NR507 / NR 507: Advanced Pathophysiology Midterm Study Guide (2022/2023) Chamberlain, Study Guides, Projects, Research of Nursing

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NR I 507 IAdvanced IPathophysiology IMidterm IStudy IGuide

Pulmonary: ▪ Review Iconcepts Irelated Ito Ianticholinergic Idrugs Iand Ithe Itreatment IforIasthma o (Block Iacetylcholine Ibinding I(primarily Iin Ilung) I-> Ibronchodilation I through I decreased I parasympathetic I response ▪ Tiotropium, IIpratropium o Short-acting Ibeta-adrenergic Iagonists I(SABA) I– Iactivate Ibeta Ireceptors Iprimarily Iin Ithe Ilung I-> Ibronchodilation Ithrough Iincreased Isympathetic Iresponse ▪ Albuterol o Oral Icorticosteroids I– Iinhibit Iinflammatory Icells Iand Ichemical Iproduction I-> Ireduce Iinflammatory Iprocess ▪ Prednisone, I prednisolone, I methylprednisolone o Long Iacting: ▪ Inhaled Icorticosteroids

• Beclomethasone, I triamcinolone ▪ Mast Icell Istabilizers
• Cromolyn ▪ Leukotriene Imodifiers
• Zafirlukast, IMontelukast ▪ Long Iacting Ibeta2 Iadrenergic Iagonists
• Salmeterol ▪ Methylxanthines
• Theophylline ▪ Monoclonal I antibodies
• Omalizumab ▪ Bronchitis Iand Iassociated Ipathogenesis o In Ibronchitis, Iinspired Iirritants Ipromote Ibronchial Iinflammation,Icausing Ibronchial Iedema, Iincreases Ithe Isize Iand Inumber Iof

mucous I glands I and I goblet I cells I in I the I airway I epithelium, I smoothImuscle Ihypertrophy Iwith Ifibrosis, Iand Inarrowing Iof Ithe Iairways. o Hypersecretion Iof Ithick, Itenacious Imucus Ioccurs Iand Icannot Ibe Icleared Ibecause Iof Iimpaired Iciliary Ifunction. IThe Ilung’s Idefense Imechanisms I are I therefore I compromised, I increasing I susceptibilityIto Ipulmonary Iinfection, Iwhich Icontributes Ito Iairway Iinjury Iand Iineffective Irepair. o Frequent Iinfectious Iexacerbations Ifrom Ibacterial Icolonization IofIdamaged Iairways Iare Icomplicated Iby Ibronchospasm Iwith Idyspnea Iand Iproductive Icough. ▪ Chronic Ibronchitis Iand Irelated Iacid/base Idisturbances, Iperfusion, Iblood Iflow Ibetween Ithe Iheart Iand Ilungs o Characterized Iby Ibronchial Iinflammation, Ihypersecretion IofImucus, Ichronic Iproductive Icough, Ipersisting Ifor Iat Ileast I 3 Iconsecutive Imonths Ifor Iat Ileast I 2 Isuccessive Iyears. o Symptoms: Iproductive Ipurulent Icough, Icopious Isputum Iproduction, Ishortness Iof Ibreath, Iwheezing, Irhonchi, Icyanosis,Iperipheral Iedema. o Ventilation Iis Idecreased Iresulting Iin Ialveolar Ihyperinflation Iand Ihypercapnia Iresulting Iin Irespiratory Iacidosis. o The Ihigh Iconcentration Iof ICO2 Icreates Ian Iunfavorable Icondition Ifor I gas I exchange I thus I causing I a I ventilation/perfusion I mismatch. o Decreased Iperfusion Iof Ithe Ipulmonary Icapillaries Iwith Ioxygenated Iblood Iresults Iin Ichronic Ipulmonary Ihypoxia. IRight Iand ILeft Ishunting I= Iblood Ipasses Ifrom Ithe IRV Ito Ithe Ilungs Ito ILVIwithout Iperfusion I(gas Iexchange) ▪ Asthma Isigns Iand Isymptoms o Coughing o Wheezing o Shortness I of I breath o Rapid I breathing o Chest Itightness ▪ Bronchioles o 3 Ilayer Itube-like Istructure Isurrounding Ithe Ilumen Ior Iair Ipassageway

o Inner Imost Ilayer ▪ Closest Ito Ithe Ilumen, Iis Icomposed Iof Icolumner IepithelialIcells Iand Imucus Iproducing Igoblet Icells o Outermost I layer ▪ Composed I of I smooth I muscle I cells, I responsible I for I the Iability Iof Ithe Iairways Ito Iconstrict Iand Idilate o Middle Ilayer I(lamina Ipropria) ▪ Embedded I with I connective I tissue I cells I as I well I as I immuneIcells. IThese Iimmune Icells Iinclude Ia Inumber Iof Idifferent Ikinds Iof IWBCs Ilocated Ihere Ito Iprotect Ithe Iairways. ▪ Alveolar Ihyperinflation Iwith Iasthma o Mast Icell Idegranulation Itriggered I by Iexcessive I amts Iof IIgE Ithat Ihave Iairingly Iformed Ithis Iindividual Ithat Iwill Ibind Ithat Iallergen IasIit Ienters Ithe Iairway Ithat Imast Icell Idegranulation Ireleases Ichemicals I that I releases I mucus I production I and I accumulation I as Iwell Ias Ichemicals Ito Icontribute Ito Ismooth Imuscle Iconstriction. IWith Ithat Iand Imucus Iplugs Ithat Iform Iresult Iin Ihyperinflation Iof Ithe Ialveoli Iand Ieventual Ierosion Iof Iairway Itissue. ▪ Polycythemia I vera o A Ichronic Ineoplastic, Inonmalignant Icondition Icharacterized Iby Ioverproduction Iof Ired Iblood Icells Iand Iplatelets Iand Isplenomegaly. o Erythrocytosis Iis Ithe Iessential Icomponent Iof IPV. IClonal Iproliferation Iof Ierythroid Iprogenitors Ioccurs Iin Ithe Ibone ImarrowIindependent Iof Ierythropoietin, Ialthough Ithe Icells Iexpress Ia Inormal Ierythropoietin Ireceptor. o More I than I 95% I of I individuals I with I PV I possess I an I acquired I point Imutation Iin Ithe IJanus Ikinase I 2 Igene, Ia Icytoplasmic Ityrosine Ikinase, Ion Ichromosome I9. IJAK2 Iincreases Ithe Iactivity Iof Ierythropoietin Ireceptor Iand Iis Iself-regulatory Iso Ithat IJAK2 IactivityIdiminishes Iover Itime. o Manifestations: ▪ Present Iinitially Iwith Ilarge Ispleen, Ifrequently Iabd Ipain Iand Idiscomfort. ▪ Increased Iviscosity, Ias Iwell Ias Ithrombocythemia Iand Iincreased Iplatelet Idysfunction, Ileads Ito Ia Ihypercoagulable

state Iwith Iformation Iof Ivenous Iand Iarterial Ithrombosis IandIvessel Iocclusion. ▪ Increased Iblood Iviscosity Iresults Iin Ia Ivariety Iof Icirculatory Ialterations Isuch Ias Iplethora I(ruddy, Ired Icolor Iof Ithe Iface, Ihands, Ifeet, Iears, Iand Imucous Imembranes) Iand engorgement Iof Ithe Iretinal Iand Icerebral Iveins. ▪ Headache, Idrowsiness, Idelirium, I mania, Ipsychotic Idepression, Ichorea, Iand Ivisual Idisturbances. ▪ Splenomegaly I and I hepatomegaly I result I from I pooling I of Iblood I in Ithese Iorgans; Iconsequently, Iindividuals Imay Idevelop Iportal Ihypertension. ▪ A Iunique Ifeature Iof IPV, Ione Ihelpful Iin Idiagnosis, Iis Ithe Idevelopment Iof Iintense, Ipainful Iitching Ithat Iis Iintensified by Iheat Ior Iexposure Ito Iwater I(aquagenic Ipruritus), Iparticularly Iwarm Iwater Iwhen Ibathing Ior Ishowering. IThe Iintensity Iof Iitching Iis Irelated Ito Ithe Iconcentration Iof ImastIcells Iin Ithe Iskin Iand Iis Igenerally Inot Iresponse Ito Iantihistamines Ior Itopical Ilotions. ▪ Mechanism Iof Iaction Iof Ianticholinergic Idrugs Ito Itreat Iasthma o (Block Iacetylcholine Ibinding I(primarily Iin Ilung) I-> Ibronchodilation I through I decreased I parasympathetic I response Cardiovascular: ▪ Cardiac Ioutput o Volume Iof Iblood Iejected Iby Ieach Iventricle Iper Iminute o HR IX ISV ▪ Cardiac Icontractility o (inotropic Istate) o Determined Iby ICa2+ Iavailability Iand Iits Iinteraction Iwith Iactin- Imyosin. o Increased Iby Isympathetic Istimulation Ir/t Iincrease Icellular Imetabolic Irate Iand Ithe Istrength Iof Ithe Imuscle Icell Itemporarily ▪ Fever, Ianxiety, Iincreased Ithyroxine o Decreased Iby Ilow IATP Ilevels I– Ilack Iof Ienergy I= Ilack Iof IstrengthIfor Imuscle Icontraction ▪ Ischemia, I hypoxia, I acidosis

▪ Preload/afterload o Preload I– Idegree Iof Imyocardial Ifiber Ilength Istretches Ibefore Icontraction ▪ Degree Iof Istretch Iinfluenced Iby Iend-diastolic Iventricular Ivolume I= Iamount Iof Iblood Ientering Iventricle Iduring Idiastole ▪ “Loading Ithe Iheart Iwith Iblood” ▪ Increased Iby ICHF, Ihypervolemia ▪ Decreased Iby Icardiac Itamponade Ior Ihypovolemia o Afterload I– Iamount I of Itension Ieach Iventricle Imust Idevelop IduringIsystole Ito Iopen Isemilunar Ivalves Iand Ieject Iblood ▪ “Unload Ithe Iheart” ▪ Influenced Iby:

• VentricleIwall Ithickness I=Imuscle Istrength o Increase Ithickness I= Idecreased Itension
• Arterial Ipressure I= Iresistance Ito Iejection o Increased Ipressure I= Iincreased Itension
• VentricleIchamber IsizeI=Iblood Ivolume Icapacity o Increased Ichamber Isize I= Iincreased Itension ▪ Increased Iby IsystemicIhypertension,Ivalve Idisease, IorICOPD I= Ipulmonary Ihypertension ▪ Decreased Iby Ihypotension Ior IvasodilationI(shock) ▪ Systole/diastole o Systole I– Ipumping o Diastole I - I filling ▪ Heart Ivalves I(when Ithey Iare Iopen I and Iclosed; Ithe Iproduction Iof IS1 I&IS2) o Ventricular Idiastole I> IAtrial Isystole I= IAV Ivalves Iclose I= IS o Ventricular Isystole I= ISL Ivalves Iclose I= IS ▪ Stenosis Iof Ithe Iheart Ivalves Iand Ieffects

o Valvular Istenosis I– Ithe Ivalve Iorfice Iis Iconstricted Iand Inarrowed, Iimpeding Ithe Iforward Iflow Iof Iblood Iand Iincreasing Ithe IworkloadIof Ithe Icardiac Ichamber Iproximal Ito Ithe Idiseased Ivalve. IIntraventricular Ior Iatrial Ipressure Iincreases Iin Ithe Ichamber Ito Iovercome Iresistance Ito Iflow Ithrough Ithe Ivalve. IIncreased Ipressure Icauses Ithe Imyocardium Ito Iwork Iharder Icausing Imyocardial Ihypertrophy. o Aortic Istenosis ▪ Causes

• Calcific Idegeneration Irelated Ito Iaging
• Congenital I bicuspid I valve
• Inflammatory Idamage Icaused Iby Irheumatic IheartIdisease ▪ The Iorfice Iof Ithe Iaortic Isemilunar Ivalve Inarrows, Icausing Idiminished Iblood Iflow Ifrom Ithe Ileft Iventricle Iinto Ithe Iaorta.IOutflow Iobstruction Iincreases Ipressure Iwithin Ithe Ileft ventricle Ias Iit Itries Ito Ieject Iblood Ithrough Ithe InarrowedIopening. ILeft Iventricular Ihypertrophy Idevelops Ito Icompensate Ifor Ithe Iincreased Iworkload. ▪ Classic I manifestations I of I aortic I stenosis
• Angina
• Syncope
• Heart IFailure ▪ Clinical Imanifestations:
• Decreased Istroke Ivolume
• Reduced Isystolic Iblood Ipressure
• Narrowed Ipulse Ipressure o MitralIStenosis ▪ Impairs Ithe Iflow Iof Iblood Ifrom Ithe Ileft Iatrium Ito Ithe IleftIventricle ▪ Impedance Ito Iblood Iflow Iresults Iin Iincomplete Iemptying Iof Ithe Ileft Iatrium Iand Ielevated Iatrial Ipressure Ias Ithe Ichamber Itries Ito Iforce Iblood Ithrough Ithe Istenotic Ivalve. IContinued increasesIin Ileft Iatrial Ivolume Iand Ipressure Icause Ichamber

dilation Iand Ihypertrophy Iand Ieventually Iresult IinIpulmonary Ihypertension ▪ Clinical Imanifestations

• Depend Ion Ithe Isize Iof Ithe Ivalvular Iorifice
• As Iit Iprogresses, Idecreased I cardiac Ioutput I occur, Iespecially Iduring Iexertion.
• JVD
• Peripheral Iedema ▪ Stroke Ivolume o Volume Iof Iblood Iejected Iby Ithe Ieach Iventricle/systole ▪ Cor IPulmonale o Inability Iof Ithe IRV Ito Iprove Iadequate Iblood Iflow Ito Ithe Ipulomary Icirculation o S/sx: IJVD, Ihepatosplenomegaly, Iperipheral Iedema o Leads Ito ILHF Ior Ibiventricular Iheart Ifailure ▪ Heart Ifailure Iand Iphysiologic Iprocesses Ithat Ilead Ito Iheart Ifailure Isymptoms o Cardiac Idysfunction Icaused Iby Ithe Iinability Iof Ithe Iheart Ito Iprovide Iadequate Icardiac Ioutput, Iresulting Iin Iinadequate ItissueIperfusion o Types: Ileft Iheart Ifailure I(CHF), Iright Iheart Ifailure I(Cor Ipulmonale),Ihigh- output Ifailure o Left Iheart I failure ▪ Inability Iof Ithe ILV Ito Iprovide Iadequate Iblood Iflow Ito Ithe Isystemic Icirculation ▪ S/sx: Ipulmonary Iedema, Idyspnea ▪ Leads Ito Ibiventricular Iheart Ifailure o SeeIabove Ifor IRight IHeart IFailure o High-output Ifailure ▪ Inability Iof Ithe Iheart Ito Ipump Isufficient Iamounts Iof Iblood Ito Imeet Ithe Icirculatory Ineeds Iof Ithe Ibody, Idespite InormalIblood Ivolume Iand Icardiac Icontractility

▪ Able Ito Iincrease Ioutput ▪ Can Ideplete Icardiac Imuscle Ireserve Iand Ilead Ito Ilow Ioutput-Ifailure Iovertime. ▪ Hypertension o Consistent Ielevation Iof Isystemic Iarterial Iblood Ipressure. o In I 2017, I HTN I was I redefined I as I SBP I of I 130 Ior I greater Ior I a I DBP IofI 80 Ior Igreater. o Isolated I systolic I hypertension I is I elevated I systolic I blood I pressure Iaccompanied Iby Inormal Idiastolic Iblood Ipressure I(<90 ImmHg). o Risk IFactors: Iage, Iethnicity, Ifamily Ihistory Iof Ihypertension IandIgenetic Ifactors, Ilower Ieducation Iand Isocioeconomic Istatus, Itobacco I use, I psychosocial I stressors, I sleep I apnea, I and I dietary Ifactors Iincluding Idietary Ifats, Ihigher Isodium Iintake, Ilower Ipotassium Iintake, Iand Iexcessive Ialcohol Iintake, Idiabetes Imellitus, Iand Iobesity o Patho: ▪ HTN Iis Icaused Iby Iincreases Iin Icardiac Ioutput, Itotal Iperipheral Iresistance, Ior Iboth. ICardiac Ioutput Iis IincreasedIby Iany Icondition Ithat Iincreases Iheart Irate Ior Istroke volume, I whereas I peripheral I resistance I is I increased I by I anyIfactor Ithat Iincreases Iblood Iviscosity Ior Ireduces Ivessel Idiameter I(vasoconstriction). ▪ Calcium Ibinding I and I troponin o Within Ieach Icell, Ithe Iproteins Iactin Iand Imyosin Iare Iarranged Iin Icontractile Iunits Icalled Isarcomeres. o Muscle Icontraction Ioccurs Iwhen Iactin Iand Imyosin Iinteract. o In Ia Iresting, Inoncontractile Istate, Itroponin Iholds Itropomyosin IinIposition Ito Iblock Imyosin-binding Isites Ion Iactin. o Changes Iin Iintracellular Iion Iconcentration Iresult Iin IelectricalIvoltage Ichanges I which I stimulate I Ca2+ I release Ifrom Ithe Isarcoplasmic Ireticulum. o The Ipositively Icharged Icalcium Iion Ihas Ia Ihigh Iaffinity Ito Ibind Ito Inegatively Icharged Itroponin. o Ca2+ Ibinding Ito Itroponin Ishifts Itropomyosin Ito Iexpose ImyosinIbinding Isites.

o Actin-myosin Iinteract Iresulting Iin Imuscle Ifibers Icontraction o ATP Iis Irequire Ito Ifacilitate Iinteraction. Hematology: ▪ Hematopoiesis o The Isite Iof Iblood Icell Iformation o Occurs Ithroughout Ilife Iand Iis Istimulated Iby: ▪ Infiltration Iof Iyellow Ibone Imarrow Iwith Ired Imarrow Icells ▪ Faster Iproliferation/differentiation Iof Istem Iand IdaughterIcells ▪ Risk I factors I and I causes I for I developing I any I type I of I anemia o Caused I by I impaired I RBC I production, I excessive I blood I loss, Iincreased IRBC Idestruction o Post-hemorrhagic I anemia I – I caused I by I acute I blood I loss I from I theIbody ▪ Severe Itrauma, I surgical, Ior IL&D Icomplications o Aplastic I anemia I – I caused I by I chemical I or I radiation I exposure I (SE Iof Icancer Itx), Iviral-induced I(hepatitis, Iepstein-barr, ICMV), Itumors, Iantibiotics I& Iother IRX(PCN, Ichloramphenicol, Iphenytoin,Idiuretics, Iantidiabetic I& Isulfa), Icongenital Idefects. o Folate IDefiency IAnemia I– Icaused I by Imalnutrition, I alcoholism, Ianticonvulsant IRx ▪ Iron-deficiency Ianemia o Caused Iby Iinadequate Idietary Iintake, Ichronic Iand/or Ioccult Ibleeding, Idecreased Iability Ito Iutilize Iiron Ifor Iheme Isynthesis. o Insufficient Iiron Ilevels Ior Iinability Ifor Imitochondria Ito Iutilize Iiron Ieffectively ▪ Decreased I hemoglobin I synthesis I resulting I in I smaller, I palerIcells ▪ Erythrocyte Ifunction Iand Ilifespan o The Imature IRBC Istructure: ▪ Biconcave, I spherical I disks I for I maximum I surface I area I forIgas Iexchange I(primary Irole)

▪ Reversible Ideformability Ito Isqueeze Ithru Icapillaries I(primary Isite Iof Igas Iexchange. ▪ Lack Ia I nucleus, I ribosomes, I and I mitochondria I (cells I cannotIdivide Ior Ido Iprotein Isynthesis; Ionly Ihave Ianaerobic Imetabolism I= Idecreased IATP Isynthesis. o Lifespan Iin I circulation I is I approximately I 100 - 120 I days. o RBCs Iare Iessentially Ia Isack Iof Ihemoglobin ▪ Sickle-cell Ianemia o Caused I by I inherited I autosomal I recessive I genetic I disorder I(inheritance Iof Itwo Iabnormal Igenes, Ione Ifrom Ieach Iparent) o Single Iamino Iacid Ichange Ion Ibeta-chain I-> Ielongated Ihemoglobin Imolecules o Oxidative Istress, Ianxiety, Ifever, Icold, Idehydration ▪ Decrease Ioxygen Ibinding Ito Ihemoglobin Iand Iincreases Isickling Itendencies o Causes I the I distortion I of I RBCs o RBCs Irupture Iafter I 10 - 15 Idays Iin Icirculation o Occlude Iblood Ivessels Iand Ispleen o High I risk I for I CVA I and I splenic I damage ▪ Thalassemia o Caused Iby Iinherited Iautosomal Irecessive Igenetic Idisorders o Single Ior Imultiple Iamino Iacid Ichanges Ion Ialpha- Iand/or Ibeta-Ichains ▪ Synthesis I of I hemoglobin I with I abnormal I chains I or I even Imissing Ialpha Ior Ibeta Ichains Icauses Idistortion I and Idysfunction Iof IRBC ▪ Minor I and I major I cooley’s I forms I of I disease: I asymptomaticIto Ilethal ▪ Pernicious I anemia o Caused Iby Ian Iautoimmune Ireaction I(GI Iinfections, IH. Ipylori), Igastritis, Igastrectomy I(loss Iof IGI Icells Iproducing Iintrinsic Ifactor) o Malabsorption Iof IB12 Idue Ito Ilowered IOF Iproduction/secretion.

▪ Decreased IDNA Isynthesis ▪ Decreased IRBC I# Iand Ialso Idecreased Imyelination ▪ Associated Ineuropathies ▪ Hemolytic I anemia o The Ilysis Iof Iblood Icells o Caused Iby Iinfection, Itransfusion Ireaction, Ihemolytic Idisease IofIthe Inewborn I(Rh Iincompatibility), Iautoimmune Ireaction, Idrug- Iinduced. o Premature Idestruction Iof IRBC Idue Ito Ienzymes/toxins Iproduced Iby Iinfectious Iagent, Imediated Iby Iown Iimmune Isystem, Ior Ithe Ieffects Iof Icertain Ichemicals/drugs. ▪ Erythropoietin o The Igrowth Ifactor Imade Iin Ithe Ikidney Iand Iliver Iin Iresponse ItoItissue Ihypoxia. ▪ Functions I of Ihemoglobin o Hemoglobin I– Ithe Ioxygen-carrying I protein Iof Ithe I erythrocyte o Hemoglobin I packed I blood I cells I take I up I oxygen I in I the I lungs I and Iexchange Iit Ifor Icarbon Idioxide Iin Ithe Itissues. o Each Ihemoglobin Imolecule Iis Icomposed Iof Itwo Ipairs Iof Ipolypeptide Ichains I(the Iglobins) Iand I 4 Icolorful Icomplexes Iof Iiron Iplus Iprotoporphyrin I(the Ihemes), Iresponsible Ifor Iblood’s Iruby IredIcolor Iand Ioxygen-carrying Icapacity. ▪ Development I of I anemia I due I to I gastrectomy o Pernicious Ianemia Idue Ito Iloss Iof IGI Icells Iproducing Iintrinsic Ifactor ▪ Effects Iof Ibeing Itransfused Iwith Iincorrect Iblood Itype o Hemolytic I anemia Genitourinary/Renal: ▪ Anatomy Iand Iphysiology Iof Ithe Ikidney o Anatomy: ▪ R Ikidney Iis Islightly Ilower Idue Ito Ithe Iliver ▪ Urine Iformed Iin Ithe Ikidneys Ipasses Iinto Ithe Iureters, InarrowItubular Ipassageways Iconnection Ito Ithe Ibladder.

▪ The Iurethra Iis Ia Ismall Itube Ileading Ifrom Ithe Ibladder Ito ItheIexterior Iof Ithe Ibody Iand Iis Ithe Ifinal Ipassageway Ifor Iurine. ▪ Inner Iportion: Iouter Irenal Icortex Iand Iinner Irenal Imedulla

• The Imedullary Istructure Iconsists Iof Ia Inumber IofIcone- shaped Iareas Icalled Irenal Ipyramids.
• The Irenal Icortex Iand Ipyramids Icompose Ithe Iparenchyma Ior Ithe Ifunctional Iportion Iof Ithe Ikidney.
• Within Ithe I parenchyma I are I specialized I microscopic Istructures Icalled Inephrons. o Nephrons Iare Ithe Ifunctional Iunit Iof Ithe Ikidney =Iultrafiltration Iunit Ifor Ifiltrate Ifrom Ithe Iglomerulus
• Nephron Iconsists Iof o Bowman’s Icapsule o Tubule Isystem ▪ Proximal Iconvoluted Itubule ▪ Loop Iof IHenle ▪ Distal Iconvoluted Itubule ▪ Collecting Iduct
• Two Icapillary Ibeds Isurround Ieach Inephron o Glomerular o Peritubular ▪ Blood Iflow
• Renal Iartery I> Iafferent Iarteriole I> Iglomerulus I> Ieffect Iarteriole I> Ipertubular Icapillaries I> Irenal Ivein o Physiology: ▪ RemovalIofInitrogenous Iwastes Igenerated Iby Iprotein Imetabolism ▪ Water Iand Ielectrolyte Ibalance Ivia Ialdosterone Iand IADH ▪ Regulation Iof Iblood I pH Ivia IH+, I HCO3- I excretion I or Ireabsorption

▪ Blood I pressure I regulation I via I aldosterone, I renin I system ▪ Hormone Iproduction I(erythropoietin, Irenin, Ivit ID. Icalcitriol) ▪ Nephron Idamage o NephronI=Ifunctional Iunit Iof Ithe Ikidney o When I a I nephron I ages I or I is I irreversibly I damaged, I the I body I is I otIable Ito Ireplace Iit. o By IageI80, Iapprox.. I40%Iof Inephrons IareInonfunctional. o 4 Iprocesses Ioccur Iin Ithe Inephron Iduring Ithe Iformation Iof Iurine: Ifiltration, Ireabsorption, Isecretion, Iand Iexcretion. ▪ Tubular Ireabsorption o I Selective Ireturn Iof Iwater Iand Isolutes I(glucose, Iions, Iamino Iacids,Iurea) IFROM Ithe Ifiltrate Iof Ithe Inephron Itubule Isystem IINTO Ithe Ibloodstream Iof Ithe Iperitubular Icapillaries. ▪ Tubular ISecretion o I Movement Iof Imaterial I(urea, INH3+, IH+, I K+, Isome IRx, Imisc Ichem.) IFROM Ithe Ibloodstream Iof Ithe Iperitubular Icapillaries IINTOIthe Inephron Itubule Isystem. ▪ Conditions Iassociated Iwith Irenal Ifailure o Prerenal I – I hypotension, I decreased I CO, I decrease I blood I volume o Intrarenal I– Iacute Itubular Inecrosis, Iacute Iglomerulonephritis,Iother Iglomerulopathies o Postrenal I– IBPH, Icalculi, Iinflammation, Itumor o ChronicRF I– IHTN, IDM, I& ISLE ▪ Calculi Iblockage Iof Iureter o Renal Icalculi I(nephrolithiasis), Ior Iurinary Istones I(urolithiasis), IareImasses Iof Icrystals, Iprotein, Ior Iother Isubstances Ithat Iare Ia Icommon Icause Iof Iurinary Itract Iobstruction Iin Iadults. o Calculi Ican Ibe Ilocated Iin Ikidneys, Iureters, Iand Iurinary Ibladder. o Renal Icalculus Iformation Iis Icomplex Iand Irelated Ito I(1) Isupersaturation Iof Ione Ior Imore Isalts Iin Ithe Iurine, I(2) Iprecipitation Iof Ithe Isalts Ifrom Ia Iliquid Ito Ia Isolid Istate I(crystals), (3) Igrowth Ithrough Icrystallization Ior Iagglomeration, Iand I(4) ItheIeffect Iof Istone Iinhibitors.

o Manifestations ▪ Renal Icolic I– Ipain Iin Ithe Iflank Iradiating Ito Ithe Igroin Iindicative Iof Iobstruction Iof Ithe Irenal Ipelvis Ior Iproximal Iureter. IColic Ithat Iradiates Ito Ithe Ilateral Iflank Ior Ilower Iabdomen Itypically Iindicates Iobstruction Iin Ithe Imidureter,Iand I bothersome I lower I urinary I tract I symptoms I (urgency, Ifrequency, Iurge Iincontinence) Iindicate Iobstruction Iof Ithe Ilower Iureter Ior Iureterovescal Ijunction. ▪ The Ipain Ican Ibe Isevere Iand Iincapacitating Iand Imay Ibe Iaccompanied Iby Inausea Iand Ivomiting. ▪ Gross I or I microscopic I hematuria I (3 I or I more I RBCs I per I high Ipower Imicroscopic Ifield) Imay Ibe Ipresent. ▪ Benign I prostatic I hypertrophy o Enlargement Iof Ithe Iprostate Igland o Current Icausative Itheories Iof IBPH Ifocus Ion Ilevels Iand Iratios Iof Iendocrine I factors I such I as I androgens, I estrogens, I gonadotropins,Iand Iprolactin Iand Ichanges Iin Ithe Ibalance Ibetween Iautocrine/paracrine Igrowth-stimulatory Iand Igrowth-inhibitory Ifactors. o Aging I and I circulating I androgens I are I associated I with I BPH I and Ienlargement. o BPH Ibegins Iin Ithe Iperiurethral Iglands, Iwhich Iare Ithe Iinner IglandsIor Ilayers Iof Ithe Iprostate. IThe Iprostate Ienlarges Ias Inodules Iform Iand Igrow I(nodular Ihyperplasia) Iand Iglandular Icells Ienlarge I(hypertrophy). I The I development Iof IBPH Ioccurs Iover I a Iprolonged Iperiod, Iand Ichanges Iwithin Ithe Iurinary Itract Iare Islow Iand Iinsidious. o As I nodular I hyperplasia I and I cellular I hypertrophy I progress, I tissueIthat Isurround Ithe Iprostatic Iurethra Iusually Icompress Iit, Ibut Ido Inot I always I cause I bladder I outflow I obstruction. I These I symptoms Iare Isometimes Icalled Ithe Ispectrum Iof Ilower Iurinary Itract Isymptoms. ▪ Symptoms Iinclude Ithe Iurge Ito Iurinate Ioften, Ia Idelay Iin Istarting Iurination, Iand Idecreased Iforce Iof Iurinary Istream. o As Ithe Iobstruction Iprogresses, Ioften Iover Iseveral Iyears, Ithe Ibladder Icannot Iempty Iall Ithe Iurine Iand Ithe Iincreasing IvolumeIleads Ito Ilong- term Iurine Iretention.

o The Ivolume Iof Iurine Iretained Imay Ibe Igreat Ienough Ito Iproduce Iuncontrolled I“overflow Iincontinence” Iwith Iany Iincrease Iin Iintraabdominal Ipressure. IAt Ithis Istage Ithe Iforce Iof Ithe Iurinary Istream Iis Isignificantly Ireduced Iand Imuch Imore Itime Iis I requiredIto Iinitiate Iand Icomplete Ivoiding. o Hematuria, Ibladder Ior Ikidney Iinfection, Ibladder Icalculi, IacuteIurinary Iretention I(hydroureter), Ihydronephrosis, Iand Irenal Iinsufficiency Iare Icommon Icomplications. o Some Imen Iinitially Ihave Isigns Iof Iuremia Iand Irenal Ifailure. o On Idigital Iexam, Ithe Iprostate Iis Ia Isoft Iand Ifirm Ienlargement IwithIa Ismooth Imucosal Isurface. ▪ Prerenal, Iintrarenal, Iand Ipostrenal Idisease Iand Iwhat Icauses Ithem o Prerenal I – I caused I by I renal I hypoperfusion I due I to I hypotension, Idecreased ICO, Ior Idecreased Iblood Ivolume o Intrarenal I– Icaused Iby IATN, Iacute Iglomerulonephritis, Iand Iother Iglomerulopathies o Postrenal I– Icaused Iby IUT Iobstruction ▪ Glomerulonephritis o Triggered Iby Ian Ievent I(infection) o Causes IAg-AB Icomplex Iformation I& Ideposition Iin Iglomerulus o Resulting Iin Iactivation Iof Icomplement Isystem I& IWBC Iinfiltration o Leading Ito Iglomerular Iinjury I& Ileakage o Causing I proteinuria/hematuria I & I coagulation I cascade IactivationI& Ifibrin Ideposition Idecreasing Icapillary Iperfusion Iand IGFR o Causing: Iedema, I increased I serum I creatinine, I azotemia, I and Ioliguria. ▪ Treatment I of I renal I failure o Management Iprinciples Idirectly Irelated Ito Iphysiologic Ialteration Igenerally Iinclude I(1) Icorrecting Ifluid Iand Ielectrolyte Idisturbances, I (2) I managing I blood I pressure, I (3) I preventing I and Itreating Iinfections, I(4) Imaintaining Inutrition, Iand I(5) Iremembering Ithat Icertain Idrugs Ior Itheir Imetabolites Iare Inot Iexcreted Iand Ican Ibe Itoxic.

o Hyperkalemia Ican Ibe Imanaged Iby Irestricting Idietary Isources Iof Ipotassium, Iusing Inon-potassium-sparing Idiuretics, Ior Iusing Ication Iion Iexchange Iresins, Iwhich Imay Ibe Iadministered Iorally I orIrectally. o Azotemia Iis Igenerally Icontrolled Iand Inutrition Imaintained Iwith IaIlow- protein, Ihigh-carbohydrate Idiet. o Drug I dosage I levels I may I require I adjustment I if I they I are Imetabolized Ior Iexcreted Iby Ithe Ikidneys. o Recovery Imay ItakeIup Ito I 1 Iyear. o Continuous Irenal Ireplacement Itherapy I(CRRT) Iis Iindicated Ifor Iuncontrollable Ihyperkalemia Ior Iacidosis Ior Isevere Ifluid Ioverload. ▪ Blood IhydrostaticIpressure o I High Ihydrostatic Ipressure Iof Ithe Iglomerular Icapillary IbedsIfacilitates Ifiltration. ▪ Kidney Ifiltration o I Glomerular Ifiltration I– Iblood Ipressure Iforces Iwater Iand IdissolvedIplasma Icomponents I(glucose, Iions, Iamino Iacids, Iurea, Iand Icreatinine I= Ifiltrate) Ithrough Ithe Iglomerulus Iand Ibowman’s Icapsule Iinto Ithe Irenal Itubule Isystem. ▪ Role I of I angiotensin I converting I enzyme I (ACE) o I Angiotensin I 1 Iis Iconverted Ito Iangiotensin III Iby IACE Iin I the IlungsIresulting Iin Isystemic Ivasoconstriction. Immunity: ▪ RoleIofImacrophages o Arrive Iwithin I 24 Ihours Iafter Iinvasion Iof Ian Iinfectious Iorganism ▪ Called I monocytes ▪ Called I macrophages I when I they I are I active I involved I in I the Iinflammatory Iresponse.