Scribd Logo
Upload

Welcome to Scribd!

  • Emily Rheumo 1

    Uploaded by

    Gela Gelashvili
    44 views34 pages
    rhuem1

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Report this Document
    rhuem1

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    44 views34 pages

    Emily Rheumo 1

    Uploaded by

    Gela Gelashvili
    rhuem1

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    of 34
    MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PA 504 - FUNDAMENTALS OF CLINICAL MEDICINE II MPONENT Component Description: An intensive study of the presentation of disorders of musculoskeletal and connective tissue system, Rheumatic diseases and the arthritides, lupus, sclerosis, vasculitis, and systemic autoimmune disorders will be discussed. Emphasis will be placed on disease recognition and patient management. Required Reading: Harrison’s Principles of Internal Medi Current Medical Diagnosis and Treatment 2014 Component Outline: Unit 1 - Overview of Musculoskeletal and Connective Tissue Diseases Unit 2 - Autoimmune Mediated Disorders Unit 3 — The Vasculitides Unit 4 The Spondyloarthropathies; Amyloidosis; Sarcoidosis Exam — Units 1-4 Unit § - The Arthritides Unit 6 — Inherited Connective Tissue Disorders; Nonarticular Rheumatic Disorders Unit 7 — Low Back and Neck Pain ‘Comprehensive Musculoskeletal Examination MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE 1 RHEUMATOLOGY COMPONENT UNIT 1: OVERVIEW OF MUSCULOSKELETAL AND CONNECTIVE TISSUE DISORDERS UNIT OBJECTIVES: After completion of this component unit, the student will be able to: 1. Discuss the appropriate approach and eval e (A) ion of the patient with musculoskeletal ‘The History and Physical Examination Diagnostic Considerations Classifications of Rheumatic Disease Treatment Modalities 2. Describe the anatomy and function of each articular structure in the musculoskeletal system (A) -Anticular cartilage, synovial membrane, bony end-plate, joint capsule and ligaments 3. Briefly describe the pathogenesis, constitutional symptoms and diagnostic findings of theumatic diseases (A) 4, Discuss the indications for specialized procedures in the management of patients with theumatic diseases (A) Joint aspirations synovial joint fluid analysis Erythrocyte sedimentation rate Autoantibodies Imaging techniques Arthroscopy (A) Denotes gore knowledge = essential to appropriately reeognize the presentation, perform the assessment, derive the diagnosis and eat the disorder as a primary eae provider (B) Denotes key knowledge - important to approptiatly recognize the presenation, perform the assessment, and diagnose the disorder as a primary eare referral (©) Denotes imnartant know ledge - helpful appropriately recognize to enhance and augment knowledge in the cote and key seas of medieal practice MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE I RHEUMATOLOGY COMPONENT. UNIT 2; AUTOIMMUNE MEDIAT DISORDERS, UNIT OBJECTIVE: After completion of this component unit, the student will be able to: 1. Discuss the etiology, patholog rheumatoid arthritis (RA) (A) and the joint and extra-articular manifestations of 2. Describe the differential diagnosis, classification criteria clinical and laboratory features, disease course, management and prognosis of rheumatoid arthritis (A) 3. Know the mechanism of action, therapeutic and side effects of drugs used in the treatment of rheumatoid arthritis (A), 4. Know the guidelines for the intra articular administration of corticosteroids in the treatment of rheumatoid arthritis (A) 5. Enumerate the extra-articular (other systems) involvement of rheumatoid arthritis and discuss the clinical manifestations of each system involvement. (A) 6. Discuss the incidence , prevalence, etiology, pathogenesis, | manifestations, laboratory diagnosis, treatment and prognosis of systemic lupus erythematosus (A) 7. Describe major criteria for classification of systemic lupus erythematosus (C) 8. Differentiate drug-induced lupus and spontaneous systemic lupus erythematosus (C) 9. Discuss the epidemiology, pathophysiology, clinical mani , diagnosis, differential diagnosis, and treatment of (B) Scleroderma Polymyositis Sjogren’s Syndrome Dermatomyositis (A) Denotes gore knowledge - essential appropriately recognize the presemation, perform the assessment, drive the diagnosis, and weat the disorder as a primary eae provider (8) Denotes key knowledge - important to appropriately recognize the presentation, perform the assessment, and diagnose the disorder as a primary ere referral (©) Denotes imnartant know edge - helpful o appropriately recognize to en sof medical practice end avgment knowledge in the core and key MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE I RHEUMATOLO¢ ‘OMPONENT UNIT 3: THE VASCULIDITES UNIT OBJECTIVES: After completion of this component unit, the student will be able to: 1. Discuss the pathogenesis, clinical manifestations, and classification criteria of vasculitis syndromes (A) Discuss the incidence and prevalence, etiology, clinical manifestations, diagnosis, differential diagnosis, and management and complications of vaset Polyarteritis Nodosa Granulomatosis with Polyangiitis (Wegener's granulomatosis) Polymyalgia Rheumatica Giant Cell (Temporal) Arteritis and Takayasus Arteritis Allergic angiitis and granulomatosis (Churg-Strauss syndrome) Briefly outline the incidence and prevalence, etiology, clinical manifestations, diagnosis, differential diagnosis, and management of the following miscellaneous vasculitides (A) Henoch-Schénlein purpura Kawasaki's disease Behget’s syndrome (A) Denotes core knowledge = essential to appropriately recognize the presentation, perform the assessment, derive the iagnosis, nd treat he disorder a a primary care provider (8) Denotes Key knowledge - important to appropriately recognize the presentation, perform the assessment, and diagnose the disorder asa primary care reterat (©) Denotes important knowledge» areas of medical practice pf to appropriately recognize o enhance and augment knowledge inthe core and key MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE 1 RHEUMA‘ IMPONENT UNIT 4: THE SPONDYLOARTHROPATHIE! UNIT OBJECTIVES: AMYLOIDOSIS; SARCOIDOSIS After completion of this component unit, the student will be able to: al 1. Describe the etiology, risk factor, criteria for diagnosis, pathophysiology, clini presentation, diagnosis, and management of spondyloarthtopathies (A) Ankylosing spondylti Reactive arthritis (Reiter's syndrome) Psoriatic arthritis 2, Describe the presentation of Juvenile onset spondyloarthropathy (B) 3. Discuss the etiology and pathophysiology, the classification, clinical manifestations, diagnosis, and treatment of amyloidosis (A) 4, Discuss the incidence and prevalence, the etiology and pathophysiology, the clinical ‘manifestations, diagnosis, management, and complications of sarcoidosis (B) (A) Denotes gare knowledge = essential to appropriately reeagnize the presentation, perform the assessment, derive the iagnosis, and wea the disorder a a primary ear provider (8) Denotes Kew knowledge - important to appropriately recognize the presentation, perform the assessment, and diagnose the lisorder asa primary cae referral (C) Denotes impartant knowledge - helpful vo appropriately rseognize to enhance and aygment knowledge inthe core and key ‘areas of medical pretice MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES. PHAS 503 - FUNDAME ‘ALS OF CLINICAL MEDICINE I RHEUMATOLOGY COMPO! UNIT 5: THE ARTHRITIDES UNIT OBJECTIVES: After completion of this component unit, the student will be able to: 1. Discuss the etiology, pathogenesis, risk factors, clinical presentation, laboratory findings, differential diagnosis, and management of osteoarthritis, gouty arthritis and pseudogout (A) 2. Discuss the etiology, pathophysiology, clinical presentation, diagnosis, and treatment of infectious arthritis (A) arthritis, Bacterial (septic) arthritis /Nongonococ Gonococeal arthritis Syphilitie arthritis Mycobacterial arthritis 3. Discuss the clinical presentation and management of fibromyalgia (A) (A) Denotes gore knowledge = essential 10 appropriately reognize the presentation, perform the assessment, derive the siagnosis, and teat the disorder asap ovider (8) Denotes Kev knowledge » important to appropriately recognize the presentation, perform the assessment, and diagnose the q (C) Denotes impartant knowledge - helpful to appropriately recognize to enhance and augment knowledge inthe core and key seas of medical practice MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE I RHEUMATOLOGY COMPONENT. INHERITED CONNECTIVE TISSUE DISORDERS; NONARTICULAR RHEUMATIC DISORDERS UNIT 6: UNIT OBJECTIVES: After completion of this component unit, the student will be able to: 1. Discuss the incidence, prevalence, classification, manifestation, diagnosis, and management of inherited connective tissue disorders (A) Osteogenesis imperfecta Ehlers-Danlos syndrome Alport syndrome Marfan syndrome 2. Discuss the clinical presentation, diagnosis, differential diagnosis, and management of periarticular disorders (A) Bursitis: Tendonitis: Rotator cuff tendonitis and Bicipital tendonitis Adhesive capsulitis (Frozen Shoulder) Medial and lateral epicondylitis (epicondylosis) Carpal tunnel syndrome (A) Denotes gore knowledge - essential to appropriately recognize the presentation, perform the assessment, derive the diagnosis and reat the disorder as a primary ear provider (2) Denotes key knowledge » important to appropriately recognize the presentation, perform the assessinet disorder asa primary care rela (©) Denotes important knowl areas ofmedical practice and disgnose the Jpfal to appropriately recognize to enhance and augment knowledge in the core and key MERCY COLLEGE GRADUATE PROGRAM IN PHYSICIAN ASSISTANT STUDIES. PHAS 503 - FUNDAMENTALS OF CLINICAL MEDICINE I RHEUMATOL :OMPON! iT UNIT 7: LOW BACK AND NECK PAIN UNIT OBJECTIVI After completion of this component unit, the student will be able to: “ @ © 1, Discuss the incidence, prevalence, pathophysiology, and the mechanism of injury for back and neck pain (A) 2. Describe the evaluation of a patient who presents with back and neck pain (A) 3. Discuss the assessment, management, and sequela of traumatic cervical spine injuries 4, Describe the types of lower back pain and know the systemic conditions that can manifest ‘as back pain. (A) Local pain Referred to the spine Originating from the spine Radicular pain ‘Associated with musele spasm Pain at rest 4. Discuss the etiology, assessment, and management of lower back and neck pain (A) 5. Differentiate acute and chronic lower back pain (A) 6. Discuss assessment and management considerations of chronic back pain (A) Denotes core knowledge - essential 10 appropriately recognize the presentation, perform the assessment, derive the diagnosis and iret the disorder as a primary ear provider Denotes hey knowledge - important to appropriately recognize the presentation, perform the assessment, and diagnose the lisorder asa primary care referral Denotes important knowledge - seas of medical practice pul to appropriately reoagnize to enhance and augment knorledge inthe core and key Aly 2: Autre MIM LiebisTep toisoere n> 2 / o> ABalems ~ GEE OR ey AUTIMVURIE. DISEASE (NIVOLVING NNO of Joints = ONSET 20-49 NO Vee CORLL IRAE Oo 6 4 tart + TETIOLEGY UNCEe TAN! RN Biber coniCpen tus) + eoe/ — CLIN CAL ees CAEEUARE PROSE NNELaMMaroey Poraenfems (onratein& 1S COMMON. S\GNL) — Can eenae EVERY dent Ny SS pee er erp dani aoa Menton. 0 WoinTs (renceeuccs de Jon) ) ~ vor COMAKIT NOLNED? Joins oF Hain (pemice), Wierers, panes, Ni Ss sion ~ ema OS SLA thes Sth ees, pla HS iJon -ULNBE DewaTon ob wep Jonurs Sicease ae =~ euronINneme peraerees se IPS aCe 2 Pasar Eat _ aes SPP feren, oe HYreeetenceD | ws Bae EC caneacruee (MeP HexD, Pe * CONE TLITIOUAL exreTEas NpER ExreNCED, Dips flexed) NORNING STIERMESS CpeeSENT IN LL PTs) TINIPRONES AS DAY ROGRESSES TAY ee Wee SEVERE APTEE eTeEMioUSs ActVvIrY wae FEVER EIGHT Loss + C-SpINE MOVEMENT CO1-CZ SUBLUXATION + INSTABILITY) CoP NITIALEY Lite MREATEMINICE COB LIGATION, - Bo-46"l» Fs — CAN LEAD Te MYELOpa THY ° CARDIAC INWOLVEME NIT — PERICARDITIS, PERICARDIAL EREUSIONS, CoupucTION, ENIEWUITIES NALA INLCOM PITERICE /BOETITS oe * PULMONARY INVOLVEMENT vascutt Ruan EPELUSIONS Coote + PRoee Ese ies) aerate TINTESENTIAL AyeseosIS —PLEURITIS apa Sx ‘ u ey ontLLntrs soceunae mlvaetentY epee ou “DEN Eves, bpiscLERITS, ScLERITIS;, SCLEROIMAUA .., ca OeueRE DUETS ScleeaL +LoouUEes, peparoconyUNcrVit 7 + DENYING oF AUc0us AEM BS rca LEAR Te SLNOME, g *SUS@ wihuryeroiD Closes = SAME atsoe aueErAces ~ SEEN KL LUNGS, SCLACAE, PERIC Fe ma WE NopuLles ae Beer) LTY Nrieeo te oN! ESPLENO MIE CAL -yypeeparneAT” OW NELITZOPENIA. —anetia ¥xtd o =. INEHRODENE aL sAteLopey 1 . ALOGAC shee ANEMIA — LeurEiA SNeUTROPENIA | Lp AA — Bboy Aen, ere- ses rsoeteue mC AWLP — NEAREST a VAALOS IS — cans LEAD TAN +SFELETAL ~ OSTEO PoROSIS EAE OstHA IA I 0S «RENAL \) PERIODAITTV REM BEAOUS NlepHropattY — S€eoNIDARY’. AWAYL.O1DOSIS = RHertatrolb \lepuLes ” Pur UIA ~ prot CAN GRENIOSINA PBA DIAGIHOOI> = SYMLOVIAL FLU SN ALVIS - LAB Fete rs om sexupanve + TITERS LJ. a. Ts . — pREs “Tong anced vDISEase Vpn Clctest —Ntost TES PEOPLE WI. oisease + Bacteria) PANT CEBU ATS Peer, EA + Peele pens 7 BO 780 sen nVRY PEOTE IN, oR > 7 940s gpeciHciTy 4 Arm eoo BE tems &6R /ceewe meme TWE PRoTEIN T mipRopoR TIN DISEASE Sith accs ) HORMocyTIeANE IA Ig comnmeterd ate CopIN: CHA A PrlleocechESIST ares nu cee Sone 7 = insbaieeiiien SUPERIMPOSED cee n ¢ seq S Euisrtwe > BAbi ogres TA wninwor ARE USUAL Rite DING ese @ Wonees -ohey — BAILIEST CHANGES INC Ves: 20 I TS of FEET RANI tage UUM ARTCULA DeLhNiea LIZATION “ mon ATER, Uni poet Jom _peviintPALCaN, IT PME WAR oArliWiGr+ EEOSIONS DEVELOP Pen CHANGES 4US0 IN C-SPAN “CLASSIFICATION CRITERIA —NEED SG “DIFFERENTIAL tiadt0siS — OSTEOKp Alp Ins owner \ Laeere Jorn —o SET Es Weise scp INNOWEMENT 2-10 LARGE Poms —l| Wo constrrumoueL 1-3 ssa onrs ——2 = ceueres oes = eesr foe ae anes —=——s — Cheb DEPKITIN Corausr) Oye —EnpiGeapl cant cremcrisisit SURAT CRYSTALS See00eY> (OR anv O Atpa ——O —SPON DYLodptHesparihes Lait Cr) RP ant Loni Cr) 2 Tie: AntiecP (a3 xuut) hee < tho @) ee om Fhuter) — Poryn yal Gnd SiewtHanta ann — —tatoe aure cop (+ 3x uLN) 3 es ase —> NeBbleppt dg Reatranrs = NORUAL ESR ! ApNoettal cep ————" oe ASNUetaL este DuRTAL, 2G Weeks ——— 2 Opes —————_ ANTI! 4 jee OF Lala ANTIE“OP ~vesuts Given As trteeS = IgM comtponteNT ¥BST eacut DEEEHD fe RieiMetne BETES oe ante A caass Har 1S arrachle BA TREATMENT “Wissies PAIDE pTOM ic RELIEE Baur Do Ke ALTER DeEALE PRGRESAL SSpapee USED OMY A CNJUNoTION WN. bans FEC OXI — tbe ee pa cox.2 INMEXTER ‘SERECTIVE + LES LIKELY T Cause Ct bESTCES?S ASE ree TCCERATION, PERFORATION, Go) Henssvecdaces —CAN fap: are Tie SIGE EAFECTS LW. PROTIN PIMP INtherroe of “RENO Sipe Fre’ INTERSTITIAL Ki, TS, PRERENAL eon, ge € tenner, ALE —TRisk WAGE ovee Go " CORNER REY PLATELET PRON + PROLOG BLEEDING IME —COX-2 INHIBITORS TRIS of THeonteonc EVENT * CORTICOSTEROIDS — eed eae INFLAMMATORY Recon + fe a vim TSE (EFFECTS LMtIT Loa THERM USE “Kuse top. vascumsse Bebo Le Ende ie 70 RE. PISEASE PROGRESSION. BEpoee DS TNO Moke TAN 1omG oF WSonte baresy LyNbees To BE TARE one *SiileTc Drtreps We terExtre TINITIAL BreuGr of cfoce “iple THeeAeY TERRCTS WIN 2-6 WeBks METH UNDROXY, SULEA ree ong ORALLY once Weeki ™ ECTS = reGitte, _ 6 = Easreie weemanav+ srasanns DAU foLsTE S 14 LEU Open A oR Wom Bocrro PENA OB LEU cover ny carci TOXICITY LA FrBeesis + C12eHos! Sconren S a INDICATED L.ANY. ne — TERATOGENIC ‘Hepa — Mech ant a ~Berosenase eS shane >» Leon pok BEASESS £0 BE fore rao “ou eee sis atheros — *HYpeoxyelroeoQuin SIDE & — SIDE Etrects — fepstoranicrye RETINAL. DawtaGe ~MTYELOSUPRESS10N = CARDIOTOXICITY. INFECTION > Blow orscea sia TB toreera TTAFES & LAasmg To look: ~OA TORE KA TREATMENT COON: J BAe AARES 2 NERCEPT Apa int ita Cot Ai TB, TORY CYTO ERLE ~ +H) A PRbIN AAAS alee ed 4 pro 3 ee KH IifereE RATE woe OEE pace Riel + FUIGSL meee AB LReactivATioN, OF CATE: re SR LYMPHOMA PIs? a peuG: INoUcED LUPUS NEURO DEFECTS ABATACE HT Se ANIA Ere 41 = IL =| INHIBITOR MK BITUXMABS ~pepets & -ceus— Creep fee Serou) piseast TOC LIZ A42> -1L-1 HhBITOR Neregreo BENNER DWENGrIVEN,’ Divreaaenuiar eregoin iNiJecr ods HAVE pew + evERYS Mo Foe up TO 2 Years + Sthu NOT Be eppeaTeo MIZE ee Th 542.4 vonaes Neue Oe cause goo eiLiTy Of CARTILAGE TERE peuer OF Mere Ss Foe (42 vem ine + ONLY StbeT + (0-40mg of TRE MOLINE weeTONIDE, Den eTEMic LUPUS BRY HEN T0sH> — General CHaRECTERISTICS PDIMMAUNE TASORDER LeabiNcr re neecante terran! And THESE qe iacie (INVOLVING WIUETIPLE © eee 7 A+ HoooarTRCTIES IMO /eD so Nee, @LNLeDI ANT “patty ‘S1OLOGY “ANTIBODY pespuctiont —> pepsrmeNl of Int AuNte com Lex! Competent Ac uATION! —> TISSUE DesTaucTIon. ‘eins +TYPES, PES iraNEOUS SLE 2 C0) P SLE Bren Legens ph. oT SYSTEMS ensaase) = BeuGe mouced tH) ~ ANA > NEGATIVE LupYys = ASS OCATED fir NES ARTHRITIS, RAYSALOS 2c AcuTe: CxrTaNleals Laspus vaeRoLO GY 2 Re CULT Gal antec Y), Anta NES USTHS Cant Te passes aL Tocttt > Lopedn al WPS = Clan cal FeaTuRes Cons TUTIONLAL SAP TOMAS FAN GUE - Macaise _ (ER Neel [rreicite Less + CUTANEOUS — puree ely Rast ~pleTOSENS mv ~biscoro LeStoNS Cee te Aarus aiseD partes Wh eepaToTe seauimG:) ~ ORAL WaeaL ULCERS ~ Alper ~eayrlauos A SpUnTee therdue HaGneS/Aat L FOLD pLPABoTs @ WAUSCULOSKELETAL Soins Pant C90 Ye SE BSS _Yemlers (MoM RR OSNE ie 6 el = ARTHRALGHAS 1S ~ Mtyacena Alor mwhrest OT oe anew + CAROL Miata 2, — peel cAgpins enebxotees) HH ENIDOCAROITS Ceiertant SACeKrS 1 BOY ee " “ 7 pnyoca2orns sarin Meee Ee, ue + Puli Na ey — pLevieiTiS _'breuear Etrusron! — pNecnonris LUNG DISE PResTecnve age cant DEVELEP 7 yTOLOGIC —Hemtorne ANEMIA < LEUKD PENA ~ DiMA pHogettA —THemieoctto pens A Pena. ~PRover WRIA « PaeysezosS “iss, Es CAS - ssuiceu von ope] sarees aL Ne pie —peeay NN . > Bi ous HI Ressay, 2 IMMUNOLOGIC. ~ IMPAIRED IMtuntie Response Gl SAE [Nomrrince, DYSPEPSIA, byspHaGra, Ic LILCeR( ~ MESENTERIC wasecune q 2 erm ~ PosTpRanioiaL Ag>meminial faint "CNS ~ PSY¥cosS - CoGNuTVE MparRMest ~Ss€izpRes > BEPRESSI ORL -HIA 7 CRANIAL eseopaahies TITRA Vee, + OCe UL SN ERSE wove Lens — Cons nenvetis IA ~ 7 en toes Bouncness ~ COTO Lntoon Spots oR P pera — DIAGNOSIS ~ Posty E Aen SCEBENLINIGr TEST US SENSITIVE Baus ACT SpECIEIG satihita eo We B, eerymeys THYROID OS EASE, CERO DERM A, 4S SoRGRESS - ANTI -0S DNA (6°%s) AND ANT 8146 (304 DOVER EpeHe burr NOT aBNsinte ae BNE 070%) — ANTI Hr sToNE LOS oA Ole oe 100% IN OR © bs en) CRUG WpucEe no ee ieee eupes) 0 (SS-4 Da 2a CSSE) ~ B TYPES of ANTI pHispteul Pid Abs a} pany sive for SpPHUS Carma i SSE RECTOR FoR vEnsnls TARTERIAL fer BOSS +r Ascasese1aG aA E (PARATIONS CoM PLERtE 7 VB — CBC + Renal “ane USUALLY BECeEASED ANTI CARDO ~ SCRITEEIA OLIPINS +L Lipe § AXTICOA ALAN CHEE pa e000 ? ; PT Has oc pipsTick proe NURIA ee + ceLeUL4R cAsTS guRoLeGne DISEASE BN GE IZURES OR + psycHos(s ¢ of Le nAAaToLeate pisoeDEe Fe acene ANEMIA $2 re yeopeni® CX qooo mel Oe CyetplopettA Ce [goorncl) 02 °C eaazcete PEMA (2190,c00met) 10, aprunsoreGne Aver oer Tau es AN Theo" 0 Suet & Tease (#) oppooene TEST poe afpthus U1. @) AWA LUpUS ~TREateNT, — Ayoro sunt Expesuee —use 6: rtarps —peR MINOR nec = conn ees TE GEE = haps ae 7 yi > CONTE OL OF | of ceeTainl 17 OLS 1 CoM Rut e oe" ri IE it OEE pein’ toe iene anti, Te Fe Riepaek™ w ask AL AG eee CNS Iyer Hearty Ln eat a peor (geieareas + ince oF Te Ge at Renn cvevept INNUED 4s PRE A ave Measuee ek a AMIDE | pronto se gore ess “TOANC) Cte eo in TO Cor eS TSAO pai AO -USEO oN cases (RESISTANT ee LEAN Helen ee ore oto pi aN ONT cea useo a bOTREPIN couStor ini Parenter _ BEL UNAAB IF Smil MET pesos —or pT plant pate sper Soeer Ae! lant COAG Gul cats spire! PROG years suievival iL BATES &. eo — nose, INFECT IS EGAN fis Dijee nAOST vor om People: — tateR, uit prcasey BRESIS 6 THE lor oresT prem 2, DRuGr (ICED 2aypes si 4 peantees aplar seP4 pc fread Se ex ea NE. y E@uAL wae 2) NEPHRITS STs #4 (PES AEE Me qlee eseNT 3). hypocom pte perertie ten soos TO DS emcee el cee ¥ Ale rnicae + ces TOM to ele af _ (Alten: ceue irepeon™ & wie, CisprEne, 2 1 , pe? x _pypearaiue, Ace PeepapRenen: WGonr21DE , CLeBRe BC . Croepen Mae PNoe AAT [gonna VE Merino PeocmbAVE @ SCLERODERMA —CGreneR SL cupeectepisTie$ > cHeantie CINECTIVE TISSUE pisoeper THrr Cal LEAD Te Wipesezen ee 1S - Pate pg Lee pune CYT eines Sint UL DROIASTS CALIS ICY AOE AL AUINT OF COLLAGEN DE pesiTiomt SimiGr M08 T Com HON IRS SLOAN AGE ee-oe8 — 2 Trees: Dipguse (20%) + LmaAreo (60 7%) ~ DIFFU WSF pe spread SEIN INVOLVEMENT - Papp oNSET SIGNI RICONT VISCERAL IIVOLNEMENT Laren LUNGutteaet Gry erueys —sken INVOLVEMENT LIMITED To prisTal BxTeeMtinies +47Ace — DeLayer onseT —CREST SME Ee + CALCINIOS |S OF DEAS + RAYMAUOS «B50 pHAGeaL tT Dxstunictio + BCLEBODACTYLY oF FINGERS « FIELANGECTASIS (OVER. DIGHTS HUME Haws) ~ CLINICAL MANIFESTATIONS APPEARS Fiest—eepeee ones : Cara aS re Fars Frias = FEMIN Gr oF Skin OF dave + EXTITErtictes EG ES COMTRACTURES DISABILITY Pps H@vententy - IFEST INITIALLY 4S ~DErta werts - ULCERATION ARGUE Fy ee . lnk. FI Gl INVOLVEMENT GR RGEE RE “AcHeoss occurs in tos parents a (eeeux Feo Ler prot Le - GrasTRic EM IN ee TLARGR MerrHEO Diver mcuLA 'N Je fund, rium + coven . puns, INVOLVEMENT < paler ce ON! C4USE oF bEA: a1 SCLEBODERTA Cee CAUSE SE TESTES tinier Disease — PULA DEY crac ES « CARDIAC INVOLVEMIENT - PERICAEDIAL ERPUSIONS » we CAN LEAD Te C+ -HeaeT Bloue _ RIGHT sIDED He mere putoisercthn + ZEN AL INVOLVEMENT AN Caisse Rape Mavicuianee HIM! wvecaleniaL INVOLV tentent F RECLERODERMA bIAGOs's = MILD ANEMIA Mae doRESENTT TSN eRe ANE SP ATEHC Ho soiree Aniena'4 eg evevaTiont UNUSH AL ~ Ra PRoTeINues ag BEMAL TRveLve eH =ANA ALMEsT A\ (+. ; , — Aan eee 7 ot jer Aittoe Unites + —ANTITDPOISOMY cease opeaine He ke DIFFUSE HMA Coot) ~ Baaumt sail Foe DY ond, ~ ReT DIFFERENTIALS uses of Zansu — CAN BE CONFUSED NI. OTHER CA be SLE MIXED Conirtecnve “rgeule DEEASE, ah ihesanene Fins Has a = SuLeRomike De = EosmMepHILic taser! s nl (Cr NCE oF BLOND seoctNoptt! LUA THY — piepieTié CHEIEO| ie pan eiag = NepHeotrenic Feteost lor DERM) by WeeatMent est S SMP ne + supPe TREATMENT ! eNe - AY NANOS Bar Haninel tecoc]ees cae AL SIDE AK RIFE DIPINE OA ~ ESOPHAGEAL werux 4 LOE mW ANoWUG) 8 BAGERIAL qveeGeotet . OC TREOTIPR (sor Aates™ ANTIBIOTICS OE BA! ree lA —Acemlhyiees foe ATM OSS &caprorel — peeousone Not cL errEOTVe a Pemvurtnte —piseen “Heres WL. SKIN TihckeninsGe 'SJOG@RENS SYHDROME —> GrenerRAL * Laipilecrtres INRLTPATE teesrieot LAC tat +SALIVA! A LMULTIORGMN (SEIN, LUNGS, HY Born vessers +eNER) * pettiey oJoereens Gpey eves +Dey WuTH four Me eTHEe gHeuM CIseace XY GLANS + Spon pry sdecaeentt Rien Bl ei = 4 —etmicaL FeaTUeES + KepartcoNJUNeTIVITIs Si1CCA cul NRUTIZATION oF eacalsen BY LYMpHoeyTE PL asma ce GLANS ~ BUENING treHiNten, epor tee ~INABIUTY “To Weae foe UN SOY ect Gilnepte sHationl /SPEACIS “ ARTHRALGIAS ARTACING, FATCNIE PAYSTIEN NE Cana gration VASCULIT 5 pleueins, cope, panceeanas NepHert > DiaGrtosi¢ ANAS #ESENTIN 13-7 Pres Bo +La present -BE+ LIE [A — Noe ocr Te, NowrAoct odie ~ LELIKOPENIA, FechiNoPHILIA 7 ER “CesT MEASURES Oulart oF TEARS feReDuceD — LIP 2 PAROTID GLAND BIOPSY —= oirrpeenmats Hee Gevepsies To content ath, =S4RCO1 Dos 16 TREATMENT enttanee OAL + OCLLSLAL _ AeTECLAL, TEARS = TapIcAl occur AE CYCLOSPORINE Tiree a SUGAe tee Cm eg eCRETIONS TDOLYMNOSIT!S HERAT ONE or oe Causes [GENEcre DUA + EnvieoMentral Tee GER susceetiea is (NOU le w> mnsevand aon Genetica UT LEADS pp IMMUNE acnveccrom! = b CRUL Ute yAecHanieets: set 25? «persists ih an pa te esr S pourmvosrttS — ceuL lear ATES Peeks —* te owl NAtvesitis peo Sounical AaM tr eSTAT ercaTuees coro t? Bon Po = HerieA CAL OXIKAAL Musee > DEVELOPS 2 Weaks oe Monts Tea (3310) 5 = pysphaGia (33 °%e eae Ce” FEEUNG BELO ever e FEATURES UNIOCUE TO peeriaron sre simS —Heroreope east (eure rer) UV IOLA CE CUS ~ = CrotreoNSPAPULES = Lae, eerrersaTous, Scat Le: onisferbiecues ” ev sien — RASH ont pace, NECK, ANT cHest es ON SHosLoees UPPEe seek, eLBONS eet STASIS S SHAIAL SIGN RAsH SS Pena elects - AELANGHES Tea caveipicaTion$ IN CHICDIEEN “> PAM FUL SNASCHILINS OF Gy react; KRONOS. LING, ENES ‘A 4 RISK OF {tact OmANict eS SASS COSCIATED HixtoiniG ~aRTdR alone oS § Stlesconoucnon! Berecrs & TINTERSTITAL LUNG Disease 3 ANT Soiree INE ee eee Creoup oF FIDINGS mucLuprHd Or CNG DISeA Bacrlaurs MeCHAaT CS —Spuaentos 1s SE +SEVERE mUSCLE ves Hanes, ALA BNIDINIGS = ~caNtHelp pjitoe pisease SEVERITY |, ALDOLACE , AST, ALT ELEVATED ~ ESZHCRP Normal bo ANTI Jo ann eon 138 MOST Contato prsins apedric 4 AssoceTeD Wl INTERSTITIAL LUNG DISEASE (Ast swareye Tse) FATED te DER Aaton tr? nS = ANTI-SRP ASS OC/ATE OWS EVERE patewesits + Dis PHAGH A ANTI = [55/14 0-ASSCATES > DETIATOLN TOSS ELAaLiGHAdtey OM. DETERMINED - ETESMIMED Hem AMOI - LL See INFILTRATES, seus cle Blopsy — Locate > DER aT OUYos its —PeelvascuLse, 4 PRRUEYSIAL scot Vos (S AsontS, © News Cris) — PAMYESITIS = Boot YS IL * DIFFERENTIALS . SLE, SoLE zo DEENA, SJOGIZENS “et Jhiotivponr te DY RAYOSATIS poTieoinlsns —peexiHar pAusore leatcnesS * PERI pHEIea. CENTEAL ONS DISORDERS YAS, oY es TH eNagrea MIS IGETEMIC VAS LIDITTES »PeUGS eR eamM eT re CORTICOSTEROIDS (acon rere oeAl eric ote \ foe GHB vio DONT eS Paleo TEE! oa = er (per, AZATHEIOP IME, gruxint elt 1 wYoreaxY cHozoeuin lx HeLe ELI RATE Sere DSEAE RVOLVE KARSOLE IE CIEMESL 9/5/2013 Rheumatology Introduction, Anatomy, Physical Exam Reynold L. Trowers, M.D. FACEP Director, Emergency Medicine Harlem Hospital Center RLT2@columbia edu Rheumatology- science of rheumatism = Rheumatism. any variety of disorders marked by inflammation, degeneration, or metabolic derangement of the connective tissue structures of the body (especially the joints and related structures) Joint anatomy * Synarthrosis (fibrous or immovable joints) * Joined by fibrous tissue 1) suture of skull = 2) gomphoses (tooth sockets) = 3) syndesmoses ({ibiofibular attachment) Amphiarthrosis (Cartilaginous joints) * Adjacent bones bound by flexible fibrocarilage * Slightly movable * Pubic symphysis, sacroiliac * Intervertebral disc * Epiphyseal plate (growing bone) 9/5/2013 Synovial Joints (diarthrosis) * United by synovial membrane * Freely movable * Plane or gliding (tarsal, metatarsals) * Hinge (interphalangeal) * Saddle (first carpo metacarpal) * Spheroidal (ball and socket) hip, shoulder, MC-P's Synovial joints * Most common joint + Well lubricated congruent cartilaginous surfaces slide freely against each other * United by joint capsule Synovial joints 9/5/2013 Joint anatomy * Articular cartilage ~ elastic, effective cushion for bones, resilient, avascular, nourished by synovial fluid + Periosteum specialized connective tissue lines bone and has bone forming potential * Tendon connective tissue muscle to bone * Ligaments fibrous tissue connects bone to ‘bone or cartilage to cartilage Synovial membrane * Highly vascular connective tissue * Multiple folds and redundancies = Does not cover the articular cartilage * Cell secrete fluid (synovium) = Synoviurn nourishes articular cartilage Synovial fluid (synovia) * Normally clear or slightly yellow = Consistency of egg whites = Non clotting * Inflammation, infection and other pathologic processes change the Characteristics of the fluid and this analysis helps with the diagnosis, Inflammation "Is the main pathologic process that produces arthritis, + Many agents have been implicated including: bacteria, viruses, crystals, antigen/antibody complexes, chemicals ‘among others Inflammation * Normal response of any foreign invader is to protect, limit injury, and remove the invader. = Unfortunately the inflammatory reaction in ‘some circumstances can cause pain, limitation of movement, and destruction of tissue Inflammatory arthritis * Body may lose its ability to distinguish normal from foreign antigens * Attacks and destroys normal tissue * In relation to the joints this may include the articular cartilage, subchondral bone, ligaments, tendons and synovial capsule itself Inflammatory response * Antigens (foreign agents) * Early mobilization of B lymphocytes to the site = Lymphocytes contact the antigens and transform into larger round cells (plasma cells) = Plasma cells produce antibodies specific for the antigenic stimulation 9/5/2013 Immune response * These antibodies bind and immobilize the antigen * Antigen antibodies complexes attract complement from the blood "+ Complement is a specialized series of proteins which act sequentially to mediate 2 large number of inflammatory effects including bacterial killing Immune response * These antigen, antibody, complement complexes are engulfed by phagocytic cells and then destroyed by the lysosomes containing enzymes found in the cells Inflammatory arthritis * 7 Recognition problem; lymphocytes seem to lose the ability to distinguish normal tissue from foreign antigens and attacks normal tissue * 7 Are there subtle changes in the normal tissue so that the body misinterprets the tissue as a foreign invader Pannus formation * Inflammation in joints triggers cells to multiply and build up in the synovium * Pannus is pathologic thickened synovial membrane * Pannus contains several substances including numerous inflammatory cells that further destroys cartilage 9/5/2013 Inflammatory arthritis * Destruction of cartilage attracts phagocytic cells with more release of enzymes Perpetuating cycles of inflammation; destruction; more inflammation * May result in significant joint damage * As clinicians itis essential for us to recognize and contro! inflammation in our patients Inflammation (manifestations) * Heat (calor) * Redness (erythema) * Swelling (edema) * Pain (dolor) Pain * Include quality, location, exacerbating or alleviating factors (i.e. motion), onset and associated factors * Most common complaint related to the jeints that induce persons to seek medical care. Swelling (edema) * Location, onset, associated with pain or ot, aggravating or alleviating factors 9/5/2013 Range of Motion * Document limitation of motion * Loss of extension * Loss of flexion * Loss of rotation 9/5/2013 Stiffness * Restriction and or discomfort at the beginning of a movement usually after rest or inactivity Weakness * Loss of motor power or muscular strength * At times difficult to distinguish muscular strength from decrease effort related to pain * Also seen with musculoskeletal disorders Systemic features = Fever = Weight loss © Anorexia * Failure to thrive = Anemia = Multi organ involvement Physical examination of the joints * Always inspect, palpate, and determine ROM (side to side comparisons) * Check for swelling, ROM, temperature change, color, creptation, muscle testing Radiologic examination of the joints * Use a simple A, B, C approach initially "A" Alignment (of axis of conjoined bones) *°B" Bone density (normal bone generally creamy with distinct smooth uninterrupted outline °C" Cartilage (normally radiolucent black space between bones) 9/5/2013 10 THE IAAT oLeGrY Fiest ligeruRe -RPET2@Coumieiepu Re, erin Sant VARIETY of isop Rem TRertees ieee ON mR aniar OL peceniepaTitn o& cy 4 , sreucrubes oe ey * CONDNIEETNE SSL, «pe —SYNARTH ROSS AWM NABLE domes - SuTuee = GromiptpesiS —SYNiesmisiS —AmplARTHeos!S -SUGHTLY WAVABLE. Syms $ —!V psc —EpVpHYSEAL PUATES — DMRTHESS(S (eoWAL FREELY MovamLe Spe esos TELM VN NERVE ie S— CAN! ALSO ees Neil Bote D> SOMETIIES Hien OSTECPINTES —

    You might also like