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· 6 : · 7 A. Acquired cardiac valvular disease · 8 B. Chronic lymphocytic leukemia • 9 C. Duodenal atresia • 10 D. Pick disease E. Rocker-bottom feet
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• 9 • 10
Image copyright © 2008 Mirza eta/; licensee BioMed Central Ltd
A i s no t correct . 1 2°/o chose this. Congenital (rather than acquired) cardiac disease is commonly associated with trisomy 21; especially common are endocardial cushion defects. EndoCArdl I cuduon5 Conoen1tal d1sorder Tnsomy Down syndrome Cardiovascular disease Endocardium B is not correct . 11°/o chose this. Down svndrome is associated with acute lvmohocvtic leukemia. not chronic lvmohocvtic leukemia. 8 s 8 Lode. Suspe-nd End Bloc:k Item: 1 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 1653 J.. Previous Next LAbf aiUI~S Notes Calculator 1 Image copyright © 2008 Mi!za • 2 eta/; licensee BioMed Central Ltd • 3 • 4 A is not correct . 12% chose this. . 5 Congenital (rather than acquired) ca rdiac disease is commonly associated with trisomy 21; especially common are endocardial cushion . 6 defects. Endocardial cushions Congenital disorder Trisomy Down syndrome Cardiovascular disease Endocardium • 7 • 8 B is not correct. 11% chose this. • 9 Down syndrome is associat ed with acute lymphocytic leukemia, not ch ron ic lymphocytic leukemia . Down syndrome Acute lymphoblastic leukemia 6-cell chronic lymphocytic leukemia Leukemia . 10 D is not correct. 3°/o chose t his. The brains of patients with Down syndrome have changes similar to those of Alzheimer disease, not Pick disease, after the age of 35. Down syndrome Alzheimer's disease
E is not correct. 8°/o chose this. Rocker-bottom feet are cha racterist ic of trisomy 18 ( Edwards syndrome) and trisomy 13 ( Patau syndrome). Rocker bottom foot Patau syndrome Edwards syndrome Trisomy
Bottom Line: Down synd rome (trisomy 21) results in infants with wide-spaced eyes and epicanthal folds. Its incidence is highest in mothers with advanced maternal age. Down syndrome has many associat ed comorbidities, includ ing duodenal at resia and endocardial cushion defects. Endocardial cushions Down syndrome Duodenal atresia Advanced maternal age Trisomy Atresia Duodenum Comorbidity Epicanthic fold
141;fil·1i•J for year:[2017 • FIRS T AID FACTS
FA17 p 59.1 Autosomal trisomies 8 s 0 Lock Suspend End Block Item: 1 of 10 - , • Mark -
· 10 Meiosis I
c :> c ::> C:> Meiosis II c ::> ~ A A A A' ""'i'"''"' Ill Ill I I Gametes II II I Ill n+ 1 n+ 1 n-1 n-1 n n n- 1 n+l I I Trisomy Monosomy Normal Mono so my Trisomy
• 8 s ~ L.odt Su~pl'nd End Block Item: 1 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 1653 J.. Previous Next LAbf aiUI~S Notes Calculator 1 • 2 FA17 p 369.1 • 3 Other intestinal disorders • 4 Acute mesenteric Critica 1 blockage of intestina 1 blood Ao w (often embolic occlusion of SMA) ..... small bowel . 5 ischemia necrosis fJ ..... abdominal pain out of proportion to physical findings. May see red "currant jelly" . 6 stools. • 7 • 8 Chronic mesenteric "Intestinal angina": atherosclerosis of celiac artery, SMA, or lMA ..... intestinal hypoperfusion • 9 ischemia ..... postprandial epigastric pain ..... food aversion and weight loss. • 10 Colonic ischemia Reduction in intestinal blood flow causes ischemia. Crampy abdominal pain followed by hematochezia. Commonly occurs at watershed areas (splenic fl exure, distal colon). Typically affects elderly. Thumbprint sign on imaging due to mucosal edema/hemorrhage. Angiodysplasia Tortuous dilation of vessels I}] ..... hematochezia. Most often found in the right-sided colon. More common in older patients. Confirmed by angiography. Adhesion Fibrous band of scar tissue; commonly forms after surgery; most common cause of small bowel obstruction mi. Can have well-demarcated necrotic zones. Ileus Intesti nal hypomotility without obstruction ..... constipation and l flatus; distended/tympanic abdomen with l bowel sounds. Associated with abdominal surge ri es, opiates, hypokalemia, sepsis. Treatment: bowel rest, electrolyte correction, cholinergic drugs (s timulate intestinal motility). Meconium ileus ln cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth. Necrotizing Seen in premature, formula-fed infants with immature immune system. Necrosis of intestinal enterocolitis mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis m. free air in abdomen, portal ve nous gas.
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• 4 · 5 · 6 · 7
• 9 • 10 ..
What was the most likely karyotype of this infant?
: A. 46 XY, deletion at Sp B. 46 XY, microdeletion at 22q11 C. 47 XY, trisomy 13 8 s 8 Lode. Suspe-nd End Bloc:k What was the most likely karyoty pe of this infant?
: A . 46 XY, deletion at Sp B. 46 XY, microdeletion at 22qll C. 47 XY, trisomy 13 D. 47 XY, trisomy 18 E. 47 XY, trisomy 21 • 8 s ~ L.odt Su~pl'nd End Block Item: 2 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 3351 J.. Previous Next LAbf aiUI~S Notes Calculator 1 The correct a nswer is 0. 59°/o chose t his. 2 This infant was born with trisomy 18, also known as Edwards' syndrome. I nfants born with this disorder exhibit severe intellectual disability, • 3 rocker-bottom feet, low-set ears, micrognathia (small j aw), congenital heart disease, clenched hands wit h overlapping fingers (as shown in the image), and a prominent occiput. These babies rarely surv ive past the age of 1 year. • 4 Edwards syndrome Rocker bottom foot Micrognathism Occiput Congenital heart defect Intellectual disability Trisomy Congenital disorder Low-set ears Cardiovascular disease . 5 6°/o . 6 A is not correct . chose this. A Sp deleticon is haracteristic of cri-du-chat syndrome, which causes microcephaly, severe intellectual disability, high-pitched crying, • 7 epicanthal folds, and ca rdiac abnormalities. Persons with this disorder generally have a normal lifespan. • 8 Microcephaly Cri du chat Intellectual disability Epicanthic fold • 9 B is not correct. 7% chose this . • 10 The 22qll syndrome, also known as DiGeorge's syndrome, results from the abnormal development of the third and fourth pharyngeal pouches. The principle defects can be remembered by the mnemonic CATCH-22, and include Cleft palate, A bnormal facies, Thymic aplasia, Cardiac defects, Hypocalcemia, and deletion of chromosome 22. Those born without fatal heart defects usually survive to adulthood . DiGeorge syndrome Palate Chromosome Aplasia Pharynx Congenital heart defect
C is not correct. 24% chos e this . Pat au's syndrome, or trisomy 13, is a ra re ca use of severe intellectual disabilit y. I nfants present with congenital anoma lies such as microophthalmia, microcephaly, cleft lip/palat e, abnormal forebrain st ructures, polydactyly, and congenital heart disease. These infa nts rarely survive past the age of 1 year. Patau syndrome Microcephaly Polydactyly Intellectual disability Congenital heart defect Cleft lip and palate Trisomy Congenital disorder Forebrain Cardiovascular disease Disability
E is not correct. 4 °/o chos e this. Down syndrome, or trisomy 2 1, is the most common chromosoma l disorder and the leading ca use of congenital intellectual disabilit y. Children born with trisomy 2 1 may present wit h int ellectual disability, flat facial profiles, prominent epicanthal folds, simian palma r crease, duodenal atresia, or hea1t defect s. The average age of death for a person with Down syndrome is 50-55 years. Down syndrome Intellectual disability Duodenal atresia Trisomy Single transverse palmar crease Congenital disorder Genetic disorder Chromosome abnormality Atresia Epicanthic fold Duodenum
Chromosome
Bottom Line: Abnormally large cranium, small jaw, low-set ears, and clenched hands with overlapping fingers are found in t risomy 18 ( Edwards' syndrome). 8 s 0 Lock Suspend End Block Item: 2 of 10 - , • Mark -
Nondisjunction in meiosis I Nondisjunction in meiosis II
Meiosis I
Meiosis II '' '' v ' ' j' Nondisjunction 8 s 8 Lode. Suspe-nd End Bloc:k Item: 3 of 10 - , • Mark -
· 6 : · 7 A. Congenital agenesis of tricuspid valve B. Defect in the septum primum • 9 C. Failure of the aorticopulmonary septum to spiral • 10 0 . Patent ductus arteriosus E. Total anomalous pulmonary venous return
8 s 8 Lode. Suspe-nd End Bloc:k Item: 3 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2850 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct a ns wer is C. 55°/o chos e this . 3 Transposition of the great vessels is a congenital ca rdiac ma lformation in which t he aorticopulmonary septum fails to spiral during • 4 development and the aort a arises from the right ventricle whereas the pulmonary artery arises from the left ventricle, com pl etely separating . 5 the systemic and pulmonary circulations. These parallel circuits prevent proper oxygenation of syst emic blood in the newborn, lead ing t o . 6 cyanosis, which is cha racterized by a blue co loration in t he extremities and lips. Surv ival with t ransposition requires the presence of a shunt to allow mixing of blood from the right (pulmonary) and left (syst em ic) sides (eg, ventricular septal defect, patent ductus arteriosus, patent • 7 foramen ovale) or surgica l correction. I nfants of women who were diabetic before pregnancy are at increased risk of atriovent ricular • 8 malformations. Additionally, this is one of the most common type of congenital heart diseases listed in the answer choices that ca uses • 9 cyanosis soon after birth . Transposition of the great vessels Aorticopulmonary septum Ventricular septal defect Patent foramen ovale Cyanosis Patent ductus arteriosus Pulmonary artery Aorta Atrial septal defect Ventricle (heart) • 10 Ductus arteriosus Foramen ovale (heart) Congenital heart defect Great vessels Septum Shunt (medical) Oxygen saturation (medicine) Congenital disorder Diabetes mellitus Pregnancy Ventricular system
Coronary artery disease
A is not correct . 7°/o chose this . Tricuspid atresia is a congenit al cyanotic heart disease, wh ich is characterized by the absence of tricuspid valve. It is commonly associated with other lesions such as atrial sept al defect (ASD) and ventricular septal defect (VSD). It results in mixing of systemic and pulmonary venous blood, leading to cyanosis. It is less common than the transposition of the great vessels and does not usua lly present immediately after birth. I t is usua lly accom panied by a heart murmur. Atrial septal defect Transposition of the great vessels Tricuspid atresia Ventricular septal defect Cyanosis Tricuspid valve Cyanotic heart defect Heart murmur Congenital disorder Atresia
Cardiovascular disease Great vessels Atrium (heart) Vein B is not correct. 9% chose t his . Atrial septal defects (ASDs) usually arise from defect s in the septum secundum; however, those associated with Down syndrome arise from defects in the septum primum. ASDs allow left-to-right shu nting of blood during diastole, increasing pulmonary pressures, and present with fixed, wide splitt ing of 5 2 . ASDs are also associat ed with Eisenmenger syndrome, which is characterized by a reversa l in shunt direction as a result of prog ressive pulmonary hypert ension and resistance secondary to ch ronic overloading of the right heart . An ASD would not result in a cyanotic appea rance. Of not e, the following congenita l heart defects are noncyanotic: ASD, ventricular septal defect, and patent ductus arteriosus. Septum primum Septum secundum Down syndrome Ventricular septal defect Eisenmenger's syndrome Patent ductus arteriosus Diastole Pulmonary hypertension Ductus arteriosus Cyanotic heart defect
Cyanosis Hypertension Congenital heart defect Congenital disorder Heart Septum Hypoplastic right heart syndrome Atrium (heart) Ventricle (heart)
D is not correct. 9°/o chose t his . 8 s 0 Lock Suspend End Block Item: 3 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2850 J.. Previous Next LAbf aiUI~S Notes Calculator 1 D is not correct. 9°/o chos e this. 2 Pat ent ductus arteriosus ( PDA) is a congen it al heart defect characterized by persistence of the communicat ion between the pulmonary artery 3 and the aorta. I n the fetus, there is no need for blood to travel to the lungs for oxygenation due t o the surrounding amniotic fluid, so bl ood in • 4 the pulmonary art ery is diverted through the ductus arteriosus into the aorta for syst emic travel. Norma lly after birt h, the ductus arteriosus closes. I f, however, the ductus arteriosus remains open, blood travels the opposite way, from t he aorta to t he pulmonary artery, due to the . 5 decreased pulmonary vasculature resistance aft er birth. This can be appreciated on physica l exam with the presence of a continuous machine . 6 like murmur. These patients can also present later with progressive pulmonary hype1tension due to increased flow through the pulmonary • 7 artery. Pat ients with PDA who require its closure are administered indomethacin or may undergo surgica l ligation. PDA would not result in a cyanotic appea rance as described in this vignet te. (Another point to remember is that newborns with cyanotic congenita l ca rdiac defects may • 8 be given prost aglandin E t o maint ain the patency of the ductus a1teriosus, to allow mixing of blood from eit her side of the heart.) • 9 Patent ductus arteriosus Jndometacin Congenital heart defect Prostaglandin Aorta Pulmonary hypertension Ductus arteriosus Pulmonary artery Ligature (medicine) Amniotic fluid Cyanosis Hypertension
. 10 Cyanotic heart defect Oxygen saturation (medicine) Circulatory system Lung Fetus Congenital disorder Heart murmur Physical examination E is not correct. 20°/o chos e this. Tot al anomalous pulmonary venous return (TAPVR) is a cyanot ic congen ital heart disease, characterized by the failure of all four pulmonary veins to make normal connection t o the left atrium . I n TAPVR the pulmonary veins drain int o the right side of the hea1t . TAPVR is commonly associat ed wtih patent foramen ovale or atrial septal defect, wh ich allows blood t o shunt from t he right side of the heart t o the left (leading to cyanosis). I t is the least common t ype of cyanotic heart disease. Atrial septal defect Anomalous pulmonary venous connection Patent foramen ovale Cyanosis Cyanotic heart defect Congenital heart defect Foramen ovale (heart) Atrium (heart) Pulmonary vein
Congenital disorder Vein Ventricle (heart) Shunt (medical) Heart
Bottom Line: Cyanot ic congenit al heart diseases include transposition of the great vessels, t ricuspid atresia, t otal anomalous pulmonary venous return, tetralogy of Fa llot, and t runcus arteriosus. I n transposit ion of the great vessels, the aortico pulmonary septum fails t o spiral during development, and the syst em ic and pulmonary circulations are completely separate such that the body does not receive oxygenated blood. Transposition of the great vessels Tricuspid atresia Aorticopulmonary septum Tetralogy of Fallot Truncus arteriosus Cyanosis Cyanotic heart defect Anomalous pulmonary venous connection Great vessels Congenital disorder Septum Atresia Tricuspid valve Cardiovascular disease Coronary artery disease
141;fil·1i•J for year:[2017 • FIRST AID FACTS 8 s 0 Lock Suspend End Block Item: 3 of 10 - , • Mark -
• 4 Congenital heart diseases · 5 RIGHT TO LEFT SHUNTS Early cyanosis-"blue babies." Often diagnosed The 5 T\: · 6 prenatally or become evident immedia te!~ l. Truncus arteriosus (I vessel) · 7 after birth. Usually require urgent surgical 2. Transposition (2 S\\ itched \'essels) · 8 treatment and/or maintenance of a PDA. 3. l'ricuspid atresia (3 = Tri) • 9 4. Tetralogy of I'a llot (4 = Tetra) • 10 5. TAP R (5 letters in the name) Persistent truncus Truncus arteriosus fails to divide into arteriosus pulmonary trunk and aorta due to lack of aorticopulmonary septum formation; most patients have accompanying VSD. 0 -transposition of Aorta leaves RV (anterior) and pu lmonary trunk great vessels leaves LV (posterior) - separation of systemic Pulmonary artery and pulmonary circulations. 1 ot compatible with life unless a shunt is present to allow mi xi ng of blood (cg, VSD, PDA, or pat·cnt foramen o,·ale). Due to failure of the aorticopulmonary septum to spiral. r--...__ Left Without surgical intervention, most infants die ventriCle within the first few months of life.
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• 9 f) Right \'entricular hypertrophy (RVH )- • 10 boot-shaped heart on CXR e Qyerriding aorta 0 \ SD Pulmonary stenosis forces right-to-left Ao" across VSD ..... RVII, "tel spells" (often caused br crying, fever, and exercise due to exacerbation of RV outflow obstruction).
Total anomalous Pulmonary veins drain into right heart pulmonary venous circulation (SVC, corona ry sinus, etc); return associated with SO and somet imes PDA to allow for right-to-left shunting to maintain CO. Ebstein anomaly Characterized by displacement of tricuspid vah-e leaflets downward into RV, artificially "atrial izing" the ventricle. Associated with tricuspid regurgitation and right H F'. Can be 8 s 8 Lode. Suspe-nd End Bloc:k Item: 3 of 10 - , • Mark -<] 1:> ""'I ~· 1!';:'1 QIO: 28 5 0 ~ Prev1o us Next Labf a lues Notes Calculator
1 & LEFT TO ·RIGHT SHUNTS Acya notic at presentation; cyanosis may occur Righl-lo-1. eft shunts: ea RLy cyanosis. 2 Left-to-Right shunts: "LateR" cyanosis. 3 years later.
• 4 F'requencr: VSD > ASD > PDA.
· 5 Ventricular septal .\!lost common congenital cardiac defect. 0 2 saturation t in RV and pulmonary artery. · 6 defect As) mptomatic at birth, mar manifest weeks · 7 later or remain asymptomatic throughout life. · 8 lost self resohe; larger lesions ma) lead to I, · 9 o,·erload and HF. · 10 Atrial septal defect Defect in interatrial septum : ; loud Sl; "ide, 0 2 saturation t in RA, RV, and pulmonary fixed split S2. Ostium secundum defects arterr May lead to paradoxical emboli most common and usually occur as isolated (S) stemic \'enous emboli use ASD to bypass findings; ostium primum defects rarer yet lun gs and become systemic arterial emboli). usually occur with other cardiac anomalies. Symptoms range from none to HF'. Distinct from patent foramen ova le in that septa are missing tiss ue rather than unfused.
Patent ductus In fetal period, shu nt is right to left (no rmal). "Endomethacin" (indomethacin) ends patency arteriosus In neonatal period, l pulmonary vasc ular of PDA; PG E keeps ductus Going (may be resistance ..... shunt becomes lefllo right necessary to sustain life in conditions such as - progressive RV11 and/or L 11 and IJ F. 1r ansposition of the great vessels). Associated with a continuous, "machine-like" PDA is normal in utero and normallr closes onl y murmur. Patency is maintained by PCE after birth. synthesis and low 0 2 tension. Uncorrected • 8 s ~ L.odt Su~pl'nd End Block Item: 3 of 10 - , • Mark -
Eisenmenger Uncorrected left-to-right shunt (VSD, ASD, syndrome PDA) - t pulmonary blood Ao,, ..... pathologic remodeling of \'asculature ..... pulmonary arterial hypertension . RVH occurs to compensate ..... shunt becomes ri ght to left. Causes late cyan osis, clubbing [!], and polycy themia. Age of onset va ri es.
OTHER ANOMALIES Coarctation of the Aortic narrowing near insertion of ductus ~Preductal aorta arteriosus ("juxtaductal "). Associated with / coarclillion / Postduc~al bicuspid aortic \'alve, other heart defects, and coarctatoo Turner s\'nclrome. Hvnerten <; ion in unnPr 8 s 8 Lode. Suspe-nd End Bloc:k Item: 3 of 10 - , • Mark -
OTHER ANOMALIES Coarctation of the Aortic narrowing near insertion of ductus ./Pr eductal aorta arteriosus ("j uxtaductal"). Associated with / coorctation Ao /""Postductal bicuspid aortic valve, other heart defects, and coo relation Turner syndrome. Hypertension in upper ~D uctus extremities and weak, delayed pulse in lower PA arteriosum extremities (brachial-femoral delay). With age, intercostal arteries enlarge due lo colla teral circulation; arteri es erode ribs ..... notched appearance on CXR. Complications include HF, t ri sk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis.
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· 6 : · 7 A. Germinal center B. Medullary cords • 9 C. Medullary sinuses • 10 0 . Paracortex E. Primary follicle
8 s 8 Lode. Suspe-nd End Bloc:k Item: 4 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 3088 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct answer is 0. 64 °/o chose t his. The abnormal development of the third and fourth branchial pouches in embryology results in a congenital T- lymphocyte deficiency, known as 3 DiGeorge syndrome. Patients wit h this syndrome present with hypoplasia of the t hymus and parathyroid glands as well as with facial and 4 ca rdiac abnormalities. Clinically, patients present with recurrent fungal and vira l infections as well as with tetany due to the hypocalcemia that . 5 accompanies hypoparathyroidism. With a deficiency of T lymphocytes, the T-ce ll- dependent lymph node structure is affected as well. . 6 Therefore, one would expect to see the paracort ex least developed, as this is the lymph node com partment that houses T lymphocytes as they await antigen presentation and subsequent B-lymphocyt e activation. • 7 Lymph node Hypoparathyroidism Hypocalcaemia 8 cell Thymus DiGeorge syndrome T cell Antigen Embryology Lymphocyte Parathyroid gland Congenital disorder Antigen presentation Hypoplasia Virus • 8 A is not correct . 18% chose this . • 9 A follicle that has a centra l pale area is ca lled a germinal cent er and consists of actively proliferating B lymphocytes. The pallor is generated • 10 because when actively proliferatcing, the hromatin of the B lymphocytes is unraveled, allowing replication, and is t herefore lacking the condensed nature that contribut es t o the dark ce nters of the dormant follicles. Both primary follicles and germinal centers are B-ce ll dependent regions of lymph nodes and are therefore norma lly developed in people with DiGeorge syndrome. Germinal center 8 cell Chromatin Lymph node Lymphocyte DiGeorge syndrome Hair follicle Lymph
B is not correct. 5% chose t his. The medullary cords consist primarily of plasma cells in their final stage of maturation int o immunoglobulin-secreting cells. This area, normally devoid of T lymphocyt es, would therefore be normally developed in a patient with DiGeorge syndrome. DiGeorge syndrome Lymphocyte T cell Plasma cell Blood plasma
C is not correct. 6 °/o chose this. Medullary sinuses of lymph nodes drain lymph from cortica lT sinuses. hey connect t o efferent lymphatic vessels. They are not necessari ly underdeveloped in a pat ient with T-cell deficiency. Medullary sinuses Lymphatic vessel Lymph node T cell Efferent nerve fiber Lymph Sinus (anatomy) Paranasal sinuses Lymphatic system
E is not correct. 7°/o chose this. The B lymphocytes are concentrat ed in lymphoid follicles locat ed in the superficial cortex. This is also the site where B lymphocytes become activat ed and begin their maturation process. If the cent er of the lymphoid follicl e is lacking a central pale area and it is homogeneously dense, it is ca lled a primary follicle. Here, B lymphocytes aggregate and are usually dormant. Lymph node Lymphocyte Hair follicle OVarian follicle Lymphatic system B cell
Bottom Line: 8 s 0 Lock Suspend End Block Item: 4 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 3088 J.. Previous Next LAbf aiUI~S Notes Calculator 1 Lymph node Hypoparathyroidism Hypocalcaemia B cell Thymus DiGeorge syndrome T cell Antigen Embryology Lymphocyte Parathyroid gland Congenital disorder Antigen presentation Hypoplasia Virus 2 A is not correct. 18% chose this. 3 A follicle that has a central pale area is ca lled a germinal cent er and consists of actively proliferating B lymphocytes. The pallor is generated 4 because when actively proliferating, the chromatin of the B lymphocytes is unraveled, allowing replication, and is t herefore lacking the condensed nature that contribut es t o the dark ce nters of the dormant follicles. Both primary follicles and germinal centers are B-cell . 5 dependent regions of lymph nodes and are therefore normally developed in people with DiGeorge syndrome. . 6 Germinal center 8 cell Chromatin Lymph node Lymphocyte DiGeorge syndrome Hair follicle Lymph • 7 B is not correct. 5% chose this. • 8 The medullary cords consist primarily of plasma cells in their final stage of maturation int o immunoglobulin-secreting cells. This area, normally • 9 devoid of T lymphocyt es, would therefore be normally developed in a patient with DiGeorge syndrome . • 10 DiGeorge syndrome Lymphocyte T cell Plasma cell Blood plasma C is not correct. 6°/o chose this . Medullary sinuses of lymph nodes drain lymph from cortica lT sinuses. hey connect t o efferent lymphatic vessels. They are not necessari ly underdeveloped in a pat ient with T-cell deficiency. Medullary sinuses Lymphatic vessel Lymph node T cell Efferent nerve fiber Lymph Sinus (anatomy) Paranasal sinuses Lymphatic system
E is not correct. 7°/o chose this. The B lymphocytes are concentrat ed in lymphoid follicles locat ed in the superficial cortex. This is also the site where B lymphocytes become activat ed and begin their maturation process. If the cent er of the lymphoid follicle is lacking a central pale area and it is homogeneously dense, it is ca lled a primary follicle. Here, B lymphocytes aggregate and are usually dormant. Lymph node Lymphocyte Hair follicle OVarian follicle Lymphatic system B cell
Bottom Line: DiGeorge syndrome is marked by congenital T-lymphocyte deficiency. DiGeorge syndrome T cell Congenital disorder
l@ljl'il·1i•J for year:[2017 • J FIRST AID FACTS
8 s 0 Lock Suspend End Block Item: 4 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 3088 ~ Prev1ous Next Labfa lues Notes Calculator 1 2 FA17 p 92.2 3 Lymph node A zol ymphoid organ that has many afferents, l or more efferents. Encapsulated, with trabeculae. 4 Functions are nonspecific filtration by m
1 & FA17p112.1 2 3 Immunodeficiencies 4 DISEASE DEFECT PRESENTATION FINDINGS · 5 B-cell disorders · 6 X-linked (Bruton) Defect in BTK, a I) rosine Recurrent bacterial and Absent B cells in peripheral · 7 agammaglobulinemia kinase gene - no B-cell enterO\·iral infections after 6 blood, l lg of all classes. · 8 maturation. X-linked reccssi'e months ( l maternal lgG). bsent/scanl) lymph nodes · 9 (t in BO\·s). and tonsils. Li,·e ,-accines · 10 contraindicated.
Selective lgA Unknown. ~ l ost common )0 ~ lajority \ symptomatic. l lgA with normallgC, l g~ l deficiency immunodeficiency. Can see \ ima) and Cl levels. t susceptibility to infections, Autoimmune giardiasis. disease, \ top), Anaphylaxis to lg \ -conta ining products. Common variable Defect in B-cell differentiation. Usua ll y presents after age 2 and l plasma cells, immunodeficiency il any causes. may be eonsidcn1bl)' delayed; l immunoglobulins. t risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infection s. T cell disorders Thymic aplasia 22ql l deletion; failure Tetany (hypocalcemia}, l T cells, l PTI I, l Ca2+. (DiGeorge syndrome) to develop 3rd and 4th recurrent viral/fungal Absent thymic shadow on pharyngeal pouches - absent infections (T-cell deficiencr}, CXR. • 8 s ~ L.odt Su~pl'nd End Block Item: 4 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 3088 ~ Prev1o us Next Labf a lues Notes Calculator
2 IL-12 receptor l Th I response. utosomal Oisse1 ninateclmycobacterial l iFt -y. 3 deficiency recess1ve. and funga l infection s; may 4 present after administration of · 5 BCC ,·accine. · 6 Autosomal dominant Deficienc\' of Th 17 cells clue to F\TI<:D · 7 : coarse Facies, cold t IgE, l IF '-y. · 8 hyper-lgE syndrome STAT3 mutation ..... impaired (non inOamed) staph) lococcal t eosinophils. · 9 (Job syndrome) recruitment of neutrophils to \ bscesses, retained primary · 10 sites of infection. Teeth, t lgE. Dermatologic problems (eczema). Bone fractures from minor trauma. Chronic T-cell dysfunction. Many oninvasi\'e Candida albicans Absent in vitro T-cell mucocutaneous causes. infections of skin and mucous proliferation in response to candidiasis membranes. Candida antigens. Absent cutaneous react ion to Candida antigens. B- and T-cell disorders Severe combined Several types includi ng Failure to thrive, chronic l T-cell receptor excision immunodeficiency defective IL-2R gamma chain diarrhea, thrush. Recu rrent circles (TRECs). (most common, X-I inked), viral, bacterial, fungal, and Absence of thr mic shadow adenosine deaminase protozoal infections. (CXR), germinal centers deficiency (autosomal Treat111ent: avoid live vaccines, (lymph node biopsr). and recessi,·e). gi\'e antimicrobial prophylaxis T cells (Row cytometry). anci iVIC; bone marrow • 8 s ~ L.odt Su~pl'nd End Block Item: 4 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 3088 ~ Prev1o us Next Labf a lues Notes Calculator
1 & Ataxia-telangiectasia t 2 Defects in ATM gene - failure Triad: cerebellar defects AFP. 3 to repair D1 A double strand ( \ taxia), spider Angiomas l lgA, lgC, and lgE. breaks - cell c\·cle arrest. (tela ngiectasia rJ), lg \ Lymphopenia, cerebellar 4 ~ ' · 5 deficiency. atrophy. ~ · 6 t risk of lymphoma and · 7 Jl c leukemia. · 8 Hyper-lgM syndrome 1ost commonly due to Se,ere p)ogenic infections i':ormal or t lg 11. · 9 defecti,·e CD40L on Th cells ea · 10 rl y in life; opportunistic ll IgG, IgA, lgE. - class switching defect; infection with Pneumocyslis, Failure to make germinal X-linked recessi,·e. Cryptosporidium, C~ rv. centers. Wiskott-Aidrich Mutation in WASp gene; \\ \TER: Wiskott-Aidrich: l to norma I IgG, Ig .\ I. syndrome leukocytes and platelets T hrombocytopenia, Eczema, t lgE, lgA. unable to reorganize actin Recurrent (pyogenic) Fewer and sma ll er platelets. cytoskeleton - defective infecti ons. antigen presentation. X-linked t ri sk of autoimmune disease recess•ve. and malignancy. Phagocyte dysfunction Leukocyte adhesion Defect in LFA-1 intcgrin Recurrent skin and mucosal t neutrophils. deficiency (type 1) (C018) protein on bacterial infections, absent Absence of neutrophils at phagocytes; impaired pus, impaired wo und healing, in feet ion sites. migration and chemotaxis; delayed (> 30 days) separation autosomal recessi,·e. of umbilica l cord. Chediak-Higashi Defect in lysosomal traffi cking Recurrent pyogenic Giant granules (IE), arrows) in • 8 s ~ L.odt Su~pl'nd End Block Item: 4 of 10 - , • Mark -
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8 s 8 Lode. Suspe-nd End Bloc:k Item: 5 of 10 - , • Mark -<] 1:> ""'I ~· 1!';:'1 QIO: 2613 ~ Prev1o u s Next Labf a lues Note s Calculator 1 2 The correct answer i s B. 46°/o chose this. 3 The AER is a region of thickened ectoderm at t he distal end (or apex) of each limb bud. It is responsible for 4 the elaboration of fibroblast growth fa ctor (FGF), a factor that stimulates mitosis of the underlying 5 mesoderm (thereby lengthening the developing limb). Dorsal-ventral patterning, on the other hand, occurs · 6 through the expression of the Wntl gene, which directs organization of the limb along the dorsal-ventral axis (see diagram). The dorsal ectoderm, rather than the AER, is responsible for dorsal-ventral patterning. · 7 Therefore, removing the distal tip of the limb bud will destroy the AER but not the dorsal ectoderm, leading · 8 to a shortened limb with intact dorsal-ventral patterning · 9 · 10 progt The underlying mesoderm, also known as the progress zone, is crucial for determining the actual limb zone structures that will form.
Ectoderm F1brobl t M.. oderm MitOSIS Gene fibroblast growth factor Umb bud Growth factor Anatom1cal terms of location Ap1cal ectodermal ndge dornl
Image coUJtesy of Sisi Chen
A i s not correct . 9°/o chose this. Removal of the limb bud tip would indeed damage the AER, but this would result in both a shortened limb and aberrant patterning along the dorsal-ventral axis. Organization along the anterior-posterior axis is directed by the ZPA, a structure situated at the base of the limb bud. AnatofTitcal ter~ of locM•on lJmb bud • 8 s ~ L.odt Su~pl'nd End Block Item: S of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2613 J.. Previous Next LAbf aiUI~S Notes Calculator 1 g y 2 A is not correct . 9 °/o chos e this. 3 Removal of t he limb bud tip would indeed damage the AER, but this would result in both a shortened limb and aberrant patterning along the 4 dorsal-ventral axis. Organization along the ant erior-post erior axis is directed by the ZPA, a structure situated at the base of the limb bud. 5 Anatomical terms of location Limb bud . 6 C is not correct. 11% chos e this . • 7 Disrupting the ZPA would give rise to a limb with aberrant ant erior-posterior axis patterning and reduced length due to loss of feedback from • 8 the ZPA necessary to maintain the AER. One would also expect t o see defects in digit patterning. Anatomical terms of location Drosophila embryogenesis Regional differentiation Anterior • 9 • 10 D is not correct. 19% c hose this . Removing the limb bud tip is more likely t o damage the AER than t he ZPA. Damage to t he ZPA would disrupt pat terning along the anterior post erior axis (as well as digit patterning), but would be unlikely t o result in a shortened limb. Anatomical terms of location Limb bud E is not correct. 1 5°/o chose this. Removal of t he limb bud tip would be more likely to damage the AER than the ZPA, a collection of mesodermal cells found at the base of the limb bud . The ZPA produces a protein ca lled sonic hedgehog, which helps direct organization of the developing limb along the anterior post erior axis. Sonic hedgehog also helps direct patterning of the digits. While t his answer choice correct ly lists t he expected effects of such a manipulation on the developing limb, these would be attributabl e to damage to t he AER rather than the ZPA. Sonic hedgehog Limb bud Mesoderm Hedgehog Germ layer Protein Drosophila embryogenesis Anatomical terms of location
Bottom Line: Removal of t he dist al limb bud would destroy the apical epidermal ridge, result ing in shortened limb length with intact dorsal-ventral patterning . Anatomical terms of location
141;fil·1i•J for year:[2017 • j FIRST AID FACTS . .
8 s 0 Lock Suspend End Block Item: 5 of 10 - , • Mark -<] 1:> ""'I ~· 1!';:'1 QIO: 2613 ~ Prev1o u s Next Labf a lu es Note s Calculator 1 FA17p 580.1 2 Important genes of embryogenesis 3 4 Sonic hedgehog gene Produced at base of limbs in zone of polari7ing activity. Involved in patterning along 5 anteroposterior axis and CNS development; mutation can cause holoprosencephaly. · 6 Wnt-7 gene Produced at apical ectodermal ridge (thickened ectoderm at distal end of each de\'eloping limb). · 7 'ecessar) for proper organitation along dorsal-\ entral axis. · 8 FGF gene Produced at apical ectodermal ridge. Stimulates mitosis of underlying mesoderm. providing for · 9 · 10 lengthening of li mbs. Homeobox (Hox) Jm·olved in segmental organiza tion of embryo in a craniocaudal direction. Code for tra nscription genes factors. Hox mutations - appendages in "rong local ions.
FA17 p 580.2 Early fetal development Early embryonic H • 1 of ctwomos.:'rnt'\ development C • I o4 clvomolock/DNA""' 1 DAY! DAYS 2·3 Zygoto <4(
DAY4 Ferti lization ~ J MOfllb OAY5 DAYO ~OC)'SI
OAYS6-10 lmplarlabon • 8 s ~ L.odt Su~pl'nd End Block Item: S of 10 - , • Mark -
DAYS6-10 I lmplantahon Ov\Jia!JOn/ 2'oocy1e )
Within week 1 hCC secretion begins around the lime of Blastocyst "sticks" at day 6. implantation of blastocyst. Within week 2 Bilaminar disc (epiblast, hypoblas t). 2 weeks = 2 layers. Within week 3 Gastrulation forms trilaminar cmbrronic disc. 3 weeks = 3 layers. Cells from epiblast invaginate - primitive streak - endoderm, mesoderm, ectoderm. 1 otochord arises from midli ne mesoderm; o,·erlying ectoderm becomes nemal plate. 8 s 8 Lode. Suspe-nd End Bloc:k Item: 6 of 10 - , • Mark -
8 s 8 Lode. Suspe-nd End Bloc:k Item: 6 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2599 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct a nswer is E. 77°/o chose this. 3 The ch ild is presenting with DiGeorge syndrome, which is due t o abnormal development of the third and fourth branch ial (pharyngeal) pouches. This leads t o hy poplasia of the thymus and parathyroid glands. Without a properly functioning thymus, T lymphocyte maturation 4 fails, resulting in impaired cell-mediat ed immunity. Thus, patients with DiGeorge syndrome often present with recurrent viral and fungal 5 infections, as in this patient . Without adequat e product ion of parat hyroid hormone, t hese patients are often hypocalcemic, leading to tetany 6 and seizures. DiGeorge syndrome ca n be summarized by the mnemonic CATCH-22: Cardiac defects, Abnormal facies, Thymic hypoplasia, I • 7 Cleft palate, and Hypocalcemia due to a microdelet ion on chromosome 22. T cell Parathyroid hormone DiGeorge syndrome Thymus Lymphocyte Cell-mediated immunity Tetany Deletion (genetics) Pharynx Chromosome Epileptic seizure Hypocalcaemia Parathyroid gland Hypoplasia • 8 Hormone Palate Virus Mycosis • 9 • 10 A is not correct . 4 °/o chose t his . The first and second branchia l arches pl ay no role in DiGeorge syndrome. For first -arch derivatives, think "M ": Mandible, Malleus, sphenoMandibular ligament; muscles of Mastication (teMporalis, Masseter, Medial and lateral pterygoids). The first arch is associated with cra nial nerve V. For second-arch derivatives, think "S" : St apes, Styloid process, Stylohyoid ligament, muscles of facial expression, Stapedius, Stylohyoid. Cra nial nerve VII is associated wit h the second arch. Lateral pterygoid muscle Facial muscles Branchial arch Facial nerve Cranial nerves Pharyngeal arch DiGeorge syndrome Facial expression Skull B is not correct. 5% chose t his . The first branchia l pouch arises in the pharynx and ext ends laterally and ce phalad to contact the first branchial cleft, forming the eustachian tube. The second branch ial pouch originates in t he oropharynx and contributes t o the middle ear and t onsils. They are not involved in DiGeorge syndrome. Pharyngeal pouch (embryology) Eustachian tube DiGeorge syndrome Pharynx Middle ear Pharyngeal groove Tonsil Pharyngeal arch C is not correct. 9 °/o chose this . The fourth and sixth pharyngeal arches do not play a role in DiGeorge syndrome. The fourth arch is responsible for muscles of the soft palate (but not the tensor veli palatini, a first arch derivative), the muscles of the pharynx (except the st ylopharyngeus), the cricothyroid, and the aortic arch. Fourth-arch muscles are innervated by the superior laryngeal bra nch of cranial nerve X. The sixth arch produces the muscles of the larynx (except for the cricothyroid) as well as the pulmonary arteries. These muscl es are innervated by the recurrent laryngeal branch of cra nial nerve X. Tensor veli palatini muscle Pharynx Larynx Soft palate DiGeorge syndrome Aortic arch Stylopharyngeus muscle Pulmonary artery Branchial arch Recurrent laryngeal nerve Vagus nerve Cranial nerves
Pharyngeal arch Artery Palate Skull D is not correct. 5°/o chose t his. 8 s 0 Lock Suspend End Block Item: 6 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2599 J.. Previous Next LAbf aiUI~S Notes Calculator 1 C is not correct. 9 °/o chose this . 2 The fourth and sixth pharyngeal arches do not play a role in DiGeorge syndrome. Th e fourth arch is responsible for muscles of the soft palate 3 (but not the tensor veli palatini, a first arch derivative), the muscles of the pharynx (except the st ylopharyngeus), the cricothyroid, and the 4 aortic arch. Fourth-arch muscles are innervated by the superior laryngeal branch of cranial nerve X. The sixth arch produces the muscles of the larynx (except for the cricothyroid) as well as the pulmonary arteries. These muscles are innervated by the recurrent laryngeal branch of 5 cranial nerve X. 6 Tensor veli palatini muscle Pharynx Larynx Soft palate DiGeorge syndrome Aortic arch Stylopharyngeus muscle Pulmonary artery Branchial arch Recurrent laryngeal nerve Vagus nerve Cranial nerves
• 7 Pharyngeal arch Artery Palate Skull • 8 D is not correct. 5°/o chose this . I • 9 The second through fourth branchial clefts form tempora ry sinuses but are obliterated before maturation. Thus, they have no derivatives in . 10 the adult. Paranasal sinuses Sinus (anatomy)
Bottom Line: DiGeorge syndrome is due to abnormal development of the third and fourth branchial pouches, and can lead t o hypocalcemia and impaired immunity. DiGeorge syndrome Hypocalcaemia
l@ljl'il·1i•J for year:[2017 • J FIRST AID FACTS
FA17 p 588.1 Branchial pouch derivatives POUCH DERIVATIVES NOTES MNEMONIC 1st pouch Middle ear cavity, eustachian Is t pouch contributes to Ear, tonsils, bottom-to-top: tube, mastoid air cells. endoderm-lined sl-ructures of I (ear), ear. 2 (tonsils), 8 s 0 Lock Suspend End Block Item: 6 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2599 J.. Previous Next LAbf aiUI~S Notes Calculator 1 FA17 p 588.1 2 Branchial pouch derivatives 3 POUCH DERIVATIVES NOTES MNEMONIC 4 5 1st pouch Middle ear cavity, eustachian Ist pouch contributes to Ear, tonsils, bottom-to-top: 6 tube, masto id air cells. endodenn-li ned st-ructures of I (ear), • 7 ear. 2 (tonsils), • 8 2nd pouch Epitheli al lining of palatine 3 dorsal (bottom for inferior • 9 tonsil. parathyroids), • 10 3 ventra I (to = thymus), 3rd pouch Dorsal wings ..... inferior 3rd pouch contributes to 3 I 4 (top = superior parathyroids. structures (thym us, left and parathyroids). Ventra l wings ..... thymus. right inferior parathyroids). 3rd-pouch structures end up below 4th-pouch structures. 4th pouch Dorsal wings ..... superior parathyroids. Ventral wings - ultimobranchial body ..... parafollicular (C) cells of thyro id. DiGeorge syndrome Chromosome 22q II deletion. Aberrant development of 3rd and 4th pouches ..... T-cell deficiency (thym ic aplasia) and hypocalcemia (fai lure of parathyroid development). Associated with cardiac defects (conotruncal anomalies).
8 s 0 Lock Suspend End Block Item: 6 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2599 J.. Previous Next LAbf aiUI~S Notes Calculator 1 • FA17 p 112.1 2 Immunodeficiencies 3 DISEASE DEFECT PRESENTATION FINDIN GS 4 5 B-cell disorders 6 X-linked (Bruton) Defect in BTK, a tyrosine Recurrent bacterial and bsent B cells in peripheral • 7 agammaglobulinemia kinase gene - no B-cell enteroviral infections after 6 blood, l lg of all classes. • 8 maturation. X-linked recessive months ( l maternal IgG) . bsent/scant y lymph nodes • 9 (t in Boys). and tonsils. Live vaccines • 10 contraindicated.
Selective lgA Unknown. Most common 1o Majority Asymptomatic. l IgA with normal IgG, IgM deficiency immunodeficiency. Can see Airway and G f levels. t susceptibility to infections, Autoimmune giardiasis. I disease, Atopy, Anaphylaxis to IgA-containing products. Common variable Defect in B-cell differentiation. Usually presents after age 2 and l plasma cells, immunodeficiency Many causes. may be considerably delayed; l immunoglobulins. t risk of autoimmune disease, bronchiectasis, lymphoma, si nopulmonary infections. T-cell disorders Thymic aplasia 22qll deletion; fai lure Tetany (hypocalcemia), l T cells, l PTH, l Ca2+. (DiGeorge syndrome) to develop 3rd and 4th recurrent viral/fungal Absent thymic shadow on pharyngeal pouches - absent infections (T-cell deficiency), CXR. • .. · ' .... 8 s 0 Lock Suspend End Block Item: 6 of 10 - , • Mark -<] 1:> ""'I ~· 1!';:'1 QIO: 2599 ~ Prev1o us Next Labf a lues Note s Calculator 1 IL-12 receptor l Th I response. Autosoma I Disseminated mycobacterial l IF -y. & 2 deficiency recess1ve. and funga l infections; may 3 present after adm inistration of 4 BCC ,·accine. 5 6 Autosomal dominant Deficiencv• ofTh 17 cells due to F\TED: coarse Facies, cold t IgE, l IF '-y. · 7 hyper-lgE syndrome STAT3 mutation ..... impaired (noninOamed) staphylococcal t eosinophils. · 8 (Job syndrome) recruitment of neutrophils to \ bscesses, retained primar) · 9 sites of infection. Teeth, t lgE, Dermatologic · 10 problems (eczema). Bone fractures from minor trauma. Chronic T-cell dysfunction. Many oninvasi,·e Candida albicans Absent in vitro T-cell mucocutaneous causes. infections of skin and mucous proliferation in response to candidiasis membranes. Candida antigens. Absent cutaneous reaction to Ccmdida antigens. I 8- and T-cell disorders Severe combined Several types including l<'ai lure to thrive, chronic l T-cell receptor excision immunodeficiency defective IL-2R gamma chain diarrhea, thrush. Recu rrent circles (TRECs). (most common, X-I inked), viral, bacterial, fungal, and Absence of thymic shadow adenosine deaminase protozoal infections. (CXR), germinal centers deficiencr (autosomal Treatment: avoid live vaccines, (lymph node biopsy), and recessi,·e). give antimicrobi
Chronic Defect of AD PI ! oxidase t susceptibility to ca t a l ase~ Abnormal dihydrorhodaminc granulomatous ..... l reactive oxygen orga nisms. (flow cytometry) test ( l green disease species (eg, superoxide) fluoresce nce). and l respirator l\'itroblue I y burst tetrazolium dye in neutrophils; X-I inked reduction test (obsolete) fails recessi,·e most common. to turn blue.
• 8 s ~ L.odt Su~pl'nd End Block Item : 6 of 10 - , • Ma rk -
3rd arch Greater horn of hyoid Stylopharyngeus (think C I IX (style- of stylophar) ngcu' pharyngeus) inner\'atcd by ~ wa llo" stylishly glossoplu1r) ngea I nerve) 4th- 6th arches Arytenoids, Cricoid, 4th arch: most phar)'ngeal 4th arch: C 1 Arches 3 and 4 form I Corniculate, constrictors; cri coth) roid , X (superior p osterior Yl of tongue; Cuneiform. Thnoid len1tor \'eli oalatini larvngeal branch) arch ) makes no 8 s 8 Lode. Suspe-nd End Bloc:k Item: 7 of 10 - , • Mark -
6 : · 7 A. Dorsal mesentery · 8 B. Lung bud • 9 C. Pancreatic islet cells • 10 D. Ureteric bud E. Ventral pancreatic bud
8 s 8 Lode. Suspe-nd End Bloc:k Item: 7 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2607 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct a nswer is E. 58°/o chose this. 3 This patient is presenting with signs and symptoms of a pancreatic adenoca rcinoma. These tumors arise most commonly in the pancreatic 4 head, and they may not manifest until an advanced stage when they have obstructed the common bile duct, resulting in j aund ice. Patients 5 with pancreatic adenocarcinoma may also experience weight loss and abdominal pain radiat ing t o the back. This patient manifests t wo other 6 signs sometimes seen in pancreatic adenoca rcinoma: migratory thrombophlebitis and a palpable gallbladder. Migratory thrombophlebitis is a condition commonly relat ed to pancreat ic ma lignancy, which leads to inflammation and painful bl ood clots in lower extremities. Given both t he 7 epidemiology of this cancer and the patient 's j aundice, it is likely that his tumor arose in the head of the pancreas, which is derived from both • 8 the vent ral and dorsal pancreatic buds. Other derivatives of the ventral bud include the uncinate process and main pancreatic duct. • 9 A is not correct . 18% chos e this. . 10 The dorsal mesentery gives rise to, among other things, the adult spleen. This patient has an adenocarcinoma of the head of the pancreas . The pancreat ic head is derived from the vent ral pancreatic bud, not the dorsal mesentery. B is not correct. 8% chose t his . This patient has adenocarcinoma of the pancreatic head. The lung bud plays a role in development of the adult lungs, but it does not contribute t o any part of t he pancreas. C is not correct. 9 °/o chose this . Pancreatic islet cells, like pancreatic acinar cells, are derived from endoderm. D is not correct. 7°/o chose this. The adult kidneys (except for the nephrons) are derived from the ureteric bud. This patient, however, presents with an adenoca rcinoma of his pancreas.
Bottom Line: Pancreatic ca ncer most commonly occurs in the pancreatic head, which arises from the ventral pancreatic bud. Symptoms of pancreatic adenoca rcinoma incl ude obst ruct ive jaund ice, weight loss, and abdominal pain rad iating to the back.
i@l;fil·1i•J for year:[2017 • J FIRST AID FACTS
8 s 0 Lock Suspend End Block Item: 7 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 2607 ~ Prev1o us Next Labf a lues Notes Calculator 1 2 141if.il;1i•l for year : 2017 • 3 FJA.ST AIO FACTS 4 5 FA17 p 380.3 6 Pancreatic Very aggressive tumor ari sing from pancreatic ducts (disorganized glandular structure \\'ith cellular 7 adenocarcinoma infiltration ); often metastatic at presentation,\\ ith a\erage survh·al - I year after diagnosis. · 8 Tumors more common in pancreatic head (- obstructi,·e jaundice). Associated with C 19-9 · 9 tumor marker (also CEA, less specific). · 10 Risk factors: Tobacco use Chronic pancreatitis (especiall y> 20 years) Diabetes Age> 50 years Jewish and African-American males Often presents with: • 1\bclominal pain radiating to back • Weight loss (due to ma labsorp tion and anorexia) • 1Jigratory thrombophlebitis-redness and tenderness on palpation of extremities (Trousseau syndrome) Obstructive jaundice with pa lpable, nontender ga llblaclcler (Courvoisier sign) Treatment: Whipple procedure, chemotherapy, radiation therapy.
FA17 p 345.2 • 8 s ~ L.odt Su~pl'nd End Block Item: 7 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 2607 ~ Prev1o u s Next Labf a lu es Notes Calculator 1 2 FA17 p 345.2 3 4 Pancreas and spleen Pancreas-deri,·ed from foregut. Ventral pancreatic buds contribute to uncinate process and main
5 embryology pancreatic duct. The dorsal pancreatic bud alone becomes the body, tail, isthmus, and accessory 6 pancreatic duct. Both the ventral and dorsal buds contribute to pancreatic head. 7 Annular pancreas- ,·entral pancreatic bud abnormall ) encircles 2nd part of duodenum; forms a · 8 ring of pancreatic ti ss ue that mar cause duodenal narro'' ing and \'Omiting. · 9 Pancreas divisum-,·entral and dorsal parts fai l to fuse at 8 weeks. Common anomalr; mostly · 10 as) mptomatic, but may cause chronic abdominal pain and/or pancreatitis. Spleen- arises in mesentery of stomach (hence is mesodermal) but has foregut supply (celiac trunk - splenic artery).
Accessory pancreatic duc:t-... Pancreatic duct
MaJOr papilla --.... Ventral pancreatic bud
process
FA17 p 217.1 • 8 s ~ L.odt Su~pl'nd End Block Item: 7 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2607 J.. Previous Next LAbf aiUI~S Notes Calculator 1 FA17 p 217.1 • 2 Paraneoplastic syndromes 3 MANIFESTA TI ON DESCRIPTION/MECHANISM MOST COMMONLY ASSOCIATED CANCER(S) 4 Cutaneous 5 6 Acanthosis nigricans llyperpigmented velvety plaques in axi lla and Cast ric adenocarcinoma and other visceral 7 neck malignancies (but more commonly associated • 8 with obesity and insulin resistance) • 9 Sign of Leser-Trelat Sudden onset of multiple seborrheic keratoses C l adenocarcinomas and other visceral • 10 mal ignancics Endocrine Hypercalcemia PTHrP Squamous cell carcinomas of lung, head, and neck; renal, bladder, breast, and ovaria n carcmomas t 1,25-(0H)z vitami n 0 3 (calcitriol) Lymphoma Cushing syndrome t ACTH Small cell lung cancer Hyponatremia (SIADH) t ADII Hematologic Polycythemia t Erythropoietin Renal cell carcinoma, hepatocell ular carcinoma, hemangioblastoma, pheochromocytoma, leiomyoma Pure red cell aplasia Anemia with low rcticulocytes Thymoma Good syndrome Hypogammaglobulinemia • 8 s 0 Lock Suspend End Block Item: 7 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 2607 ~ Prev1o us Next Labf a lues Notes Calculator 1 ' Pure red cell aplasia Anemia with low ret i culocyte~ 2 Thymoma 3 Good syndrome Hypogammaglobulinemia 4 Trousseau syndrome Migratory superficial thrombophlebitis 5 Non bacterial Deposition of sterile platelet thrombi on heart 6 denocarcinomas, especially pancreatic 7 thrombotic (marantic) valves · 8 endocarditis · 9 Neuromuscular · 10 Anti-NMDA receptor Psychiatric disturbance, memory deficits, Q,·arian teratoma encephalitis seizures, dyskinesias, autonomic instabilil), language dysfunction Opsoclonus- "Dancing eyes, dancing feet" euroblastoma (children), small cell lung myoclonus ataxia cancer (adults) syndrome Paraneoplastic Antibodies against antigens in Purkinje cells Small cell lung cancer (anti-Hu), gynecologic cerebell ar and breast cancers (anti-Yo), and llodgkin degeneration lymphoma (anti-Tr) Paraneoplastic Antibodies against llu an ti gens in neurons Small cell lung cancer encephalomyelitis Lambert-Eaton Antibodies against presynaptic (P/Q-type) Ca2+ Small cell lung cancer myasthenic syndrome channels at ll\ lJ Myasthenia gravis Antibodies against postsynaptic Ch receptors Thymoma at 'YIJ • 8 s ~ L.odt Su~pl'nd End Block Item: 8 of 10 - , • Mark -
4 5 6 7 · 8 • 9 • 10
Which of the following is t he most likely embryologic explanation for this malformation?
: A. Expansion of the fo ramen cecum B. Fa ilure of fusion of the lateral palatine processes C. Failure of fusion of the medial palatine processes D. Failure of fusion of the nasal processes E. Incomplete formation of the nasal septum
8 s 8 Lode. Suspe-nd End Bloc:k Item: 8 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 2600 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct ans wer is 0. 38°/o chose this. 3 The image shows a unilat eral cleft lip. This results from t he failure of fusion of the maxillary and medial nasal processes. The maxillary 4 process is a derivative of t he first branch ial (pharyngeal) arch, and the medial nasal processes develop from mesenchymal accumulation on the medial side of t he nasal placodes. Their failure to fuse t ogether causes a so-called cleft in the palate t hat makes t he nasal cavity and the 5 mouth contiguous. Although a cleft palate can simultaneously occur wit h a cleft lip, we are unable t o determine so in this image. 6 Cleft lip and palate Nasal cCPJity Medial nasal prominence Palate Maxillary prominence Lip Pharynx Mesenchyme Pharyngeal arch 7 A is not correct . 2°/o chose this. 8 The foramen cecum is the remnant of t he thyroglossal duct, located at the back of the tongue. The closest pathology t o an "expansion of t he • 9 foramen cecum " would be a thyroglossal duct cyst, formed when the duct persists. This would not cause a cleft lip or cleft palate. • 10 Thyroglossal duct Thyroglossal cyst Cleft lip and palate Cecum Cyst Palate Lip B is not correct. 21% chose this. Failure of fusion of only the lateral palatine processes would produce a cleft palate without a cleft lip and t hus cannot be t he explanation for the condition shown in the image. The primary palate is formed by the intermaxillary segment, and the secondary palate is formed from t he lat eral and median palatine processes and the nasal septum. Palatine process of maxilla Nasal septum Palatine bone Cleft lip and palate Nasal bone Palate Secondary palate Septum C is not correct. 34% chose this. A cleft palat e, not a cleft lip, is due t o failure of fusion of the lateral palat ine processes, the nasal septum, and/or t he medial palatine process. Although a cleft palat e ca n simultaneously occur with a cleft lip, we are unabl e to determine so in this image. Cleft lip and palate Nasal septum Palatine process of maxilla Palate Lip Palatine bone Septum Nasal bone
E is not correct. 5°/o chose this. The formation of t he nasal septum is involved in a cleft palate, not a cleft lip. Cleft lip and palate Nasal septum Palate Lip Septum Nasal bone
Bottom Line: The maxillary process is a derivat ive of the first branchial arch. Branchial arch Maxillary prominence Pharyngeal arch
8 s 0 Lock Suspend End Block Item: 8 of 10 - , • Mark -<] 1:> ""'I ~· 1!';:'1 QIO: 2600 ~ Prev1o us Next Labf a lues Notes Calculator
1 FA17 p 588.2 2 3 Cleft lip and cleft Cleft lip-failure of fusion of the maxi llary and 4 palate medial nasal processes (formation of 1° palate). 5 Cleft palate-failure of fusion of the two lateral 6 palatine shelves or failure of fusion of lateral 7 palatine sheh-es with the nasal septum and/or 8 median palatine shelf (formation of 2° palate). · 9 · 10 Cleft lip and cleft palate ha'e distinct, uvw multifactorial etiologies, but often occur Oeft palate (partial) ~ Cl~ft Up together.
FA17 p 586.2 Branchial (pharyngeal) Composed of branchial clefts, arches, pouches. CAP covers outside to inside: apparatus Branchial clefts-deri\·ed from ectoderm. Also Clefts = ectoderm called branchial grooves. Arches= mesoderm + neural crest Branchial arches-derived from mesoderm Pouches= endoderm (muscles, arteries) and neural crest (bones, ca rtilage). Pharyngeal floor Branchial pouches-derived from endoderm. __.--earulage / 1 Nerve c..____ Artery II •• Ill - • 8 s ~ L.odt Su~pl'nd End Block Item: 9 of 10 - , • Mark -
8 s 8 Lode. Suspe-nd End Bloc:k Item: 9 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 1847 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct answer is E. 46°/o chose this. 3 Congenital rubella infection can result in deafness, patent ductus arteriosus, pulmonary artery stenosis, cataracts, and microcephaly. 4 Patent ductus arteriosus Microcephaly Pulmonary artery Ductus arteriosus Congenital disorder Rubella Stenosis Congenital rubella syndrome Stenosis of pulmonary artery Cataract Hearing loss 5 Pulmonic stenosis Infection 6 A is not correct . 12% chose this. 7 Bone deformity of the nasa l bridge, or saddle nose, is seen in congenitally acquired syphilis. 8 Syphilis 9 B is not correct. 19% chose this. • 10 Brain ca lcifications may result from mat ernal cytomegalovirus infection and Toxoplasmosis gondii infection, not German measles . Toxoplasmosis Cytomegalovirus Measles Rubella Human brain Brain Infection
C is not correct. 12% chos e this. Chrondrodystrophy is an aut osomal recessive disorder. Autosomal recessive Recessive Altosome Dominance (genetics)
D is not correct. 11% chose this. Cryptorch idism occurs when the test es fail t o descend int o the scrotum during fetal development. Cryptorchidism is a rare congenita l defect associat ed with mat ernal Epst ein-Barr virus infect ion, not German measles. Epstein-Barr virus Cryptorchidism Rubella Scrotum Measles Testicle Congenital disorder Prenatal development Virus Infection
Bottom Line: Rubella (German measles) is one of the ToRCHeS infections that can lead t o congenital anomalies includ ing patent ductus arteriosus, pulmonary artery stenosis, cataracts, and deafness. The ToRCHeS infections can cross t he placental barrier, often result in congenita l abnormalities, and include the following : Toxoplasmosis, Rubella, Cytomegalovirus, Herpes/HIV, and Syphilis. Patent ductus arteriosus Rubella Pulmonary artery Measles Congenital disorder Ductus arteriosus Hearing loss Stenosis Placenta Pulmonic stenosis Cataract
l@);fil ~ 1hl for year:l 2o17 y FIRST AID FACTS 8 s 0 Lock Suspend End Block Item: 9 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 1847 J.. Previous Next LAbf aiUI~S Notes Calculator 1 FA17 p 290.1 2 3 Congenital cardiac DISORDER DEFECT 4 defect associations Alcohol exposure in utero (fetal alcohol VSD, PDA, ASD, tetralogy of Fallot 5 syndrome) 6 Congenital rubella PDA, pulmonary artery stenosis, septal defects 7 8 Down syndrome AV septal defect (endocardial cushion defect),
9 VSD, ASD • 10 In fant of diabetic mother Transposition of great vessels Marfan syndrome MVP, thoracic aortic aneurysm and dissection, aortic regurgitation Prenatal lithium exposure Ebstein anomaly Turner syndrome Bicuspid aortic valve, coarctation of aorta Williams synd rome Supravalvular aortic stenosis 22qll syndromes Truncus arteriosus, tetralogy of Fallot
FA1 7 p 163.1 RNA viruses VIRAL FAMILY ENVELOPE RNA STRUCTURE CAPSID SYMMETRY MEDICAL IMPORTANCE Reoviruses No OS linear Icosahedral Coltivirusa - Colorado tick fever 10-12 segments (double) Rotavirus-cause of fata l diarrhea in children
Picornaviruses 0 SS ® linear Icosahedral Poliovirus-polio-Salk/Sabin vaccines-IPV/OPV 8 s 0 Lock Suspend End Block Item: 9 of 10 - , • Mark -
4 delivery (especially HSV-2). 1 onspecilic signs common to many ToRCHeS infections include 5 hepatosplenomegaly, jaundice, thrombocytopenia, and growth retardation. 6 Other important infectious agents include Streptococcus agalactiae (group B streptococci), E coli, 7 and Listeria monocytogenes- all causes of meningitis in neonates. Parvovirus Bl9 causes hydrops 8 fetal is. 9 AGENT MODES OF MATERNAL TRANSMISSION MATERNAL MANIFESTATIONS NEONATAL MANIFESTIONS • 10 Toxoplasma gondii Cat feces or ingestion of Usually asymptomatic; Classic triad: chorioretinitis, undercooked meat lymphadenopathy (rarely) hydrocephalus, and i ntracran ia I calcifications, +1- "blueberry muffin" rash m.
Rubella Respiratory droplets Rash, lymphadenopathy, Classic triad: abnorma 1iti es polyarthritis, polyarthralgia of eye (cataract) and car (deafness) and congenital heart disease (PDA); ± "blueberry muffi n" rash. "I (eye) • ruby (rubella) earrings." Cytomegalovirus Sexual contact, organ Usually asymptoma ti c; Hearing loss, seizures, petech ial 8 s 0 Lock Suspend End Block Item: 9 of 10 - , • Mark -
HIV Sexual contact, neecllestick Variable presentation depending Recurrent infections, chronic on CD4+ cell count diarrhea Herpes simplex virus-2 Skin or mucous membrane Usually asymptomatic; herpetic Men ingoencephal it is, herpetic contact (vesicular) lesions (vesicular) lesions Syphilis Sexual contact Chancre (1°) and disseminated Often results in stillbirth, rash (2°) arc the two stages hydrops fcta lis; if child I ikely to result in fetal infection survi,·es, presents with facial abnormalities (eg, notched teeth, saddle nose, short 8 s 8 Lode. Suspe-nd End Bloc:k Item: 10 of 10 - , • Mark -
8 s 8 Lode. Suspe-nd End Bloc:k Item: 10 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 18 56 J.. Previous Next LAbf aiUI~S Notes Calculator 1 2 The correct answer is A. 69°/o chose this. 3 This is a case of co ngenitally acquired cytomegalovirus (CMV) infection. Fetuses exposed to CMV during t he first trimester may experience intrauterine growth retardation and may be afflict ed with cent ra l nervous system damage, with hearing and sight impairments. I ntellectual 4 disabilit y will occur along with microcephaly. 5 Cytomegalovirus Microcephaly Intrauterine growth restriction Central nervous system Intellectual disability First trimester Visual impairment Nervous system Pregnancy Infection Delayed milestone 6 B is not correct. 12% chose this. 7 Epstein-Barr virus, t he ca use of infectious mononucleosis, is a rare ca use of congenital defects. These defects include cataracts, hypotonia, 8 cryptorchidism, and micrognathia. Cryptorchidism Epstein-Barr virus Infectious mononucleosis Micrognathism Hypotonia Virus Congenital disorder Cataract 9 10 C is not correct. 8 °/o chose this . Herpes simplex virus can result in a variety of congenit al defects, abortions, and neonatal encephalitis. It ca n be associated with skin rashes and microcephaly but is not commonly associated with hearing loss. Microcephaly Herpes simplex virus Encephalitis Herpes simplex Virus Congenital disorder Hearing loss Infant Rash
D is not correct. 4°/o chose this. Congenital HIV results in neonat al AIDS. HIV HIV/AIDS Congenital disorder Infant E is not correct. 7°/o chose this. Congenital syphilis can result in cranial nerve VIII deafness, mulberry molars, saber shins, saddle nose, and Hutchinson teeth. Hutchinson's teeth syphilis Congenital syphilis Vestibulocochlear nerve Saddle nose Congenital disorder Molar (tooth) Hearing loss
Bottom Line: Congenital CMV manifests with hearing loss, petechial rash, hepatosplenomegaly, and microcephaly. Periventricular calcifications are seen on CT of the hea d. Microcephaly Hepatosplenomegaly Petechia Purpura Congenital disorder Rash Hearing loss Cytomegalovirus
141;fil·1i•J for year:[2017 • FIRST AID FACTS 8 s 0 Lock Suspend End Block Item: 10 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 18 56 J.. Previous Next LAbf aiUI~S Notes Calculator
1 FA17 p 178.1 2 ToRCHeS infections 3 Microbes that may pass from mother to fetus. Transmission is transplacental in most cases, or via
4 delivery (especially HSV-2). onspecific signs common to many ToRCHeS infections include 5 hepatosplenomegaly, jaundice, thrombocytopenia, and growth retardation. 6 Other important infectious agents include Streptococcus agalactiae (group B streptococci), E coli, 7 and Listeria monocytogenes- ail causes of meningitis in neonates. Parvovirus Bl9 causes hydrops 8 fetal is. 9 AGENT MODES OF MATERNAL TRANSMISSION MATERNAL MANIFESTATIONS NEONATAL MANIFESTIONS 10 Toxoplasma gondii Cat feces or ingestion of Usually asymptomatic; Classic triad: chorioretinitis, undercooked meat lymphadenopathy (rarely) hydrocephalus, and i ntracran ia I calcifications, +1- "blueberry muffin" rash m.
Rubella Respiratory droplets Rash, lymphadenopathy, Classic triad: abnormali ties polyarthritis, polya rthralgia of eye (cataract) and car (deafness) and congenital heart disease (PDA); ± "blueberry muffin" rash. "I (eye) • ruby (rubella) earrings." Cytomegalovirus Sexual contact, organ Usually asymptomatic; Hearing loss, seizures, petechial 8 s 0 Lock Suspend End Block Item: 10 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 1856 ~ Prev1o u s Next Labf a lues Notes Calculator 1 Cytomegalovirus Sexual contact, organ Usually asy mptomati c; Hearing loss, seizures, petechial 2 tran mononucleosis-like illness 3 splants rash, ''blueberry muffin" rash, 4 periventricular calcifica ti ons rn
5 6 7 8 9 10 HIV Sexual contact, needlestick Va riable presentation depending Recurrent infections, chronic on C D4+ cell count diarrhea Herpes simplex virus-2 Skin or mucous membrane Usually as) mptomatic; herpetic Af eningoencephalitis, herpeti c contact (vesicular) lesions (vesicular) lesions Syphilis Sexual contact Chancre (1 °) and disseminated Often results in stillbirth, ra sh (2°) arc I he I wo stages hydrops fctalis; if child likely to result in fetal infection survives, presents "·ith facial abnormalities (eg, notched teeth, saddle nose, short maxilla),saber shins,C VII I deafness
FA17 p 160.2
Herpesviruses Enveloped, OS, and linear viruses • 8 s ~ L.odt Su~pl'nd End Block Item: 10 of 10 ~ , • Mark <::J [:::> ""I ~· ~'j QID: 18 56 J.. Previous Next LAbf aiUI~S Notes Calculator • 1 FA17 p 160.2 2 Herpesviruses Enveloped, OS, and linear viruses 3 4 VIRUS ROUTE OF TRANSMISSION CLI NICAL SIGNIFICANCE NOTES 5 Herpes Respiratory Gingivostomatitis, keratoconj uncti vitis fJ, Most common cause of sporadic 6 simplex secretions, sa liva herpes labialis m, herpetic whitlow on finger, encephalitis, can present as altered 7 virus-1 temporal lobe encephalitis, esophagitis, mental status, seizures, and/or 8 erythema mu lti fo rme. aphasia. 9 10 Herpes Sexua I contact, Herpes genital i s ~. neonatal herpes. Latent in sacral ganglia. Vi ral simplex perinatal meningitis more common with virus-2 HSV-2 than with HSV-1. Varicella- Respiratory Varicella-zoster (chickenpox [!], shingles 0}, Latent in dorsal root or trigeminal
Zoster virus secretions encephalitis, pneumonia. ganglia; C V1 branch (HHV-3) Most common complication of shingles is post- involvement can cause herpes herpetic neuralgia. zoster ophthalmicus. Epstein-Barr Respiratory Mononucleosis- fever, hepatosplenomegaly, Infects B cells through CD21. virus (HHV-4) secretions, pharyngitis, and lymphadenopathy (especially Atypical lymphocytes on peripheral saliva; aka posterior cervical nodes 0 ). Avoid contact sports blood smear [!!-not infected B "kissing disease," until resolution due to risk of splenic rupture. cells but reactive cytotoxic T cells. (common in Associated with lymphomas (eg, endemic EE> Monospot test-heterophile teens, young Burkitt lym phoma), nasopharyngeal antibodies detected by agglutination adults) carcinoma (especially Asian adults), of sheep or horse RBCs. lymphoproliferative disease in transplant Use of amoxicillin in mononucleosis patients. can cause characteristic
•.,.., .,,..., ,J .,..,.,,.,,.,, .] ... •• -rn t-h • 8 s 0 Lock Suspend End Block Item: 10 of 10 - , • Mark --<) [::> ""'I ~· 1!';:'1 QIO: 1856 ~ Prev1o u s Next Labf a lues Notes Calculator 1 oss 2 Congenital CM 3 Human Sali va Roseoh1 infantum (exanthem subitum): high Roseola: fe,·er first, RO\ ie (checks) 4 herpes- fevers for se\'eral days that can cause seizures, later. 5 viruses 6 followed by diffuse macular rash HHV-7-less common cause of 6 and7 roseola. 7 8 Human Sexual contact Kaposi sarcoma (neoplasm of cnclothclial cells). Can also affect Cl tract and lungs. 9 herpesvirus Seen in HIV/A IDS and transplant patients. 10 8 Dark/violaceous plaques or nodules representing \'ascular pro Iiferations.
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