7 a aoa nia Pathology For Paramedics Nias " INFLAMMATION" (vido) INFLAMMATION: Itis the reaction of living tissues to all types of injuries. ae LE Lure Ppt iM Siri nis ADVANTAGES AND DISADVANTAGES OF _INFLAMMATION: The advantages and disadvantages of inflammation are as under; ESC re tl VL Firs yg) U1 98 oF hy gee } Inflammation is a protective response against injury. <1 ALF es pleat irk } Inflammation tends to destory the invading microorganisms. -< etutizLic i firg } Inflammation tries to inactivate the toxins of microorganisms. VAIL eltnsL£e } Inflammation helps in healing and repair of issues. -<-doatLefiPinsectUr } Inflammation helps in releiving infections. emt i PS Sirk } Inflammation may be potentially harmful in some conditions e.g. Viral Encephalitis etc. ctr ml Piuite From sh2 LP Wem Pir < } Healthy tissues can be damage if healing process fails due to continuous inflammation. we SIP ein IE no MoS REL Sin FY ti & ikutinctir & TYPES OF INFLAMMATION: There are two types of inflammation i.e, wupbinbenl fir ~usl Stee e | inte A vind viLiL2 1 ACUTE INFLAMMATION. 2. CHRONIC INFLAMMATION. | debe Usmania Pathology For Paramedics By Dr. Muhammad Usman | ——~ Scanned with CamScanner* Jamania Pathology For areata ese a ‘ACUTE. INFLAMMATION: It is an immediate and early response to an injury so it is the first line of defense against any kind of injury. 2A nS A SABRE L 22S pay pan i SA cHANGES_IN_ ACUTE INFLAMMATION: There are two types of changes occur in acute ion which are discussed below; Pint sn teh Wie rL yas 251990 oF pea Mil 29S | ubeFr(A) | Ub eAk-(B) inflammati ES: The following are vascular changes in acute inflammtion; AdeS nen biente™ Weel byes ysl 9 (A) } Initially vasoconstriction occurs in small blood vessels. Ut Vigntaddde ter, € > After vasoconstriction the process of persistant vasodilatation occurs rapidly. At ae tb lIOS € } Then change in blood flow occurs which increases the blood velocity due to dilatation of (A). VASCULAR CHAN arterioles that increases vascular permeability. Fluid is lost from the blood and the blood viscosity is increased that slows down blood flow called stasis of blood. tbe Fett bd eZ L Pe ub RAS SoA AILS TIAL & pense IPURK Ie tyne Sy eiP renter This increasd vascular permeability & fluid exudation widens the intercellular junctions Which allows passage of large amount of fluid that produces tissue swelling called edema. eg i rerrl eS E LM infty EPO ME IP PIM RL LIBR & >From dilated vessels leukocytes comeout & engulf the bacteria or toxins & tissue debris. Litt te atbol tifre iL oaah Uite wel ore Paisndio « dics By Dr. Muhammad Usman Scanned with CamScanner . Far Paramet3 _ ys F hemical substances which are responsible for reaction like Histamines, Serotonins, 2 tagiandins, Bradykinins, Leucotrins & complement system comes out and activate. é - pros! a bpm f eed tool SASt oes ehesguih octet WEL UE LP EMAL YI & eraymaticaigestion of tissues & debris occurs Lb iL Pitted boi BIA & YY En » Finally restoration of injured tissue comes to its normal structure and function. tet Voy frre teh tut « 8). CELLULAR. cH 5: The following are cellular events in acute inflammtion; eee p Brute beoutcl Pinel jubas ylplen(B) of blood flow near to the vascular endothelium. SAS tebe SE odes i } ADHESION: In adhesion the inflammatory cells attach to the endothelial cells. It is due tothe presence of adhesion molecules on the surfaces of both cells. Spuitdpbath iLodtbic editor _tptaady) through the intracellular junctions. 2 Be sLusimar tudtbic lire nL tir aS le ite | “i } CHEMOTAXIS: In chemotaxis the inflammatory cells are attracted and moved to the si Serotonins, Prostaglandins, ofinjury. It is due to the chemical substances like Histamines, | : ke 6 x soothe vwillyltLeG/e pibrivgewtin tu SE, emu, sa ¢ metre aly drtled dE tae ‘ Bradykinins, Leucotrins etc. + ? PHAGOCYTosis: In phagocytosis the microorganisms and other injurious agents are —eYTOSIS: ®guied and destroyed by the inflammatory cells. PI | watt Lo iptie Mrasolsic psiust Sir PSIL eng Se 5 € — naire Rv Dr. Muhammad Usman Scanned with CamScanner_—\————— _ vewsp pewweyny “1g Ag Sojpawered 104 ABojoyeg ejuewsp, a “ewuysy le1youoigé “SI]OD aanesa9d/N, a1uosyDe “sineday [esa ‘o1uosyg? {62 sisoqy pue sisouoau anssy pasayeos s! esau} es Auouwod ‘anssy ayy jnoyBnowyy paiayeos Jayjes sewojnuesB JO WO} ay} U! JOU aJe S]jao asa “S4ND90 Base payaye ayy ul sayAooyduiA] paziisuas pue saBeydosoew ‘sjjao ewsejd jo uonrinunose ayy ody siuy ul: NOILVWAVTANI OINOHO SNOLVWOINNVEO-NON "Z| } PEMA dapxenpapn- | » AOpapa- Pepi Ppa y FOP ATL AWS OFA, RTH yf Are gi PIPE ETO Sig MM: DV rue OPAL DAAT BAT | “sisoplooueg< “SISOOIIIS = “sisowse|doysiH® “sisojnozeqny | | Bs s]j99 quer’ Burujequoo i si29 ewsejd pue sayAo0yduid] jo se\}09 & Aq pajozjoue sjjoo plojauyide yo uoneBasB6e | adoososo}W a4 S! YOIYM BWO}NUeJG [199 plojeyyide yo UOREWIO) ayy Aq pazuajoeseYD | S| UoneUWeE|U! D1U04Yd Jo adAy SIU, .| HYPERPLASIA. 2.| HYPERTROPHY. -. ATROPHY. = METAPLASIA. 1. HYPERPLASIA: The enlargement of an organ or tissue caused by an increase in the PES ts reproduction rate of its cells. sthontkL Hire BEE LEAS. CAUSES OF HYPERPLASIA: Few common causes of hyperplasia are as under; Ui bionra taper Sb A: lage y SF Uj ye (a). Hyperplasia due to tissue loss, it is also called compensatory hyperplasia. | tin duirKteed Sra SL yx PL PRG Sun Ala (b). Hyperplasia due to hormonal stimulation. we bre SL br Parlier nsiSin a Ab MECHANISM OF HYPERPLASIA: The mechanism of hyperplasia is by mitotic division ELEN L BALA ea AE Li A: OW 4d b FY ye! EXAMPLES OF HYPERPLASIA: Few common examples of hyperplasia are as under; ebotepead CLL AL: athe U5! (a). Enlargement of uterus during pregnancy. ateax€ SGrg on L (b). Enlargement of breasts during pregnancy. thank useryinL lb (c). Thyroid gland hyperplasia. abn AerSid0- (c Usmania Pathology For Paramedics By Dr. Muhammad Usman) ———————" Scanned with CamScanneroo Seer re eee reeeeereeeeee eH ysmania pathology —— 1S Jp, CHROMOSOMES: The nucleus is arranged in 45 minute strips called chromosomes. chromosomes are arranged in pairs of 23. One member of each pair brings inheritance fromthe male parent and another from female. Genes are present on chromosomes. (fone ve oP GURL So PAL, pri Tee taier Se Lit fon tec HALAL Appr hohe SPE aS ott Su SosLiie 5} bre eto Sei Bituk® spre wEuigi hii eyyriONS OF THE CELL: Cell performs following functions; puNTIONS OF T™ : iffusion, active transport etc. \ INGESTION e- DIGESTION done by lysosomes. AL Gr Ate, | ENERGY PRODUCTION done by mitochondria. me bel EEM tet < SYNTHESIS e.9- Granular ER produces proteins & smooth ER produces lipids. : ig LE Sib hei nl Sache bbs Sassen ile Lag MOVEMENT e.g. ciliary movement of ciliated epithelium and flagellum of sperm. AAS PE SI ASINL EGER LE CELLULAR ADAPTATION : It is a natural phenomenon of a body in which each cell of the body has the capacity to adjust itself to the best of its capacity to escape injury & survive inresponse to the external or internal stimuli. sete La HALE L ebay SUR LTLE £6 BIL: tata) 5 ghee NECHANISM OF CELLULAR ADAPTATION : The mechanism of cellular adaptation is as unde, se SiG ak DESI Me: gS aby oF pba! pighee ‘HPERPLASIA i.e. Increase in cell numbers. ar SLI LUE Wy pels UHPERTROPHY i.e. Increase in cell size. tI PALE EI SIS age “AROPHY i.e. Decrease in cell size. eS EAL EI ssh! ! "TAPLASIA i.e. Changes in cell type. ted eB pute by Ge Pate *down regulation of specific cellular receptors. eit e6LAES ny ew protein synthesis by target cell Scanned with CamScannerFe uewsn pewweyniy 20 8S © OEE aad aq Kew Jana} papes6 yBiy |Z yuas [quasaud aq Aew 4000} popes6 MOT 1 > quosead aq yb sisosqid Zz > quasge s| eweps re ea > quasge Aysow s! sIso4qi4 — yuaseid Ajsow s| ewapyz “quourwosd 7 ‘yeurwosd asow “| oue abeydosoew pue sjtudosnn | _7 JOYOYS S! UO!EINP 7 fis aso ade $ySejqosg!y ‘S}|29 ewseld|.. ‘sayfooydwik7 ‘sabeydouoew | | se6uo] s uoneanp $1 [eis] I] | a Re ainoy lestem ES SEE SF COA BD I TIS ZF" YL DIP Ps imojaq uani6 ase UOeWWWEYU! 9]U0IYO Pur BNE ujoamyaq seousJoyIp AY. Rroyesndsey < TAC : pyar Sanyeg JonrTé wena Z pt “sysoaaaé| | SSM SOP: AT PTIW IPD ‘ase UORPWWEYU! 9}U0IYD Jo BWODNo oy, {NOILVWWVTANI ONG? drupe” Drniannprar pap apie || J Pa —— ieee HUELL ASLAN AI yeas Nd ruqez parade hil 7# BAT SH Eee Sep dng sae : J a Sis IME A Pampatergy TEV lb LL Soipouereg 704 ABojoured eeu | Scanned with CamScanner Pa 3 go SWwooINo — =aee aa, Usmania Pathology For Paral IS. aie ‘Osis. : Wk, 5, TRAUMATIC NECR' / Wika rosis, coagulation of Protoplasm OC ¥ IS. ‘OXIC NECROSI: — = ION NECROSIS: In this kind of nec! . 4. COAGULATI ai high temperature causing sudden death of the tissues org je to - ccurs du : : gear f the blood or slow supplying to certain organs of the body, For tion of to sudden obstruct example, Kidneys, Lungs, Spleen etc. Mill pis LRLTEL PN: sey SS + op Lesa ibe Eine Mgnt OE (ERLE EN ey 83st ytigg Lem beir 7 Sa 2H Li bre t3 bes 3 Luh hove dentrer 23a ie den il pred pid « «hun. AEE Ub + -< in, Pte 2. CASEATION NECROSIS: It generally occurs in tubercular and syphilitic infections, In this condition, a cheesy meterial is seen in the ulcers formed in the body due to the effect of infection caused by tuberculosis and syphilis. LA LM Bherhtile Une Xie Minh SS ty as -< debe tutitusiine of the cells and tissues is followed by liquefaction, The dead tissues become soft and surrounded liquid material due to autolytic decomposition. It is 3. LIQUEF, ‘ACTION NECROSIS: In this type of necrosis, death by some sort of generally found in Pi proteolytic enzymes. Sha ont ke EP ancreas, central nervous system or any other tissue rich in mle OMIT 3 i, PENAL IBS GulibiC range pipi_d re£it mesentery or the tissues rich in fats, nt Hig, AACE aed wbal tyne rfp PU seid ou Scanned with CamScannerUsmania Pathology For Paramedics NECROSIS: Necrosis means the local death of tissues stil) atte! hed to the living body which aS. vs occurs suddenly, A he rely oe PSOELS ay ee tbsesyy Soa Ss CAUSES OF NECROSIS: The following are the main Causes of necrosis: BME rage, F vans 55 1, PHYSICAL AGEN Ts, ©.9. Injuries, Heat Stroke, Extreme Cold, Burns etc. ANIL bi, cids like Phosphorus, Caustic Soda and Salts of Mercury tee git eu whet 2. CHEMICAL AGENTS e.g, Strong A Carbolic Acid, Sulphuric Acid, Arsenic, ete. cabal Ek eG, FEM PENG Ke WEP wie etsy Wha 2 3. MICRO-ORGANISMS e.g. Toxins of Diphtheria, Poliomyelitis, Herpes-zoster, Typhoid etc. retaiLutir£ x spoT SubideGsit Sl jo3 the tissues die suddenly. c Sua LSI SREAL at PSehi butte MTT We of a 4 ethan ede SM bicaS Oberst 27 TPES OF NECROSIS: The following are the varieties of necrosis; TS SRUROSIS: Use BSE Epladl SF yay Ss ‘COAGULATION NECROSIS. — 2 CASEATION NECROSIS. — S-UQUEFACTION NECROSIS. =~ Scanned with CamScanneris " GANGRENE " (ay Sey yoRENE! Itis the necrosis of tissues with superadded putrefaction = (Gangrene = Necrosis + Infection + Putrefaction) ety Keen APE EA repay SSI: eS roti + thre lip Sdnanit =e A) causes OF GANGI NE: The causes of gangrene are as follows; suditvcpalg Hh sia sey Fe SE () Arterial obstruction due to Thrombosis. athe She lL ei SEW {iyAnterial obstruction due to Artherosclerosis. ath She Le be Fey TGA (ii) Arterial obstruction due to Embolus. ater She lL Ayity, AGFA) (wv) Arterial obstruction due to Diabetes. athe Sher L, “SE Liv) (Infection due to Boils. other en lA tutk Li.) Fab Pug uti) athe Pies Lo KA Ei) (vi) Infection due to Carbuncles. fecctead clint (vii) Infection due to Gas Gangrene. (vii) Infection due to Gangrene of Scrotum. tong Mel Miekbue (viii) ee ae oF (i) Trauma due to, Crush injuries or Pressure sores. pL ittntgdre pK siPilin) pesctdabadiaci 0)Physical agents e.g. Burns, Frostbite or Chemicals. -A¢,wevitbtiPet ato ee Tres oF GANGRENE: There are three types of gangrene; adie BS AT p52 SS \).DRY GANGRENE, ABA) ®.WET GANGRENE. ~gA8) (9-GAS GANGRENE, ALAC) Uemania Dathalnau Far Paramedics By Dr. Muhammad Usman Scanned with CamScannerUsmania Pathology For Paramedics OS 5. TRAUMATIC NECROSIS: As a result of injury, the tissues are damaged, so that ng —~ Reg, occurs which is partly inflammatory in character.The common site for this king OF ne, tl roy is the breast. terse Kr, ec Drp brs HE L228 sf Ee Vir Sod Sirs SSG if SoS Pure L itr ig 6. TOXIC NECROSIS: In this variety, when the toxins are of very strong nature fale 5 only cause inflammation but also necrosis of tissues for example Typhoid may caus necrosis of the peyer’s patches, Poliomyelitis can cause necrosis of the anterior horn ce and herpes-zoster can cause necrosis of the posterior root ganglion cells, Vinci Bei; oe SL, PLIES IE GBs Fr ESR es, MECHANISM OF NECROSIS: There are two ways that cause the basic morphologic, 63k L898 aS yuny changes of necrosis; 1. ENZYMATIC DEGRADATION OF CELLS: In this process the hydrolytic enzymes a, released from the lysosomes of the invading white blood cells that convert proteins; cells into liquid. WAAL tthe preter WL RLM plat OT tad SF 53 Seth Abe t0her LE Sage 2. DENATURATION OF PROTEINS: In this process the proteins of the cells denature including the enzymatic proteins thus blocking the cellular proteolysis in this way th cellular out lines are retained. Ke SPE ee MENS, ALP EK ESN 5b 9 2 8T tata S <2 Fifi AesTbyglK fee dy yee, SS ————_ Usmania Pathology For Paramedics By Dr. Muhammad Usman |§ ——————~ Scanned with CamScanner