By A. Arakos. New School of Architecture and Design.
Mycoplasma pneumoniae Unilateral or bilateral enlargement of hilar Common in children discount 100mg lasix overnight delivery, rare in adults buy generic lasix 40 mg on-line. Psittacosis lasix 40 mg fast delivery, infectious mononucleosis (also spleno- (Fig C 14-1; see Fig C 13-1) megaly) discount lasix 40mg on line, rubeola, echovirus, varicella. Unilateral in pertussis (whooping cough) and (Figs C 14-2 and C 14-3) tularemia (ipsilateral hilar enlargement in 25% to 50% of tularemic pneumonias); bilateral involve- ment in anthrax and plague. Diffuse, reticular interstitial infiltrate Fig C 14-2 with a focal area of consolidation in the right upper lobe. Air-space consolidation involving the Note the striking right hilar and mediastinal adenopathy right middle lobe and a portion of the right upper lobe. Presenting sign in up to one-third of patients (Fig C 14-4) (primary carcinoma arising in a major hilar bronchus or metastasis from a small primary tumor in adjacent or peripheral parenchyma). Prominent right mediastinal lymphadenopathy associated with an ill-defined primary malignant lesion (arrow). Pulmonary involvement or pleural asymmetric (unilateral node enlargement is effusion occurs in about 30%. Leukemia (Fig C 14-7) Symmetric enlargement of hilar and medias- Lymphadenopathy occurs more commonly in tinal nodes in approximately 25% of patients. Metastases (lymphangitic Unilateral or bilateral enlargement of hilar or Usually associated with a diffuse reticular or reti- spread) mediastinal nodes. Lateral view of the chest shows subtle Fig C 14-7 enlargement of a retrosternal (internal mammary) Leukemia. Typical Usually associated with a diffuse nodular or (see Fig C 13-5) eggshell calcification (in approximately 10% of reticulonodular pattern throughout both lungs. Sarcoidosis Bilaterally symmetric enlargement of hilar and Approximately half of patients have diffuse (Fig C 14-8) paratracheal nodes develops in up to 90% of parenchymal disease. The outer borders of the enlarged hila resolves as the parenchymal disease develops, are usually lobulated. The bilateral symmetry is unlike tuberculosis, whereas the lack of retrosternal involvement is unlike lymphoma. Pulmonary Langerhans Symmetric enlargement of hilar and medias- Early diffuse micronodular pattern that may cell histiocytosis tinal nodes is a rare manifestation. Lack of lymph node enlargement in a patient with diffuse interstitial pulmonary disease favors a diagnosis of histio- cytosis X rather than sarcoidosis. Idiopathic pulmonary Symmetric enlargement of hilar nodes primarily Episodes of pulmonary hemorrhage produce hemosiderosis/ occurs in the acute stage. Goodpasture’s syndrome Cystic fibrosis Unilateral or bilateral hilar node enlargement is Diffuse increase in pulmonary markings with hy- an uncommon finding. Bronchopulmonary Symmetric enlargement of hilar and medias- Rare manifestation of this plasma cell dyscrasia. Drug-induced changes Bilateral hilar or mediastinal lymph node en- May develop during diphenylhydantoin or trime- largement. Affected zones show air trapping on expiration and overinflation at full lung capacity. Bulla/bleb Sharply defined, air-containing spaces that are Predominantly unilateral. Unlike local obstructive (Figs C 15-1 and C 15-2) bounded by curvilinear, hairline shadows and emphysema, the vascular markings are absent vary in size from 1 cm to an entire hemithorax. Foreign body aspiration Segmental distribution with lower lobe predom- Most common manifestation of foreign body as- (see Fig C 31-3) inance (especially on the right). An opaque foreign body may be demon- air trapping on expiratory films and often local strated. Compensatory overaeration Overinflation and oligemia of the remaining Lobar collapse or agenesis causes overdistention of (Fig C 15-3) lobe(s). The chest wall is asym- metric, and the ribs are somewhat close together on the left. Metastases to hilar lymph nodes occasionally compress a bronchus and cause oligemia. Thromboembolic disease Affected segment often shows moderate loss of Almost invariably associated with obstruction of a (Fig C 15-4) volume but may still appear hyperlucent due to major lobar or segmental pulmonary artery. The (Fig C 15-5) expiration (mediastinal shift toward the normal hilar and peripheral vessels are small. Congenital lobar emphysema Severe overinflation of a pulmonary lobe Approximately one-third of cases apparent at birth (Fig C 15-6) (especially the right upper or the right middle (others noted several weeks later). Because the deflation of the right lung is normal, the mediastinum has swung sharply to the right. The left pulmonary artery is present, although diminutive, differentiating this appear- ance from congenital absence of the left pulmonary artery. Severe overdistension of the left upper lobe causes marked radiolucency of the left hemithorax along with depression of the ipsilateral hemidi- aphragm and displacement of the mediastinum into the right hemithorax. The hyperinflated left upper lobe has her- niated into the right side of the chest (arrows). Note the small and widely separated bronchovascular markings in the lu- cent left lung. If the malformation does not communicate predominates, simulating infantile lobar with the bronchial tree, it contains only fluid and emphysema. The lesion expands the ipsilateral hemi- thorax by depressing the hemidiaphragm and shifting the mediastinum toward the contralateral side. May supplied partly or completely by systemic arteries be associated with an anomalous draining vein (left-to-right shunt). Other cardiopulmonary that forms a broad, gently curved shadow anomalies are common. Pulmonary branch stenosis Ipsilateral lung is hypoplastic and has reduced Very rare anomaly in which the involved lung is volume, and there is an absent or diminutive supplied by a hypertrophied bronchial circulation. No air trapping on forced expiration The anomalous artery is usually on the side (unlike Swyer–James syndrome). Anomalous origin of left Hyperlucent right lung due to air trapp- Very rare anomaly in which severe compression pulmonary artery from ing and overinflation (anomalous vessel com- may collapse the lung. Compression of the trachea right pulmonary artery presses the right main bronchus). An esophagram shows pathognomonic posterior displacement of the esophagus and anterior displacement of the trachea by the interposed anomalous artery. Frontal radiograph of an infant’s chest and abdomen at 1 hour of age demonstrates a large lucent mass in the right hemithorax with shift of the medi- astinal structures to the left. In the lower right chest, the mass appears multicystic and resem- bles air-filled loops of bowel. Tuberculosis Overinflation and oligemia due to partial Primarily involves the anterior segment of an bronchial obstruction from ipsilateral hilar upper lobe or the medial segment of the middle lymph node enlargement. Staphylococcal infection Characteristic thin-walled cystic spaces develop Cystic spaces usually appear during the first (pneumatocele) in approximately 50% of affected children. May week of a pneumonia and tend to disappear (see Fig C 11-2) be large and even fill an entire hemithorax. Probably results from check-valve obstruction of a communication between a peribronchial abscess and the bronchial lumen. Hydrocarbon poisoning Inhalation in children can lead to the formation Ingestion or inhalation of hydrocarbons is the (Fig C 15-8) of pneumatoceles simulating those in staphy- leading cause of poisoning in children. Broncholith Overinflation and oligemia due to partial Erosion of a calcified lymph node (usually from bronchial obstruction from an endobronchial histoplasmosis) into the bronchial lumen. Disparity in thickness of the supraclavicular soft (Fig C 15-9) tissues and axillary folds. Most commonly due to patient rotation, which technique projects the soft tissues and the spine over one side of the chest while rotating them off the opposite, more lucent side (especially prominent in women with large pendulous breasts). The lower portion of the right lung appears hyper- lucent, whereas the apex seems comparatively opaque. The heart tends to be small and relatively vertical, and there are often single or multiple bullae.
Prolactin causes the production of milk generic lasix 40mg fast delivery, and oxytocin release (via the suckling reflex) causes the contraction of smooth-muscle cells in the ducts to eject the milk from the nipple cheap lasix 100 mg amex. It contains more protein and less fat than subsequent milk lasix 100 mg without a prescription, and contains IgA antibodies which impart some passive immunity to the infant buy discount lasix 40 mg on line. Most often it takes one to three days after delivery for milk production to reach appreciable levels. The expulsion of the placenta at delivery initiates milk production and causes the drop in circulating estrogens and progesterone. The physical stimulation of suckling causes the release of oxytocin and stimulates prolactin secretion, causing more milk production. Week 1 begins with fertilization of the egg and ends with implantation of the blastocyst onto the endometrial surface. It begins at conception (day 0) and ends with the entry of the morula into the uterine cavity (day 3). The conceptus is traveling down the oviduct as it passes through the 2-cell, 4-cell, and 8-cell stages. The intrauterine phase begins with entry of the morula into the uterus (day 3) and ends with implantation of the blastocyst onto the endometrial surface (day 6). The outer layer will become the trophoblast or placentae, and the inner cell mass will become the embryo. Postconception week 3: most significant event is the migration of cells through the primitive streak between the epiblast and hypoblast to form the trilaminar germ disk with ectoderm, mesoderm, and endoderm layers. Postconception weeks 4–8 (period of major teratogenic risk): during this time, the major organs and organ systems are being formed. Testosterone stimulation is required for development to continue to form the vas deferens, seminal vesicles, epididymis, and efferent ducts. If a genetic male has an absence of androgen receptors, the Wolffian duct will also undergo regression. If a genetic male has an absence of androgen receptors, external genitalia will differentiate in a female direction. Hormones Primordia Female Male Major Determinant Factors Gonadal Germ cells Oogonia Spermatogonia Sex chromosomes Coelomic Granulosa Sertoli cells epithelium cells Leydig cells Mesenchyme Theca cells Rete testis Mesonephros Rete ovarii Ductal Paramesonephric Fallopian Testis hydatid Absence of zY chromosome (Müllerian) tubes Vas deferens Testosterone Mesonephric Uterus Seminal Müllerian-inhibiting factor (Wolffian) Part of vesicles Mesonephric vagina Epididymis tubules Gartner’s Efferent ducts duct Epoophoron Paroophoron External Genitalia Urogenital sinus Vaginal Prostate Presence or absence of testosterone, Genital tubercle contribution Bulbourethral dihydrotestosterone, and 5-alpha reductase Urogenital folds Skene’s glands enzyme Genital folds glands Prostatic Bartholin’s utricle glands Penis Clitoris Corpora Labia spongiosa minora Scrotum Labia majora Table I-1-5. A teratogen is any agent that disturbs normal fetal development and affects subsequent function. The nature of the agent, as well as its timing and duration after conception, is critical. There are critical periods of susceptibility with each teratogenic agent and with each organ system. The stages of teratogenesis are as follows: From conception to end of second week: embryo either survives intact or dies because the three germ layers have not yet been formed Postconception weeks 3–8: period of greatest teratogenic risk from formation of the three germ layers to completion of organogenesis After week 9 of postconception: teratogenicity is low but adverse effects may include diminished organ hypertrophy and hyperplasia The types of agents that can result in teratogenesis or adverse outcomes are as follows: Infectious: Agents include bacteria (e. Ionizing radiation: No single diagnostic procedure results in radiation exposure to a degree that would threaten the developing pre-embryo, embryo, or fetus. No increase is seen in fetal anomalies or pregnancy losses with exposure of <5 rads. Second- and third-trimester fetuses are remarkably resistant to chemotherapeutic agents. Medications (account for 1–2% of congenital malformations): The ability of a drug to cross the placenta to the fetus depends on molecular weight, ionic charge, lipid solubility, and protein binding. Category B: animal studies have failed to demonstrate a risk to the fetus but there are good studies in pregnant women. Examples include metformin, hydrochlorothiazide, cyclobenzaprine, amoxicillin, pantoprazole. Category C: animal studies have shown an adverse effect on the animal fetus; there are no good studies in humans but potential benefits may warrant use of the drug in pregnant women. Category D: human studies have shown an adverse effect on human fetus but potential benefits may warrant use of the drug in pregnant women. Category X: human studies have shown an adverse effect on human fetus and risks clearly outweigh benefits in pregnant women. After 2015 The A, B, C, D, and X risk categories in use since 1979 have now been replaced with narrative sections and subsections to include pregnancy (includes labor and delivery), lactation (includes nursing mothers), and females and males of reproductive potential. While the new labeling improves the old format, it still does not provide a definitive “yes or no” answer in most cases. The Pregnancy subsection will provide information about dosing and potential risks to the developing fetus, and registry information that collects and maintains data on how pregnant women are affected when they use the drug or biological product. Terminology for Perinatal Statistics Terminology Definition Abortion Pregnancy loss prior to 20 menstrual weeks Antepartum death Fetal death between 20 menstrual weeks and onset of labor Intrapartum death Fetal death from onset of labor to birth Fetal death Fetal death between 20 menstrual weeks and birth Perinatal death Fetal/neonatal death from 20 menstrual weeks to 28 days after birth Neonatal death Newborn death between birth and the first 28 days of life Infant death Infant death between birth and first year of life Maternal death A woman who died during pregnancy or within 90 days of birth Table I-1-7. Terminology for Perinatal Losses Terminology Definition Birth rate Number of live births per 1,000 total population Fertility rate Number of live births per 1,000 women ages 15–45 years Fetal mortality rate Number of fetal deaths per 1,000 total births Neonatal mortality rate Number of neonatal deaths per 1,000 live births Perinatal mortality rate Number of fetal + neonatal deaths per 1,000 total births Infant mortality rate Number of infant deaths per 1,000 live births Maternal mortality ratio Number of maternal deaths per 100,000 live births Table I-1-8. Indicators for genetic counseling during pregnancy include the following: Advanced maternal age: women age ≥35 at increased risk of fetal nondisjunction trisomies (e. Polyploidy refers to numeric chromosome abnormalities in which cells contain complete sets of extra chromosomes. The most common polyploidy is triploidy with 69 chromosomes, followed by tetraploidy with 92 chromosomes. An example of triploidy is an incomplete molar pregnancy, which occurs from fertilization of an egg by two sperm. Structural alteration refers to a condition in which chromosomal material is deleted, gained, or rearranged. An example of a chromosomal deletion is del (5p) or cri du chat syndrome, which is a deletion of the short arm of chromosome 5. Mosaicism refers to the presence of ≥2 cytogenetically distinct cell lines in the same individual. Gonadal mosaicism can result in premature ovarian failure and predispose the gonad to malignancy. Carriers of balanced reciprocal translocations have 46 chromosomes, with both derivative chromosomes present. Offspring may also have 46 chromosomes but only one of the derivative chromosomes is present. Robertsonian translocation always involves the acrocentric chromosomes and is caused by centric fusion after loss of the satellite region of the short arms of the original acrosomic chromosome. The karyotype of a balanced Robertsonian translocation will appear to have only 45 chromosomes; however, the full complement of genetic material is present, and there are no clinical effects. The offspring may have 46 chromosomes but have double the genetic material of a particular chromosome. The 2 most common aneuploidies in miscarriage are trisomy 16 and monosomy X (50% of these abnormalities are autosomal trisomies, with trisomy 16 the most common). Turner syndrome (45,X) (also known as gonadal dysgenesis or monosomy X) (1 in 2,000 births) is most often the result of loss of the paternal X chromosome; 98% of these conceptions abort spontaneously. Obstetric ultrasound shows the characteristic nuchal skin-fold thickening and cystic hygroma. Physical findings include tall stature, testicular atrophy, azoospermia, gynecomastia, and truncal obesity. Down syndrome (trisomy 21) (1 in 800 births) accounts for 50% of all cytogenetic diseases at term. The syndrome is characterized by intellectual disability, short stature, muscular hypotonia, brachycephaly, and short neck. Typical facial appearance is oblique orbital fissures, flat nasal bridge, small ears, nystagmus, and protruding tongue. Congenital heart disease (endocardial cushion defects) is more common along with duodenal atresia. Birth Rate and Rate of Down Syndrome versus Maternal Age Edward syndrome (trisomy 18) (1 in 5,000 births) is more frequent with advancing maternal age; 80% of cases occur in females. About 15% of all birth defects are attributable to Mendelian disorders; of these, 70% are autosomal dominant. Autosomal dominant Transmission occurs equally to males and females, and serial generations are affected. Autosomal dominant examples include the following: Polydactyly Marfan syndrome Neurofibromatosis Huntington chorea Myotonic dystrophy Osteogenesis imperfecta Achondroplasia Polycystic kidneys Autosomal recessive Transmission occurs equally to males and females, but the disease often skips generations. If both parents are heterozygous for the gene, 25% of offspring will be affected, 50% will be carriers, and 25% will be normal.
It is a common childhood illness characterized by a “slapped cheek” appearance on the face lasix 40 mg with amex. Fetal infection: Almost all fetal losses are linked to infections occurring prior to 20 weeks cheap lasix 40 mg line. Transient isolated fetal pleural or pericardial effusions may be seen that resolve spontaneously prior to delivery 40mg lasix mastercard. Neonatal presentation: While fetal hydrops can occur order 100 mg lasix mastercard, most intrauterine parvovirus infections do not have an adverse outcome. Maternal infection: Maternal parvovirus B-19 infections are mild and generally do not include the rash seen in children. Pregnant women exposed to or with symptoms of parvovirus infection should have serologic testing for IgG and IgM antibodies. A positive IgG and negative IgM is consistent with maternal immunity so the fetus is protected. A positive IgM antibody is consistent with acute infection and should initiate obstetric ultrasound assessment starting at 22 weeks, looking for evidence of fetal hydrops as well as fetal Doppler screening for anemia. Fetal infection: The greatest risk of serious perinatal sequelae appears to be with 1st and 2nd trimester infections. Ultrasound abnormalities seen with congenital infections include fetal growth restriction, ventriculomegaly, microcephaly, and intracranial calcifications. Neonatal presentation: Newborn findings other than listed above include ocular abnormalities (e. Maternal infection: Clinical signs consistent with Zika infection are maculopapular rash, arthralgias, conjunctivitis and fever. Zika can also be transmitted though sex without a condom with an infected person even if there are no symptoms. Symptomatic or Zika-exposed women should undergo serum and urine nucleic acid test and IgM serology as soon as possible through 12 weeks after. Positive blood tests should be followed up by prenatal ultrasound and repeated monthly looking for findings listed above. At 12 weeks’ gestation she experienced a flulike syndrome with right upper quadrant pain. Vertical transmission from mother to fetus or neonate occurs mainly during the viremia of a primary infection. However, because the result of primary infection is predisposition to a residual lifelong latency, fetal infection can occur with reactivation. Fetal infection: Transplacental infection rate is 50% with maternal primary infections regardless of the pregnancy trimester, but <1% with recurrent infections. Only 10% of infected infants have clinical disease, which includes petechiae, mulberry skin spots, meningoencephalitis, periventricular calcifications, hepatosplenomegaly, thrombocytopenia, and jaundice. On examination she had localized, painful, ulcerative lesions on her right vaginal wall. Transplacental transmission from mother to fetus can occur with viremia during the primary infection but is rare. Fetal infection: The transplacental infection rate is 50% with maternal primary infections. Those who survive have severe sequelae: meningoencephalitis, intellectual disability, pneumonia, hepatosplenomegaly, jaundice, and petechiae. Maternal infection (two types): Primary herpes results from a viremia and has systemic manifestations: fever, malaise, adenopathy, and diffuse genital lesions (vagina, cervix, vulva, and urethra). Transplacental fetal infection is possible; however, in 2/3 of cases the infection is mild or subclinical. Recurrent herpes results from migration of the virus from the dorsal root ganglion but is localized and less severe, with no systemic manifestations. Fetal infection results only from passing through a birth canal with lesions present. Sharing contaminated needles, having sexual intercourse with an infected partner, and perinatal transmission are the most common modes of transmission. Fetal infection: Transplacental infection occurs, but the major route of vertical transmission is contact with infected genital secretions at the time of vaginal delivery. With elective cesarean section without labor and before membrane rupture, the perinatal infection rate may be <5%. Mode of delivery: Vaginal delivery should be planned at 39 weeks, with the following guidelines: Avoid amniotomy as long as possible. If viral load ≥1,000 copies/mL, offer cesarean section at 38 weeks without amniocentesis. She admits to a past history of substance abuse but states she has been clean for 6 months. With her second pregnancy, she experienced a preterm delivery at 34 weeks’ gestation of a male neonate who died within the first day of life. She states that at delivery the baby was swollen with skin lesions and that the placenta was very large. She was treated with antibiotics but she does not remember the name or other details. Syphilis is caused by Treponema pallidum, a motile anaerobic spirochete that cannot be cultured. Syphilis does not result in a state of immunity or latency; the infection can be eradicated by appropriate treatment but reinfection can occur over and over again. It is spread as a sexually transmitted disease by intimate contact between moist mucous membranes or congenitally through the placentae to a fetus from an infected mother. Fetal infection: Transplacental infection is common with vertical transmission rates of 60% in primary and secondary syphilis. Without treatment, manifestations of early congenital syphilis include nonimmune hydrops, macerated skin, anemia, thrombocytopenia, and hepatosplenomegaly. Neonatal infection: Late congenital syphilis is diagnosed after age 2 years and includes “Hutchinson” teeth, “mulberry” molars, “saber” shins, “saddle” nose, and 8th nerve deafness. Maternal infection (four types): Primary syphilis is the first stage after infection. Papules become painless ulcers with rolled edges (chancres) which appear 2–3 weeks after contact at the site of infection, most commonly the vulva, vagina, or cervix. Around 2–3 months after contact, fever, malaise, general adenopathy, and a maculopapular skin rash (“money spots”) are seen. The treponema-specific tests do not correlate with disease activity and remain positive in spite of treatment. Tertiary syphilis is a symptomatic stage with symptoms dependent on which organ system is affected by the classic necrotic, ulcerative nodules (gummas). Maternal Syphilis Prevention includes the following: Vaginal delivery is appropriate with cesarean section only for obstetric indications. Follow the principles of avoiding multiple sexual partners, and promote use of barrier contraceptives. Even if the gravida is penicillin-allergic, still give a full penicillin dose using an oral desensitization regimen under controlled conditions. The Jarisch-Herxheimer reaction is associated with treatment and occurs in 50% of pregnant women. It is associated with acute fever, headache, myalgias, hypotension, and uterine contractions. She received 2 units of packed red blood cells two years ago after experiencing postpartum hemorrhage with her last pregnancy. Sharing contaminated needles, having sexual intercourse with an infected partner, and perinatal transmission are the most common ways of transmission. Fetal infection: Transplacental infection is rare, occurring mostly in the third trimester. The main route of fetal or neonatal infection arises from exposure to or ingestion of infected genital secretions at the time of vaginal delivery. Of those neonates who get infected, 80% will develop chronic hepatitis, compared with only 10% of infected adults. Chronic hepatitis: Cirrhosis and hepatocellular carcinoma are the most serious consequences of chronic hepatitis. Prevention includes: Vaginal delivery is indicated with cesarean section only for obstetric indications. On pelvic examination the fetal membranes are seen bulging into the vagina, and no cervix can be palpated. Two years ago she underwent a cervical conization for cervical intraepithelial neoplasia.