SiMPTOW Spontirousppain (Stootng) NEURONAL PROCESSES, MECHANISMS Peripheral nociceptor hyperoxotabilty Ectopic impulse gine, ‘Seclatorsin deal rot ganglion Ifamnation within nerves Gyrokino release Het cou Mechanica stinut Hisamne Contraldoroa! horn hryperexctilty Contra sorsitzation Saspral eve! Gngoirg Cine neces Ineveaced syaote trarsmssicn Aroiication of Ciberinpa Gaingot A-fber nput (mechanical dynamic Fyperagesay Gatngotas-tber npit (rectnica parcute hryperagesad Ietrapnal histor iter suronsh (larctaral degeneration) Gasaeaic opoidege Changes insupraspin! ‘dsscering macaaticn Inniptery conto! (feradienaine, 5-7) ¢ Faction contro! TARGETS Sexier channels otokines TTRPUI weentor ‘TRPMBrecepter ASIC receptor? receptor Histamine Ht receptor rosy: fon chanel (0-6) Postsyraptc: NMDA reoeptoss INR? recaptors Soaum chanel trocetar cascades OABAy receptos frscoptort 1 meoptors HT receptors (OPTIMAL CONPOUNDS: Selective sodtar-chamel doser Oytekine antagonists Cyooonygenase Docker TRPV receptor antagonists TRPME receptor amgoriss ASIC rocopior antagonists sc recoptor antegon: Hi-receptoraniageists etachatea Booker, 2. hands NMDA eceptor antagonists Niktreceptor ataporists Soucthe sedum-chamel Boer MAPK mecator GABA agonists serezeptoragonate 2-mcanter agonists Na/sHtreupane door AVAILABLE, ‘ComPouNos Lidocaine. cabanazepia ‘nearer Tanotiging, TOA TWE-santagerists Nsaos? ‘Capsaicin cram Monitor? Prentataning| ‘synpathat Block, Ten TA pies Gabapentin, regabaln| ketamine Carpanaieoine? enidne ‘CA, verafaine, slonetineTable - Underlying causes of acute dyspnea and diagnostic findings Gus Signs endaymptons Radiologicimaping ECO findings Other diagnonic dues Proumohorox Sudden rst of Chest rediogroph: ——_Usvely normal —— ea, chet pain, agnosic font shi eerebeeliac tle yertinone percussion, absence pied monary Sudden onset of dyepnea; Chest rodcgroph: May bo rormol May hove fever nbolsm undafyngrisk face” maybe noma’or orimay shaw —_-hattopys, este ad es rt ee txcmiraionnayshow — Geatnomelties ” cbnomltiey, _thvomooss pal to abronatts, indecngial’ — CTscanning othe Hguorenaispresure Spiral chest CT Prwaves chester pulmonary yee eel ea accented rulmoric spacfe wih good abnornaltion—_disgrosie fecond hearfsound—_Sensiviy Flmonary _Angine, gallon rhythm Chest rodcprooh: —_Alnomay Palmenary capil tien” “sinavacep rtyfnTalnonary deme, Show evens’ weds presse” fies Giaged toca: Sfieharal’ eras eau) sihovote pric perroph ender ache changes monary Precipiatng fac, Chest radiograph: Usually normal PUmenary capil fiona” ersosng ypox) ———_pumonery Seema, y wedge posure.” feat] eelonid Breed Sihowete a Odor ifedion” dyspnea maybe infos, cronges idenicaion of only synpiom in tray besten pohhogeic organism fmmunecompromsed _nmunoconpromied a mee ‘shma/——__ Hsory of awa, Usualy normal Usval normal Spiromety reals cet i. bee - Y 4 greeters eae aye Brorchits “PEO Dice Nl eee pulronay cal owe normal or Bll tes ove westctne foros Soh long boses faexonodular changes Sec Gators Chast CT san: biatral sna corey reiconodular changes ete ete ea te el Seeteteoe) podne ormyemiedl svaed daphrogm alecrophvidloie surgery Chest huorescepy: required for diagnosis ee Feychogenic_Repeand epiodes, __Nomal Normal Diagnosis of exon syed peychdlogeal sess; be accompanied By wheezing_— Myocardial infarction Myocardial dysfunction Systolic Diastolic giteonenkincy aoeies af J + Cardiac output “LVEDP aes 4 Stroke volume Pulmonary congestion { ‘ two! ¥Systemic Hypotension * Peroxynitrite perfusion | every perfusion pressure va Ischemia Vasodilation Compensatory " +SVR vasoconstriction wera dysfunction DeathWhat happens in hypovolemic shock In mic shock, voscular volume loss causes ex- ‘neme tissue hypoperfusion. h fowl had bes ot fiom hemonhoge or hid melee ‘shifting. External ‘oss can result from se- compensatory mechanisms in ‘on attempt fo increase vascular ‘volume. If compensation is un- decompensation and death may ocat Internal or exteinal fid loss Decreosed intravascular fluid volume Diminished venous return Reduced prolod (illiag pressure) Decrecsed stroke volumeInsulin deficiency cS glucagon excess A Blood ketones | A Blood glucose x Vomiting Cellular dysfunction Osmotic diuresis Fluid and electrolyte depletion oedema Sc Cerebral |PN Teles (Ufo) Cy Corre) Cardiac aero) re pa} BT ETS) |) function Overt cardiac failure Congestioneontractity Cardiogenic High were Shock Sympathetcovar activity leads to inorder to neniretaniry B®Tissues Affected by Autoimmunity Multiple Sclerosis Hachmeto's itis Graves Disease Bones_ — -“ Rheumatoid Arthritis Leukemia, * Ankylosing Spondylitis ‘Lupus Polymyaigia Rheumatica ieecinani Dysglyeemia we eg, er ™ — \ Lee Muscular Dystrophy Gi Tract - ce \ron's Disease ae: = Siew coms *s = Nerves Lungs Perphest Neuropathy Asha kczena. Diabetic Neuropathy weoeeer's sclaisclertic Granuiomarosis vitiligo