NR 507 PATHOPHYSIOLOGY WEEK 5 TD2 Alterations in Endocrine Function Discussion Part Two (NR507)

Exam (elaborations) NR 507 PATHOPHYSIOLOGY WEEK 5 TD2 Alterations in Endocrine Function Discussion Part Two (NR507) Week 5: Alterations in Endocrine Function - Discussion Part Two Loading... This week's graded topics relate to the following Course Outcomes (COs). 1 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1) 2 Differentiate the epidemiology, etiology, developmental considerations, pathogenesis, and clinical and laboratory manifestations of specific disease processes. (PO 1) 3 Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions. (PO 1, 7) 4 Distinguish risk factors associated with selected disease states. (PO 1) 5 Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1) 6 Distinguish risk factors associated with selected disease states. (PO 1) 7 Explore age-specific and developmental alterations in physiologic and disease states. (PO 1, 4) Discussion Discussion Part Two (graded) • Is there any genetic component to the top of your differential? • What tests would you order? Responses Lorna Durfee 5/29/2016 7:51:34 PM Discussion Part Two vAo tmhritese a-mfteorn teha-toinldg .b Habey o bftoeyn choams eas siwntool lyeonu urp cplienri cb ewlliyth ( dthiset emnatiionn c)o amftpelra fienet dtihnagt ahne dfr aecqtuse fnutslsyy awlel itghhet .time. The vomiting has become more frequent this past week, and he is beginning to lose What is your differential diagnosis at this time? Is there any genetic component to the top of your differential? What tests would you order? Doctor Brown and Class: My differential diagnosis is: Pyloric Stenosis tMhec Cpyanlocrei,c Hspuheitnhcetre, rB trhaasth iesr cs,a uansedd R boyt eh y(2p0e1rt4r)o pexhpyl. a iInt itsh aat c poymlomriocn s tdeinsoorsdise ri st haant ocbasnt raufcfeticotn of ianpfparnotxs iomf aetietlhye r5 oinn e1 t0o0 t0w. oW whieteeks sa orer uthsrueael ltyo affofuerc tmedo nmthosr.e aTsh aer ien fcuidlle tnecrem f oinrf manatlse sv eisrs us pmroemthaetru irne tihnef afnintsa.l tTrihme ecsateurs ein o pf rtehgisn acnocnyd ictiaonn r iasi sneo tth ken loikwenli,h hooowd eovfe pr,y gloarsitcr isnt esneocrseisti.o nT hbey ctahues e aodf mthien iosvtreartpiorond oufc tpiroons toafg glaansdtriinc Ese icsr eatsisooncsi actoeudl dw biteh binyc srteraessesd t hinatc iadfefencctes othf ep ymloorthice rs.t e Enoxsteisr nal i(nMcrceCaasnedce i nect iadle.,n 2c0e 1o4f, ppy. l1o4ri8c8 s)t.e nTohseirse i nap cpheialdrsre tno wbeh oa hgaevnee taic f caomninlye cmtieomn baes rt hthearet hisa sa nth e problem (McCance et al., 2014, p. 1488, 1489). Is there a genetic component? sOtelinvoes aisn din E an rdeogmis t(r2y0 f1ro6m) s tDateen tmhaatr kth. e Treh ew raess uanlt ewxaasm siingantiifoinca onft ffaammiilliiaall aaggggrreeggaattiioonn owfi pthy lao 2ri0c0 - freosldu lhtsi gwheerre r astiem ailmaro wngit hd imzyagtoertinca lt waninds poart esribnlailn cgosn. t Trihbeu thioenrist,a abnildit yth ees ctiomnactleu swioans w87a sp ethrcaet nt. The isntetrnaoustiesr iins eo benscvuirroen bmuet natp wpaarse nntolyt iims pmourtlatinfat.c tTorhiea la. u Tthhoerrse r melaayte bteh aat gtheen eettiico lporgeyd iospf opsyiltoiorinc and (eOnvliivroe namnde nEtadlo fmac, t2o0rs1.6 )N. eTohneartea al phpyepaerrsg taos tbrien ae mgeian eatnicd cgoanstnreicc thioynp earsa tchideritey i sm aany icnocnretraisbeudte i(nMcicdCeannccee o eft payl.l,o 2ri0c1 s4t,e pn.o 1si4s8 i8n, c1h4i8ld9r)e.n who have a family member that has the problem What test to be ordered? oDfi ahsy epte ratlr.o (p2h0i1c2 p) yrleolraitce sttheanto uslitsr.a sPoyulnodri ecx satemnionsaitsi osnh oisw tsh ae tbheisctk menoidnagl iotyf tohfe c mhouiscceu flaorr ldaiyaegrn aonsdis faanidlu craen o af ltlhoew p fyolro rdiicr eccatn oabl stoer rvealtaixo nc aouf stihneg pgyalsotrriicc coauntlaelt (oDbisatsr uect.t iaoln, .2 0U1l2tr,a ps.o 2u4n7d) i. s Plehsyss iincavla sive emxoavmaibnlaet imonas ws itlhle p sriozvei doef aan c hoalinvcee i tno t ohbe sueprvpee rg raisgthritc q pueardirsatanlts i(sM. cTChaenrcee w, Hillu beeth ae rf,i rBmra, sshmearsll,, &an d iRmobtea,l a2n0c1e4s,. p A. 1ls4o8, 9w).e Wneee ds htoo uinldv ecshteigckat eel feocrt rcohlyrotensi cd muea tlon usterviteioren falunidd w aneidg helte lcotsrso l(yMtec Cance et al. 2014, p. 1489). References Costa Dias, S., Swinson, S., Torrão, H., Gonçalves, L., Kurochka, S., Vaz, C. P., & Mendes, V. (2012). Hypertrophic pyloric stenosis: tips and tricks for ultrasound diagnosis. Insights into Imaging, 3(3), 247-250. doi:10.1007/s-x McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2014). Alterations of Digestive Function in children. In Pathophysiology: The biologic basis for disease in adults and children (7th ed., pp. 1488, 1489). St. Louis, MO: Mosby. Olive, A. P., & Endom, E. E. (2016). In T. W. Post (Ed.), UpToDate. Infantile hypertrophic pyloric stenosis. Retrieved from pyloric-stenosis Rechel DelAntar 5/31/2016 8:54:20 PM Differential Diagnosis Hello Professor and Class, Differential Diagnosis This is a case of a three-month-old boy with a chief complaint of increased vomiting after ingestion of food, which has become more frequent in the last week. Also presents with abdominal distention after eating, irritability and is starting to loose weight. Differential Diagnosis at this time would be: Pyloric Stenosis = is an obstruction of the pyloric sphincter caused by hypertrophy of the sphincter muscle from the stomach to the first part of the duodenum (pylorus). It is one of the most common disorders of early infancy and affects infants between the ages of either 1 and 2 weeks or 3 and 4 months. Occurs largely among males 5 out of 1000 whereas in females 1 out of 1000 and occurs more among Caucasians than African American or Asians, and full-term infants are affected more often than premature infants (McCance, K.L. et. al., 2013). Symptoms: Vomiting is the primary symptom which is non bilious and projectile. There is abdominal distention because the food is unable to pass to the intestines due to the obstruction. Patients like this are often hungry and become irritable. Dehydration occurs as vomiting increases and leads to weight loss or failure to gain weight. Also, Stomach contractions may occur. These are wave-like contractions (peristalsis) that ripple across your baby's upper abdomen soon after feeding, but before vomiting. This is caused by stomach muscles trying to force food through the narrowed pylorus. Etiology: The causes of Pyloric stenosis are multifactorial, some genetic and some multifactorial. Ina study done in Denmark of children born between 1977 to 2008 involving 1,999,738 children, This nationwide study documented strong familial aggregation of pyloric stenosis, with a nearly 200-fold increase among monozygotic twins and 20-fold increase among siblings. Familial aggregation of pyloric stenosis was pronounced even in more distant relatives with a heritability of 87%. Although the study also shows that it is more predominant in males, there is no evidence as yet for a sex-related heritability of pyloric stenosis. Male predominance is also a characteristic of other gastrointestinal diseases, such as Hirschsprung, intussusception, and rotavirus gastrointestinal infections, and suggests that males might be more susceptible with respect to the development, maturation, and function of the gastrointestinal tract (Krogh, C. et. al., 2011). Diagnostic testing: Diagnosis can be made through physical exam. Palpation of the abdomen reveals an olive sized “mass” in the epigastric region. Plain abdominal x-ray will sometimes how a dilated stomach, Upper GI series will show the narrowed pyloric outlet filled with a thin stream of contrast material; a "string sign" or the "railroad track sign". Abdominal Ultrasound is a diagnostic imaging technique, which uses high frequency sound waves to create images of the t organs to be able to see any abnormalities such as pyloric stenosis. Blood tests will also reveal low blood levels of potassium and chloride in association with an increased blood pH and high blood bicarbonate level due to loss of stomach acid (which contains hydrochloric acid) from persistent vomiting (Children’s Hospital of Wisconsin, 2016). References: Children’s Hospital in Wisconsin. (2016). Pyloric Stenosis. Retrieved from program/conditions/pyloric-stenosis/. Krogh, C., Gortz, S., Wohlfahrt, J., Biggar, R., Melbye, M. and Fischer, T. (2011). Pre-and Perinatal Risk Factors for Pyloric Stenosis and their Influence On the male predominance. Retrieved from content/early/2012/05/01/. McCance, K.L., Huether, S.E., Brashers, V.L. and Rote, N.S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7 ed.). St. Louis, MO: Mosby. th 5/Lanre Abawonse 31/2016 11:03:20 PM Discussion Part Two What is your differential diagnosis at this time? Pyloric stenosis (PS) This occurs when the circumferential muscle of the pyloric sphincter becomes thickened, resulting in elongation and narrowing of the pyloric channel. Peralta (2015) stated that PS is progressive narrowing of the pyloric canal, occurring in infancy. Onset is usually at 3–6 weeks of age; rarely in the newborn period or as late as 5 months of age. It is less common in African American and Asian populations and more common among Caucasians. In PS the circular muscle of the pylorus thickens as a result of hypertrophy and hyperplasia. This produces severe narrowing of the pyloric canal between the stomach and the duodenum, causing partial obstruction of the lumen. Over the course of time complete obstruction occurs, which then results in palpable pylorus hypertrophy as an olive-like mass in the upper abdomen. With this distension and obstruction the patient will experience colicky abdominal pain from peristalsis attempting to overcome the obstruction. The earliest sign obstruction is projectile vomiting of 3 to 4 feet when the child is in a sidelying position, dehydration from loss of large quantities of fluid and electrolytes into the vomiting and weight loss, as is significant for the patient. Gastroesophageal reflux (GERD) is defined as the transfer of gastric contents into the esophagus. This represents symptoms or tissue damage that resulst from GER. GER becomes a disease when complications such as failure to thrive, bleeding, or dysphagia develop. GERD is associated with respiratory symptoms, including apnea, bronchospasm, laryngospam and pneumonia. Peralta (2015) contends that GER is reflux of gastroduodenal contents into the esophagus, larynx, or lungs, with or without resultant esophageal inflammation with symptom that include vomiting, weight loss, failure to thrive and usually resolves by 18 months. GER is associated with our patient in question because GER is related to dysfunction of the lower esophageal sphincter (LES), delay in gastric emptying, poor clearance of esophageal acid, and the susceptibility of esophageal mucosa to acid injury. Transient relaxation of the lower esophageal sphincter is the mechanism that leads to GER. Gastric distention, increased abdominal pressure caused by coughing, central nervous system disease and delayed gastric emptying are some the LES contributor. At infancy the child might present with symptoms like failure to thrive, abdominal distension, and episodes of vomiting. Other symptoms include ribbon like, foul-smelling stools, explosive diarrhea, visible peristalsis, and appearing significantly ill. While our patient displays problem in GERD, it won’t be the primary diagnosis for this patient. Intussusception is the most frequent cause of intestinal obstruction in children between the ages of three months and three years. Lee, Zeddun, and Borum (2015) contend that intussusception is the invagination of a portion of intestine into itself of which may involve any part of small intestine or ileocolic (95%) or colocolic segment. At this proximal segment, the bowel telescopes into a more distal segment, pulling the mesentery with it. As the mesentery gets compressed and angled, it results in lymphatic and venous obstruction. The pressure within the intussusception increases as the edema from the obstruction increases. Thus, the pressure increases, equaling arterial pressure, and arterial blood flow stops, resulting in ischemia and the pouring of mucus into the intestine. The venous engorgement leads to leaking of blood and mucus into the intestine forming the classic sign of currant jelly stool. Other associated symptoms are sudden abdominal pain, vomiting, tender distended abdomen, and fetal positioning when the child is in pain screaming. Part of the problem experienced by the patient is related to this diagnosis, however, it won’t be an appropriate diagnosis for this patient. Is there any genetic component to the top of your differential? Peralta (2015) suggested that recent studies have identified linkage to chromosome 11 and multiple loci and chromosome 16. The incidence is higher in firstborn boys, a five times increased risk with affected 1st-degree relative and strong familial aggregation and heritability. What tests would you order? In order to Identify the problem of pyloric stenosis, Peralta (2015) noted that abdominal US is the study of choice, this will help to see the thickened and elongated pyloric muscle and redundant mucosa. An Upper GI series can reveal strong gastric contractions; elongated, narrow pyloric canal (string sign); and parallel lines of barium in the narrow channel (double-tract sign or railroad track sign). It is also essential to get the chem 7 to check the electrolyte profile for hypokalemia, hypochloremia and metabolic alkalosis. Other tests are available but the listed ones here are essential for this patient. Reference Lee, W., J., Zeddun, S., &Borum, M., L. (2015). Intussusception. In F. J. Domino (Ed.), The 5-minute clinical consult 2015 [electronic resource].Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Peralta, R. (2015). Gastroesophageal reflux. In F. J. Domino (Ed.), The 5-minute clinical consult 2015 [electronic resource].Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Peralta, R. (2015). Pyloric Stenosis. In F. J. Domino (Ed.), The 5-minute clinical consult 2015 [electronic resource].Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Sarah Boulware reply to Lanre Abawonse 6/1/2016 2:58:26 PM RE: Discussion Part Two Lanre, stood ouI tf otou nmde y boeucra puoses ta vt ewryo rikn ftoordmaya twivee .w Yeoreu ro dpiefrfaetrienngt ioanl daina ginnfoasnits wofi tihn tiunstususssucsecpetipotnio n ianncdl uadfteedr tmhiys raesa pdainrtg os ff omr yc ldaisfsf earnedn tmiayl. eI xdpeecriideendc eto t olodoayk afut rwthoerrk i nI ttoh othuigsh ct oIn sdhiotiuolnd. have iAntcecrmoridttienngt ,t oa bKdaonmgi annadl pPaeitne rths a(t2 i0n1c4r)e,a as ekse iyn sfyremqputeonmcy o wf iinthtu tsismues.c eBpettiwone eins sthued dpeenr,i ods of pmauinc otuhse pcrheislde nits iuns uthaell syt opoali na nfrde ep.o Ass icbhliel dv owmililt icnlags. sSicyamllpyt oflmexs tahreei ru shuipalsl yw choennf iuns epda iwn,i thha ve dgaeshtyrdoreanttieornit,i tsh. eIrne sfoorme ei nctaussessu sthcee pptaiotine nsth moualyd oanlwlya ypsre bsee nint wthieth d lieftfheraerngtyi aflo fro prr poefoduiantdri c ilentthuasrsguysc. eUplttiroans oaunndd i sh aths ea fsiresnts-liitnivei ttye sot ff o9r7 .d9e%te catnindg s pinetcuisfiscuistyce opft i9o7n..8 % for detecting Thanks, great post! Sarah Bouwlare Reference Kang, P. & Peters, A. (2014). Intussusception