病生章节之各种疾病整理

1、病生各种疾病整理 ?sodium and water imbala nee 1. Hyp ertonic dehydration conception : The dehydration in which the water loss is in excess of salt loss and the ECF of the body is hypertonic is termed of hypertonic dehydratio n etiology : 1. In sufficie nt water in take :( Un able to obta in water ;)Deficie

2、nt Thirst Reflex ;)Difficulty in swallowi ng 2. Excessive water loss (pure water or hypotonic fluid): (1) the skin(burns, excessive persp irati on) )the lungs (hyp erve ntilati on of any cause) ( the In testi ne (GI hemorrhages, diarrhea, vomiti ng) (4) the kid neys (Diabetes insipi dus, osmotic diu

3、resis ) cli ni cal mani festati ons Degree Volume of water loss (% of body weight) Cli nical mani festati on Mild Moderate Sever 2-5 5-10 10-15 Thirst, Oliguria Severe thirst,dry ness of mucosa,fever Delirium, stupor, coma 2. H ypo tonic dehydration conception : The dehydration in which the salt los

4、s is in excess of water loss and the ECF of the body is hypotonic is termed of hypotonic dehydrati on. etiology : ( Excessive amount of sodium can be lost in gastr oin testi nal secreti ons. (Vomiti ng, diarrhea or gastric sucti on) Sodium deficit may result from excessive sweat ing. Sodium deficit

5、may result from excessive water loss from kid ney (proIon ged diuretic thera py, adre nal deficie ncy or low aldostero ne or renal tubular acidosis) cli nical mani festatio ns Degree Volume of sodium loss (per kg of body weight) Cli nical mani festa Mild Moderate Sever 0.5g/Kg 0.5-0.7g/Kg 0.75-1.25g

6、/Kg Fatigue, dizz in ess, p ale Loss of skin turgor, cramps, ap athy, hypotension Oliguria, shock, stupor 3.lsotonic dehydration concep ti on :The dehydrati on in which the con tract ion of ECF was in duced by proportion ate loss in both sodium and water and the ECF of the body has the no rmal osmol

7、ality is termed of isot onic dehydrati on. etiology: 1. Excessive water loss (Isot onic fluid) 2. I mproper or incompi ete treatme nts to hypotonic or hypertonic dehydrati on ?Disorders of Potassium Metabolism 1. Hyp okalemia concep ti on: Serum K+ 5.5mmol/L, a medical emerge ncy etiology and p atho

8、ge nesis ? In adequate excreti on of K Renal failure, hypo aldoster oni sm, K sparing diuretics ? Redistribution of K in the body tissue injury, hypo xia, acidosis, in suli n deficie ncy, familial hyp erkalemic p eriodic p aralysis ? In creased in take of K rapid IV K Admi nistratio n Clin ical mani

9、 festati ons I .Effects on neuromuscular excitability n .Effects on the heart .Effects on excitability 2 Effects on autorhythmicity 3. Effects on con ductivity 4. Effects on con tractility 川.Effects on acid-base balanee ?Acid -Base Bala nee and Disturba nee I. Metabolic acidosis concep ti on: is def

10、i ned as p rimary decrease in p lasma HCO3- concen trati on Excessive in take of fixed acids, salicylate drug Excessive p roducti on of fixed acids, e.g., hypo xia Decreased acid excreti on, e.g., renal dysfu nction Excessive loss of bicarb on ate, e.g., diarrhea etiology : a) b) c) d) Divided by AG

11、: ? High AG type a) b) c) Fixed acid- IhCQ- Increased p roduction of organic acids. Acid intake -salicylate etc. Retention of sulfates, p hos phates etc. ? Normal AG type hyperchloremic a) HCl, NHtCI in take b) J/HCC3 reabsor pti on or rege nerati on in renal tubules: Renal tubular acidosis ( RTA )

12、; Renal failure ; Carbonic an hydrase in hibitor c) HCC3 losses in alime ntary tract: Diarrhea d) Hyperkalemia : Paradoxical alkaluria Compensation : 1) Extracellular bufferi ng - immediately 2) Resp iratory compen sati on-rapi dly 3) In tracellular bufferi ng- in 2-4 h 4) Renal compensation- Start

13、to work in several hours, more efficient than respiratory compen sati on Alterati on of metabolism and fun cti on 1) Cardiovascular system a) pH7.2 myocardial contractility b) pH 7.0 t J cardiac out put c) Cardiac arrhythmia d) Vasodilati on 2) Central nervous system : Depression. Coma ( pH 7.55) is

14、 dan gerous. 4. Respi ratory alkalosis concep ti on: Caused p rimarily by PaCO2 decrease etiology: alveolar hyperven tilati on Compen sati on (1) Bufferi ngsystems: week. Renal compen sati on Alteratio n of metabolism and fun cti on a) CNS: hypocapnia, vasoc on stricti on. con fusi on, seizure, coma

15、, etc b) Hypo xia C)cra mping d) Hyp okalemia - p aresis, arrhythmia ? Hy poxia concep ti on :tissue cells can ctbta in eno ugh oxyge n or can fully utilize oxyge n ,which cause alterati ons or cha nges in metabolism, fun cti on and structure 1. H ypo tonic hypo xia Characterization: PaO2 J Mecha ni

16、sm: O2 up take J 1) PO2 in inspired air J 2) Pulmonary dysfu ncti on Hypoven tilation Ven tilati on-P erfusi on Imbala nee Imp aired diffusi on blood-gas membra ne 3) Shu nt 2. Hemic hypo xia J affinityJ Characterizati on: HB amount Mechanism: 1) Anemia RBC/HB J 2) CO 3) Methemoglob in emia 3. Circu

17、latory hypo xia Characterizatio n: blood flow CO J ; regi onal arterial ste no sis Mechanism: A . Ischemia: whole heart failure B . con gesti on 4. Histogenous hypo xia Characterization: 02 utilization J Mechanism: histotoxic cyanide; cell or mitochondrial injury; vitamin deficiency Hypotonic Hemk C

18、trculalor/ HKlogenou PaO； SaO； I /N 1 /N CaOj CaOmax i/N - C咖 Functional and metabolic alterati ons 1. Resp iratory system ? 4000m high f Respiratory rate and depth t ? Hyperventilation ? Severe hypoxia: f pulmonary edema; f inhibition of respiratory center 2. Circulatory system ? Cardiac out put t

19、? Redistributi on of blood flow ? Pulmonary Vasoc on strict ion (HPV) 3. Hematological system Severe Hypoxia f Cellular damage(cellular swelling; J synthetic metabolism;mitochondria da mage; t ROS ;lysosome damage) ? Pulmonary hypertension -right ven tricle ? Myocardiac systolic and diast olic dysfu

20、 nction ? Cardiac arrhythmia ? J Venous return ? Ischemia-re pefusion injury Conception : Aggravated ischemic injury during reperfusion Causes of rep erfusi on : Recover from cardiac arrest ; Orga n transplan tati on ; Lys ing thrombi Mecha ni sms Oxidative Injury 1. Membra ne Lipid Peroxidati on (1

21、) . Destructio n of membra ne structure; (2) .ln direct in hibiti on of membra ne p rote in (3) . Facilitate the p roduct ion of free radical and other bioactive substa nces 2. P rote in den aturalizati on and in activati on of en zymes 3. DNA disr up ti on and chromosome aberrati on Calcium overloa

22、d 1 Disorder of Na+-Ca2+excha nge (1) Higher Na+i activate Na+-Ca2+exchanger directly (2) Higher H+i activate Na+-Ca2+exchanger indirectly 2. Defects in membrane p ermeability (1) .Cell membrane injury (2) .Mitochondria and sarc opl asmic reticulum injury Neutr op hil activati on and Others Na+i t;G

23、ene activation ;Neutrophil activation Structural and Fun cti onal Chan ges Heart: Rep erfusi on arrhythmia ; Myocardial stunning Brain :edema ; cell death ? Coagulati on-An ticoagulati on Bala nee And Imbala nee Disseminated/diffused intravascular coagulation(DIC) conception : A disorder of widespre

24、ad micro-vascular thrombosis caused by activation of coagulati on cascade with: Bleedi ng. Shock, Orga n dysfu nction. Hemolytic an emia Pathoge nesis The tissue factor release t systemic activation of coagulation Endothelial lesion t imbalanee of coagulation and anticoagulation Blood cells damage E

25、ntrance of p rocoagula nt substa nces into blood In flue ncing Factors Mononu clear p hagocyte system dysfu nction Hep atic dysfu nction Hyp ercoagulable status Microcirculati on dysfu ncti on Metabolic and fun cti onal cha nges Bleedi ng Organ dysfu nction Shock Microa ngiop athic hemolytic an emia

26、 ? SHOCK Defin iti on: an acute, systemic and severe reduct ion of tissue p erfusi on characterized by in adequate blood flow and oxyge n delivery to the tissue of the body result ing in metabolic and functional disturba nces Mani festati ons: Hypotension; Hypop erfusi on Dulled sen sorium; Rapid an

27、d weak pu Ise; Cold and clammy skin; Oliguria Pathoge nesis: Bleedi ng nJ Effectively circulatory blood volume n Symp athetic-adre nal system activati on n Extensive constriction n Hypoperfusion Hemorrhagic shock Pathogenesis: Ischemic Anoxia Phaser Stagnant Anoxia Phaser Organ Dysfunctional Stage I

28、schemic Ano xia Phase 1. Co mpen satory Mecha ni sms:Sy mp athetic-adre nal system activatio n 1) Autotra nsfusi on 2) Aut op erfusi on 3) Redistributi on 2. Cli nical Ma nifestatio ns J Pulse Pressure=JJ Systolic Pressure - t Diastolic Pressure J Urine out put; Cold and moist skin Stag nant Ano xia

29、 P hase Clinical Manifestations : Oliguria;anuria; coma Organ Dysfu nctio nal Stage Clinical Manifestations : DIC; MODS 探 Hyp ody namic shock (Cold Shock): Characterized by an in adequate or falli ng cardiac out put, vasoc on strict ion (in creased SVR) 探 Hyperdyn amic shock (Warm shock): Characteri

30、zed by a no rmal to high cardiac out put and systemic vasodilati on (decreased SVR). Functional and Metabolic Chan ges Cell metabolism : Lactic acidosis Intracellular: K+ J Na+ tCaTt cellular edema Cell injury : Apoptosis ; Necrosis Orga n dysfu nction ?Res pi ratory Failure Definition : External re

31、spiratory dysfunction results in PaO2 decreased Etiology and p athoge nesis: I . Ventilatory disorder 1. Restrictive restricted inspi rati on (1) Neuromuscular paralysis(2) Complianee of thorax J (3) Lung complianee 丸4) Pleural effusion, pneumothorax 2. Obstructive (1) Airway resista needys pn ea; F

32、orced exp irati onSmall airway closed n . Diffusion disorder 1 Reduced alveolar membra ne Lung consolidation (肺实变,atelectasis (肺不张)，pulmonary lobectomy (肺切除) 2 Alveolar membra ne thicke n Pulmonary Edema, hyali ne membra ne formatio n, pulmonary fibrosis 川.Ventilation-perfusion imbalanee 1. Local hy

33、poventilationFunctional shunt 2. Local hypop erfusi onDead-s pace like ven tilati on Functional shu nt Abnormal I VVQ PmCO, 1 Tt :V CrtCOj TT 丄 N HjiOj JI TT I aOj it 1 1 IV . An atomic shunt Alterati ons of metabolism and fun ctio n PaQ 60mmHg Compen sati on 50mmHg Compen sati on 80mmHg Deco mpen s

34、ati on NormflU Total Dead-s pace like ven tilatio n Abnomrial Normal Total lung 0.8 VPK =0川 Paq u L CaO； I- u * -O S OJS . Increased affinity of SR and Block L-type Ca* channel Sensitivity of p -AR to ME/ Hyperkalemiainflux H* bi nd to Troponin Metabolic disorder 厂工+ SR Ca*handling dysfunction Ca*in

35、flux| Tni binding to Ca* dysfunction Mitochondria dysfunction Energy metabolic dysfunction Pulmonary heart disease; Pulmonary encep hal op athy( Hypo xia;Acidosis ) ? Cardiac in sufficie ncyHeart failure Defin iti on : Heart failure is the in ability of the heart to supply adequate blood flow and ge

36、n erate a cardiac out put sufficie nt to meet the metabolic dema nds of the body . Etiology :P rimary myocardial dysfu ncti on; Ven tricular overload Pathoge nesis I Reduced con tractility 1. Damaged cardiomyocyte : (1) Necrosis; (2)A pop tosis 2. Metabolic dysfu ncti on of myocardium (1) Disorders

37、in liberatio n of en erge (2) Disorders in store of en ergy (3) Disorders in utilizati on of en ergy 3. Dysfu nction of excitati on-con tracti on coup li ng (1) Dysfu nction of Calcium in flux Recep tor op erated calcium cha nnel dysfu nction Reduced calcium cha nnel p rote in level (2) Dysfunction

38、of Calcium handling by SR SR Ca2+ up take SR storage; SR release dysfu nction (3) Dysfunction of Ca2+ binding to troponin H+ comp ete with Ca2+ binding to troponin Reduced sen sitivity of immature TnC to Ca2+ 探H+ fT myocardium contractility J .Myocardium damageStructural damage nDiastolic dysfu ncti

39、on 1 Slower Ca2+ restoration （复位） 2 myos in-actin comp lexes dissociati on dysfu nctionATPJ 3 Diastole potential energy （势能）Ventricular systole J 4 Ventricular complianee （顺应性）J 川 Myocardial remodeli ng 1. overload of myocardium 2. decompensation （失代偿） IV Development from sin gle ven tricle to both

40、1. Afterload t T Diastole dysfunction 2. Heart chambers enl arged 3. Hypoxia, Acidosis V Asynergia （不协调）of ventricular contraction and relaxation Develo pment of HF 1. Compen satory mecha nism Cardiac compen sati on In creased heart rate In creased p reload Myocardial hypertrophy Extra cardiac compe

41、n sati on In creased blood volume Redistributi on Erythrocytosis （红细胞增多） Oxygen utility t 2. Deco mpen sati on The enl argeme nt of myocardiumnot followed by in creased con tractility Alterati ons of metabolism and fun ctio n In adequate CO; Venous con gesti on ?He patic In sufficie ncy He patic Enc

42、e phalo pathy 肝性脑病 concep ti on : A comp lex, poten tially reversible disturba nee in cen tral n ervous system that occurs as a con seque nee of severe liver diseases etiology: En doge nousHE -25% Fulminant hep atic failure ExogenousHE -75% Portal-systemic encephalopathy ; PIasma level of ammonia p

43、athoge nesis : 1）Am monia in toxicatio n, 探 Overproduction In testi nal mucosa con gesti on, edema, bacterial activity in creased Digesti on function reduced, lots of p rote in stay in the in test inal tract Hep atore nal dysfu nction, decreased urine excreti on Kidney p roduces ammonia 探 Cleara nee

44、 imp airme nts Disrup ted urea cycle ATP deficie ncy, En zyme in activati on. Substrate deficie ncy Portal-systemic shunt, intestinal ammonia doesngo to the t ornithine cycle 2) False n eurotra nsmitters, 3) am ino acid imbala nee, 4) GABA hyp othesis cii ni cal mani festati ons : 1)Slee ping disord

45、er,A pathy,Childish ness 2) Con fusi on 3) Drows in ess 4) Coma 十一 .Renal Failure V Acute Renal Failure concep ti on: A p athological p rocess that the kid neys lose the function abrup tly and thus leads to disturba nee of internal homeostasis. Pathoge nesis 1. Alterati on in renal hemody namics KfuhI pvrrusloQ i RualusirJrtlaji Rrua chemif-iTfperfniou injury KruftI lirtyvrli即塞yiikHlity 2. Glomeruli injury Inft百 Ikuuiiifee jviirtiuu (-g十Ab* ralripped Ju Ilf gloiuctnil) 5f sanpifll pinohlrrntiaD BlOifk T.hf gliillKTHlI I Attjt 1 pviDsIly (Kf=LPAA) gikI 3. Tubular lesi ons (1) Tub