may persist for decades and is often refractory to antimicrobial therapy and
is frequently associated with multiple or large calcific lesions in the liver and spleen.
Many other common illnesses can mimic the most common clinical presentation of
brucellosis.
Treatment of acute brucellosis first choice:
Adults: Doxycycline, 100 mg orally twice daily, PLUS rifampin, 600-900 mg
orally daily for 4-6 weeks
Children: Doxycycline,2 2 mg/kg orally twice daily, PLUS rifampin, 15 mg/kg orally daily
for 4-6 weeks
Treatment of acute brucellosis second choice:
Adults: Doxycycline, 100 mg orally twice daily for 4-6 weeks, PLUS streptomycin, 1 g IM
daily for the first 15 days
Children: TMP/SMX,3 2.5 mg/kg orally of TMP component 4 times daily, PLUS rifampin,
15 mg/kg orally daily for 4-6 weeks
Treatment of Endocarditis-Meningitis-Spondylitis-Localized Forms first choice
Adults: Doxycycline, 100 mg orally twice daily, PLUS rifampin, 600-900 mg orally daily
for 6 mo, PLUS streptomycin, 1 g IM daily for the first 2-3 weeks
Children: Doxycycline,2 2 mg/kg orally twice daily, PLUS rifampin, 15 mg/kg orally daily
for 6 mo, PLUS streptomycin, 10 mg/kg IM twice daily for the first 7-14 days
Treatment of Endocarditis-Meningitis-Spondylitis-Localized Forms second
choice
TMP/SMX,3 2.5 mg/kg orally of TMP component 4 times daily, PLUS rifampin, 15 mg/kg
orally daily for 6 mo, PLUS gentamicin, 1.5-2 mg/kg (IV or IM) in three daily doses for
the the first 7-14 days
a) Amikacina
b) Trimetoprim-sulfametoxazol
c) Gentamicina
d) Eritromicina
e) Cefutoxima
Enteritis caused by Shigella species may be watery (Shigella sonnei, Shigella boydii) or
dysenteric (Shigella dysenteriae, Shigella flexneri). Risks include ingestion of fecally
contaminated food or water and contact with infected individuals. Definitive diagnosis
requires microbiologic isolation and identification of Shigella species or molecular
evidence of infection. Early in the course of disease, when bacteria are present in the
small intestine, patients develop acute, watery diarrhea; fever; and abdominal pain.
Patients may become toxemic and fever may reach as high as 104 °F. Later in the
course of disease, the primary site of infection is the colon. In this phase, fever
continues, but is usually less pronounced. The pain that is present is usually in the
lower abdominal quadrants. Stools become dysenteric, consisting of a mixture of
neutrophils, blood, mucus, and debris. Frequent, small-volume or fractionated stools
may occur, and tenesmus is often present. Patients experience pain upon rectal
examination. Colonoscopy discloses hyperemic and friable-to-ulcerated colonic
mucosa. Patients with acute diarrhea, which may be watery to dysenteric; fever;
MX-Biomedical Research Group / JD-MD Bioinformatics Labs 54
JD-MD Medicine and Technology
ENARM 11ª PARTE by JD-MD
a) Miconazol
b) TMP-SMX
c) Praziquantel
d) Amikacina
e) Anfotericina B
a) Dapsona + rifampicina
b) Isoniazida + etambutol
c) Ciprofloxacina + etambutol
d) Isonicida + ciprofloxacina
e) Ceftrixona + amikacina
The manifestations of leprosy involve the skin, upper respiratory system, peripheral
nerves, and, in men, testes. The peripheral neuropathy that is seen in leprosy results in
impaired sensation of fine touch, temperature, and pain, whereas proprioception and
vibratory sensation are intact. Such loss of sensation leads to recurrent trauma and
ulceration in the extremities. For example, loss of sensation in the feet can lead to
chronic nonhealing ulcers, especially at the metatarsal heads. Large nerve trunks may
also be affected. A common nerve trunk that is affected in leprosy is the ulnar nerve at
the elbow, which results in clawing of the fourth and fifth digits of the hand, dorsal
interosseus muscle atrophy, and loss of sensation in the hand along the ulnar nerve
distribution. The lepromatous or multibacillary form of leprosy is characterized by
symmetric skin nodules, plaques, and thickened dermis. Usually, the ear lobes and
extremities are affected. Diffuse lepromatosis is seen usually in patients from Mexico,
who show areas of diffuse dermal infiltration and no focal lesions. Untreated,
lepromatous leprosy results in a high level of continuous bacteremia. Peripheral
neuropathy is symmetric and generalized. There is a characteristic deformity
associated with this type of leprosy, "saddle-nose deformity," which occurs because of
infiltration of the upper respiratory system and nasal cartilage. Other upper respiratory
system effects include chronic nasal congestion and epistaxis. The tuberculoid, or
paucibacillary, form of leprosy is characterized by one or few hypopigmented macules,
which are anesthetic and variable in size. These macules have distinct and elevated
borders. Peripheral neuropathy in this form of leprosy is usually asymmetric and affects
large nerves. Neural leprosy is characterized by functional impairment of large nerve
trunks without skin lesions. The upper respiratory system is not involved. M leprae
Infection. Leprosy generally requires a long duration of treatment, and compliance is a
major problem. Lepromatous leprosy requires a longer treatment time course than
tuberculoid leprosy because of the greater number of organisms involved. Currently,
the recommended treatment is dapsone and rifampin for 6 months for
tuberculoid leprosy. Dapsone alone is not recommended because of reports of
emerging resistance. For lepromatous leprosy, dapsone with rifampin or clofazimine for
24 months is recommended. Nonetheless, there have been reports of relapses even
after such long courses of treatment. Other agents such as ethionamide,
prothionamide, the aminoglycosides, minocycline, clarithromycin, and the
fluoroquinolones may also prove to be beneficial.
a) Ciprofloxacina
b) TMP-SMX
c) Ceftriaxona
d) Amoxicilina
e) Neomicina
This clinical syndrome is caused by the neurotoxin of C botulinum. There are seven
types (A-G) of neurotoxin, all of which inhibit the release of acetylcholine at the level of
peripheral neuromuscular junctions. In the majority of cases, the disease is acquired by
ingestion of preformed toxin in home-canned vegetables, fruits, and fish. In Japan, the
former Soviet Union, Scandinavia, and the Great Lakes region of the United States,
type E toxin causes disease in people who consume raw or lightly smoked fish. There
are four categories of botulism: Food borne (most common), Wound botulism caused
by the absorption of toxin from a wound contaminated by C botulinum (the rarest
form), Infant botulism resulting from in vivo elaboration of toxin by colonizing
organisms in the bowel, Undetermined, which refers to cases that occur in individuals
> 1 year old in whom no food or wound source is identified. Symptoms and signs arise
12-36 h after food ingestion and consist of acute onset and progressive flaccid
paralysis involving the facial musculature and the cranial nerves bilaterally, then
descending symmetrically to the pharynx, thoracic region, and the upper and lower
extremities. This evolves into respiratory failure without impairment of consciousness.
Fever is classically absent. In cases of infant botulism, which is found in children 6 days
to 11 months old, constipation is the initial symptom, followed by lethargy, feeding
difficulties, altered cry, floppiness, ophthalmoplegia, and respiratory failure. Treatment
is mainly supportive; antitoxin made from equine serum can be used. In the United
States, it is obtained through state health departments or the Centers for Disease
Control. The standard dose is one vial intravenously and one vial intermittently. It may
be repeated every 4 h in severe progressive cases. Clinical trials evaluating its efficacy
are lacking. Full recovery takes from 3 months to 1 year. Risk of death ranges from 4 to
25%, depending on the promptness with which the diagnosis is made.
a) Pseudomona sp.
b) Streptococcus pneumoniae
c) Streptococcus pyogenes
d) Klebsiella sp.
e) Haemophylis influenzae
Acute otitis media is a bacterial infection of the mucosally lined air-containing spaces of
the temporal bone. Purulent material forms not only within the middle ear cleft but also
within the mastoid air cells and petrous apex when they are pneumatized. Acute otitis
media is usually precipitated by a viral upper respiratory tract infection that causes
auditory tube edema. This results in accumulation of fluid and mucus, which becomes
secondarily infected by bacteria. The most common pathogens both in adults and
in children are Streptococcus pneumoniae, Haemophilus influenzae, and
Streptococcus pyogenes. Acute otitis media is most common in infants and children,
although it may occur at any age. Presenting symptoms and signs include otalgia, aural
pressure, decreased hearing, and often fever. The typical physical findings are
erythema and decreased mobility of the tympanic membrane. Occasionally, bullae will
be seen on the tympanic membrane. Although it is taught that this represents infection
with Mycoplasma pneumoniae, most cases involve more common pathogens. Rarely,
when middle ear empyema is severe, the tympanic membrane can be seen to bulge
outward. In such cases, tympanic membrane rupture is imminent. Rupture is
accompanied by a sudden decrease in pain, followed by the onset of otorrhea. With
appropriate therapy, spontaneous healing of the tympanic membrane occurs in most
cases. When perforation persists, chronic otitis media frequently evolves. Mastoid
tenderness often accompanies acute otitis media and is due to the presence of pus
within the mastoid air cells. This alone does not indicate suppurative (surgical)
mastoiditis. The treatment of acute otitis media is specific antibiotic therapy, often
combined with nasal decongestants. The first-choice antibiotic treatment is either
amoxicillin (20-40 mg/kg/d) or erythromycin (50 mg/kg/d) plus sulfonamide (150
mg/kg/d) for 10 days. Alternatives useful in resistant cases are cefaclor (20-40
mg/kg/d) or amoxicillin-clavulanate (20-40 mg/kg/d) combinations. Tympanocentesis
for bacterial (aerobic and anaerobic) and fungal culture may be performed by any
experienced physician. A 20-gauge spinal needle bent 90 degrees to the hub attached
to a 3-mL syringe is inserted through the inferior portion of the tympanic membrane.
Interposition of a pliable connecting tube between the needle and syringe permits an
assistant to aspirate without inducing movement of the needle. Tympanocentesis is
useful for otitis media in immunocompromised patients and when infection persists or
recurs despite multiple courses of antibiotics. Surgical drainage of the middle ear
(myringotomy) is reserved for patients with severe otalgia or when complications of
otitis (eg, mastoiditis, meningitis) have occurred. Recurrent acute otitis media may be
managed with long-term antibiotic prophylaxis. Single daily doses of sulfamethoxazole
(500 mg) or amoxicillin (250 or 500 mg) are given over a period of 1-3 months. Failure
of this regimen to control infection is an indication for insertion of ventilating tubes.
a) Ultrasonografia
b) Rectosigmoidoscopia
c) Tomografia computarizada
d) Colonoscopia
e) Colon por enema
Colonic diverticulosis increases with age, ranging from 5% in those under age 40, to
30% at age 60, to more than 50% over age 80 years in Western societies. In contrast, it
is very uncommon in developing countries with much lower life expectancies. Most are
asymptomatic, discovered incidentally at endoscopy or on barium enema.
Complications in one-third include lower gastrointestinal bleeding and diverticulitis.
Colonic diverticula may vary in size from a few millimeters to several centimeters and
in number from one to several dozen. Almost all patients with diverticulosis have
involvement in the sigmoid colon; however, only 15% have proximal colonic disease. In
most patients, diverticulosis is believed to arise after many years of a diet deficient in
fiber. The undistended, contracted segments of colon have higher intraluminal
pressures. Over time, the contracted colonic musculature, working against greater
pressures to move small, hard stools, develops hypertrophy, thickening, rigidity, and
fibrosis. Diverticula may develop more commonly in the sigmoid because intraluminal
pressures are highest in this region. The extent to which abnormal motility and
hereditary factors contribute to diverticular disease is unknown. Patients with diffuse
diverticulosis may have an inherent weakness in the colonic wall. Patients with
abnormal connective tissue are also disposed to development of diverticulosis,
including Ehlers-Danlos syndrome, Marfan's syndrome, and scleroderma. Perforation of
a colonic diverticulum results in an intra-abdominal infection that may vary from
microperforation (most common) with localized paracolic inflammation to
macroperforation with either abscess or generalized peritonitis. Thus, there is a range
from mild to severe disease. Most patients with localized inflammation or infection
report mild to moderate aching abdominal pain, usually in the left lower quadrant.
Constipation or loose stools may be present. Nausea and vomiting are frequent. In
many cases, symptoms are so mild that the patient may not seek medical attention
until several days after onset. Physical findings include a low-grade fever, left lower
quadrant tenderness, and a palpable mass. Stool occult blood is common, but
hematochezia is rare. Leukocytosis is mild to moderate. Patients with free perforation
present with a more dramatic picture of generalized abdominal pain and peritoneal
signs. Plain abdominal films are obtained in all patients to look for evidence of free
abdominal air (signifying free perforation), ileus, and small or large bowel obstruction.
In patients with mild symptoms and a presumptive diagnosis of diverticulitis, empiric
medical therapy is started without further imaging in the acute phase. Patients who
respond to acute medical management should undergo complete colonic evaluation
with colonoscopy or barium enema after resolution of clinical symptoms to corroborate
the diagnosis or exclude other disorders such as colonic neoplasms. In patients who do
not improve rapidly after 2-4 days of empiric therapy and in those with severe disease,
CT scan of the abdomen is obtained to look for evidence of diverticulitis,
including colonic diverticula and wall thickening, pericolic fat infiltration, abscess
formation, or extraluminal air or contrast. Endoscopy and barium enema are
contraindicated during the initial stages of an acute attack because of the risk of free
perforation, though sigmoidoscopy with minimal air insufflation is sometimes required
to exclude other diagnoses. Most patients can be managed with conservative
measures. Patients with mild symptoms and no peritoneal signs may be managed
initially as outpatients on a clear liquid diet and broad-spectrum oral antibiotics with
anaerobic activity. Reasonable regimens include amoxicillin and clavulanate potassium
(875 mg/125 mg) twice daily; or metronidazole, 500 mg three times daily; plus either
ciprofloxacin, 500 mg twice daily, or trimethoprim-sulfamethoxazole, 160/800 mg twice
daily orally, for 7-10 days or until the patient is afebrile for 3-5 days. Symptomatic
improvement usually occurs within 3 days, at which time the diet may be advanced.
Patients with increasing pain, fever, or inability to tolerate oral fluids require
hospitalization. Patients with severe diverticulitis (high fevers, leukocytosis, or
peritoneal signs) and patients who are elderly or immunosuppressed or who have
serious comorbid disease require hospitalization acutely. Patients should be given
nothing by mouth and should receive intravenous fluids. If ileus is present, a
nasogastric tube should be placed. Intravenous antibiotics should be given to cover
anaerobic and gram-negative bacteria. Single-agent therapy with either a second-
generation cephalosporin (eg, cefoxitin), piperacillin-tazobactam, or ticarcillin
clavulanate appears to be as effective as combination therapy (eg, metronidazole or
clindamycin plus an aminoglycoside or third-generation cephalosporin [eg, ceftazidime,
cefotaxime]). Symptomatic improvement should be evident within 2-3 days. The
antibiotics should be continued for 7-10 days, after which time elective evaluation with
colonoscopy or barium enema should be performed. Approximately 20-30% of patients
with diverticulitis will require surgical management. Surgical consultation should be
obtained on all patients with severe disease or those who fail to improve after 72 hours
of medical management. Indications for emergent surgical management include free
peritonitis and large abscesses. Patients with fistulas or colonic obstruction due to
chronic disease will require elective surgery. Patients with a localized abdominal
abscess can be treated acutely with a percutaneous catheter drain placed by an
interventional radiologist. This permits control of the infection and resolution of the
immediate infectious inflammatory process. In this manner, a subsequent single-stage
elective surgical operation can be performed in which the diseased segment of colon is
removed and primary colonic anastomosis performed. In patients in whom catheter
drainage is not possible or helpful or in cases requiring emergency surgery, it is
necessary to perform surgery in two stages. In the first stage, the diseased colon is
resected and the proximal colon brought out to form a temporary colostomy. The distal
colonic stump is either closed (forming a Hartmann pouch) or exteriorized as a mucous
fistula. Weeks later, after inflammation and infection have completely subsided, the
colon can be reconnected electively.
a) Glomerulonefritis
b) Feocromocitoma
c) Síndrome nefrótico
d) Insuficiencia suprarrenal
e) Tumor renal
a) Streptococo beta-hemolítico
b) Diplococo Pneumoniae
c) Haemophylus influenzae
d) Mycoplasma pneumoniae
e) Bordetella pertussis
symptoms, including rhinorrhea, mild cough, and low-grade fever. During this stage,
which typically lasts 1-2 weeks, the disease is highly communicable. The paroxysmal
stage is marked by sudden attacks or paroxysms of severe, repetitive coughing, often
culminating with the characteristic whoop (tos coqueluchoide-whooping cough-
Tos espasmódica en la que la primera inspiración ocurre con la glotis
semicerrada, produciendo un ruido característico) and frequently followed by
vomiting. A marked lymphocytosis usually accompanies this stage of the disease, with
lymphocyte counts sometimes exceeding 50,000/mm3 and usually representing 70%
or more of total circulating leukocytes. The paroxysmal stage typically lasts 1-4 weeks
and can be associated with a variety of complications, including secondary bacterial
infections such as pneumonia and otitis media, toxic central nervous system
manifestations such as seizures and encephalopathy, and effects of increased
intrathoracic and intra-abdominal pressure such as pneumothorax, hernia, and rectal
prolapse. The beginning of the convalescent (recovery) stage is marked by a reduction
in frequency and intensity of coughing spells. After clinical pertussis, immunity to
disease is lifelong. Although most cases of pertussis follow a characteristic course,
exceptions exist. In infants < 3 months, the catarrhal stage is usually no longer than a
few days, and the paroxysmal and convalescent stages are extremely protracted, with
coughing spells that continue throughout the first year of life. In infants < 6 months,
apnea is a common manifestation, and the whoop is often absent. Paradoxically, in
infants, cough and whoop may become louder and more classic during convalescence,
reflecting growth in body mass and increased strength. In immunized children, all three
stages are shortened, and in adults, only a protracted cough may be present. Post-
tussive vomiting is common in pertussis at all ages and is a major clue to the diagnosis
in adolescents and adults. With subsequent respiratory illnesses over the next several
months, paroxysmal coughing may recur, though not because of recurrence of active
Bordetella infection.
Most patients can be managed with conservative measures. Patients with mild
symptoms and no peritoneal signs may be managed initially as outpatients on a clear
liquid diet and broad-spectrum oral antibiotics with anaerobic activity. Reasonable
regimens include amoxicillin and clavulanate potassium (875 mg/125 mg) twice daily;
or metronidazole, 500 mg three times daily; plus either ciprofloxacin, 500 mg twice
daily, or trimethoprim-sulfamethoxazole, 160/800 mg twice daily orally, for 7-10 days
or until the patient is afebrile for 3-5 days. Symptomatic improvement usually occurs
within 3 days, at which time the diet may be advanced. Patients with increasing pain,
fever, or inability to tolerate oral fluids require hospitalization. Patients with severe
diverticulitis (high fevers, leukocytosis, or peritoneal signs) and patients who are
elderly or immunosuppressed or who have serious comorbid disease require
hospitalization acutely. Patients should be given nothing by mouth and should receive
intravenous fluids. If ileus is present, a nasogastric tube should be placed. Intravenous
antibiotics should be given to cover anaerobic and gram-negative bacteria. Single-
agent therapy with either a second-generation cephalosporin (eg, cefoxitin),
piperacillin-tazobactam, or ticarcillin clavulanate appears to be as effective as
combination therapy (eg, metronidazole or clindamycin plus an aminoglycoside or
third-generation cephalosporin [eg, ceftazidime, cefotaxime]). Symptomatic
improvement should be evident within 2-3 days. The antibiotics should be continued for
7-10 days, after which time elective evaluation with colonoscopy or barium enema
should be performed. Approximately 20-30% of patients with diverticulitis will require
surgical management. Surgical consultation should be obtained on all patients with
severe disease or those who fail to improve after 72 hours of medical management.
Indications for emergent surgical management include free peritonitis and large
abscesses. Patients with fistulas or colonic obstruction due to chronic disease will
require elective surgery. Patients with a localized abdominal abscess can be treated
acutely with a percutaneous catheter drain placed by an interventional radiologist. This
permits control of the infection and resolution of the immediate infectious inflammatory
process. In this manner, a subsequent single-stage elective surgical operation can be
performed in which the diseased segment of colon is removed and primary colonic
anastomosis performed. In patients in whom catheter drainage is not possible or
helpful or in cases requiring emergency surgery, it is necessary to perform surgery in
two stages. In the first stage, the diseased colon is resected and the proximal colon
brought out to form a temporary colostomy. The distal colonic stump is either closed
(forming a Hartmann pouch) or exteriorized as a mucous fistula. Weeks later, after
inflammation and infection have completely subsided, the colon can be reconnected
electively.
a) Cólera
b) Shigelosis
c) Giardiasis
d) Botulismo
e) Tétanos
Symptoms and signs fo botilusm arise 12-36 h after food ingestion and consist of acute
onset and progressive flaccid paralysis involving the facial musculature and the cranial
nerves bilaterally, then descending symmetrically to the pharynx, thoracic region, and
the upper and lower extremities. This evolves into respiratory failure without
impairment of consciousness. Fever is classically absent. In cases of infant botulism,
which is found in children 6 days to 11 months old, constipation is the initial symptom,
followed by lethargy, feeding difficulties, altered cry, floppiness, ophthalmoplegia, and
respiratory failure.