- Information
- AI Chat
General Pathology 3
Introduction to pathology
Recommended for you
Related Studylists
Jerry 2Preview text
SHOCK
SHOCKDefinitionacute cells and reduction Shockhypotensionof isaeffective life-threatening circulatingand clinical hypoporfusionbloodsyndrome volume(hypotension);.of cardiovascuand lar collan inadequate apse ) Acute characterised Inadegual perfusionmductionby: perfectionofan cellular
Tissues (hypoperfusion). If uncompensated,
Sport
Rom
Scom
Unknown interruption adrenal of sympathetic insufficiency vasomotor in which sthe upply iii) Hypoadrenal torespondshock. normallyHypoadrenal to the shockstress occurs of trauma,from
Surgery or illness.
Pathogenesis shock involve following 3 derangements: Reduced effective circulating blood volume general, Reduced all forms supply of released ofoxygen from to shockinduced the cells and cellular tissues injury. With resultant These derangements anoxia, Inflammatoryinitiallyset in mediators and toxins compensatory mechanisms (discussedbelow) but eventually a vicious cycle of cell injury and severe cellular dysfunction lead to breakdown of organ function (Fig. 5) 1. Reduced effective circulating odvolume. It may resultby eitherofthefollowingmechanisms: i) by actual loss of blood volume as occurs in hypovolaemic shock; or il) by decreased cardiac output without actual loss of blood >
(normovolaemia)asoccurs in cardiogenicshock andseptic shock 2 tissue oxygenation <
Following reduction in the effective circulating blood volume from either of the abovetwomechanisms and from any of the etiologic agents, there is decreased venous return to the heart resulting in decreased cardiac output. This consequently causes reduced supply of oxygen to the organs and tissues and hence tissue anoxia, whichsets incellular injury. 3. Release of inflammatory mediators to
cellular injury, innate immunity of the body gets activated as a body defense mechanism and release inflammatory mediatorsbuteventuallytheseagentsthemselves becomethecause ofcellinjury Endotoxins inbacterial wall in septic shock stimulate massive release of pro-inflammatory mediators (cytokinesis a similar process of release of these agents takes place in late stages of shock from other causes. Several pro-inflammatory inflammatory mediators are released from monocytes-macrophages, other leucocytes and other body cells, the most important being the tumour necrosisfactor- (TNF)-a and interleukin-1 (IL-
- cytokines > Massive hemorrhage ,hours, massive burns, dany hes,
WATHOGENESIS OF HYPOVOLAEMIC SHOCK Hypovolaemic shock occurs from inadequate circulating blood volume due to various causes. The majoreffects of hypovolaemicshockare duetodecreased cardiac output and low intracardiac pressure The severity of clinical features depends upon degree of blood volume lost, haemorrhagic shock is divided into 4 types:< 1000 ml: Compensated 1000-1500 ml: Mild 1500-2000 ml: Moderate >2000 ml: Severe Accordingly, clinical features are increased heart rate (tachycardia), low blood pressure (hypotension), low urinary output [oliguria to anuria) and alteration in mental state (agitated to confused to lethargic). Injonction. Mayocandite, Venhicaler mmphone
1Myocardial
PATHOGENESIS OF CARDIOGENIC SHOCK Cardiogenic shock resultsfrom asevereleft ventricular be dysfunction from various causes. The resultant decreased cardiac output has its effects in the form of decreased tissue perfusion and movement of fluid from pulmonary vascularbedinto pulmonary interstitialspace initially (interstitial pulmonary oedema) and later into alveolar spaces(alveolar pulmonary oedema).
PATHOGENESIS OF SEPTICISHOCK Septic shock results most often from Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Grampositive bacteria. Inseptic shock, there is immune system activation andseveresystemic inflammatory response to infection as follows:
Neurogurie shack Anestlate accident on afinal land anjiny
- Activation of macrophage-monocytes. Lysis to
lipopolysaccharide, LPS-LBP into binds circulation to CD14 where it important binds of the Gramnegative surfacelipopolysaccharide-binding ofthebacteriamonocyte/macrophages and releases IL-1. protein endotoxin, The effects(LBP). which aofThetheseare
various in shock shock temperature cascades have are pale (clotting, face, to Feeble hypoxic sunken and complement,cell irregulareyes,injury
pulse due
kinin). These include the following": 1 respiratory distress syndrome(ARDS) 2. Disseminated intravascular coagulation (DIC) 3. Acute renal failure (ARF) 4. Multiple organ dysfunction syndrome (MODS) With progression of the condition, the patient may develop stupor, coma and death.
THROMBOSIS
Thrombosis is the process of formation of solid mass incirculation fromthe constituents offlowing blood; the mass itself is called a thrombus. In contrast, a blood clot is the mass of coagulated blood formed in vitro e.g atest tube
Haematoma is the extravascular accumulation of blood clot e. into the tissues. Haemostatic plugs are the blood words,clots haemostaticformed in healthyplug at the individuals cut end atof the ablood site of vessel bleedingmay bee. considered in injury to the the simplest blood vessel. form Inof
other
following developing thrombosis. harmful in Haemostatic the effects: unruptured plugs 1. Ischaemic cardiovascular areuseful injury. asthey system Thrombi stop may the maybe escape decrease life- threatening of blood or stop and by the causing plasma, blood supply one whereas of to thethrombipart of
Vinchow's riad (1)Injury to endo thelium
(1) Statis onherbulent blood flow
(1 ) Hyper
thrombogenic influence of subendothelium. ii) It elaborates a few anti-thrombotic factors (thrombosis inhibitory factors) e. a) Heparin-like substance which accelerates the action of antithrombin III and inactivates some other clotting factors. b) Thrombomodulin which converts thrombin into activator of protein C, an anticoagulant. c) Inhibitors of platelet aggregation such as ADPase, PG12 or prostacyclin. d)
Tissue plasminogen activator which accelerates the fibrinolytic activity. ili) It can release a few prothrombotic factors which have procoagulant properties (thrombosis favouring factors) e.
2. ROLE OF PLATELETS
i) Platelet adhesion. The platelets in circulation recognise the site of endothelial injury and adhere to exposed subendothelial collagen (primary aggregation); von Willebrand's factor is required for such adhesion between platelets and collagen.
calcium, antiheparin] granules granules 15) Platelet 5-HT containing are release releasedand(serotonin), cationic reaction fibrinogenobronectin, totheproteins The exterior b) and Dense Twoepinephrine plateletderived bodies types thencontainingof platelet undergo growth ADP granulesreleasefactor, (adenosine reaction areplateletreleased: diphosphate),byfactor which a) 4 Alpha(anthe ionicplatelet
3 ROLEsolid OF mass COAGULATIONof fibrin. The SYSTEM Coagulation mechanism is the conversion of the plasma fibrinogen
with factor Va and platelet factor 3, inthe presence ofcalcium ions. factor X which forms a complex
4, ALTERATION there OF is axialBLOOD flowFLOW. Turbulence means unequal flow while stasis means slowing. i) leucocytes and redcells. The of platelets blood in are whichpresent the most intherapidly-movingslow-moving laminar central stream streamadjacent consists to ofthe
central flow endothelialof stream blood layeris while disturbed.(Fig. the 5.21).peripheral WhenH) Turbulencestream slowsdown,consists and stasisof most occur slow-moving in thrombosis cell-free in which plasma the normal close toaxial
arteries causes: to and passage Trauma branches of to fatty1bones In majoris Pathogenesis Locally arteries and branches 3. Attachment to vessel wall Firmly adherent Loosely attached or Iving free 4. Gross appearance Head pale, tail red No distinction in head and tail;smooth surfacedrydullsurface5. Microscopy Platelets and fibrin in layers, Mixed withblood clot,Linesof Zahn seenlinesof Zahn raremarrowin circulation, concussions of bones, after orthopaedic surgical procedures etc. Trauma to soft tissue e g. laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue. ii) Nontraumatic causes: Extensiveburns DiabetesmellitusFattyliver Pancreatitis Sickle cellanaemia
Decompression sickness Inflammation of bones and soft tissues Extrinsic fat or oils introduced into the body.
PATHOGENESIS. The following mechanisms are proposed to explain the pathogenesis of fat embolism These may be acting singly or in combination, i) Mechanical theory. Mobilisation of fluid fat may occur followingtrauma totheboneorsofttissues fromthe injured area may enter venous circulation and finally most of the fat is arrested in the small vessels in the lungs. Some of the fat globules may further pass through into the systemic circulation to lodge in other organs: ") Emulsion instability theory. This theory explains the pathogenesis of fat embolism in non-traumatic cases. According to this theory, fat emboli are formed by aggregationof plasma lipids(chylomicrons and fatty acids) due to disturbance in natural emulsification of fat. iii) Intravascular coagulation theory, In stress, release of some factor activates disseminated intravascular coagulation (DIC) and aggregation of fat
emboli; iv) Toxic injurytheory to this theory, the smallbloodvessels of lungs are chemically
injured by high plasma levels of free fatty acid, resulting in increased vascular permeability and consequent pulmonary oedema.
blood GasEmbolism vesselscausing Air, nitrogen damage and toother tissue. gases Two can main produce forms bubbles of gas embolism-air within the circulation embolism and andobstruct the decompression sickness are described below.
AirEmbolismAir embolism occurs when air is introduced into venous or arterial circulation.
VENOUS AIR EMBOLISM. Air may be sucked into systemic veins under the following circumstances: i) Operations on head and neck, and trauma. The accidental opening of a major vein of the neck like jugular, or neck wounds involving themajorneckveins,mayallowairto be drawnintovenous circulation. #1) Obstetrical operations and trauma. During childbirth by normal vaginal delivery, caesarean section, abortions and other procedures, fatal air embolism may result from the entrance of airintotheopened-
uputerine venous sinusesandendometrialveins) Intravenousinfusionof blood and fluid. Air embolism may occur during intravenous blood or fluid infusions if only positive pressure is employed. iv) Angiography. During angiographic procedures, air may be entrapped into a large vein causing air embolism. The effects of venous air embolism depend uponthe following factors: i) Amount of air introduced into the circulation. The volume of air necessary to cause death is variable but usually 100150 ml of airentry is considered fatal. # Rapidity of entry of a smaller volume of air is important determinant of a fatal outcome iii) Position of the patient duringorsoon after entry ofairisanother factor, The air bubbles may ascend into the superior vena cava if the position of head is higher than the trunk (e in upright position) and reach the brain) General condition of the patient e. in severely ill patients, as little as 40 ml of air may have serious results The mechanism of death is by entrapment of airemboliin thepulmonaryarterialtrunkinthe rightheart airintheformoffrothpass further out into pulmonary arterioles, they cause widespread vascular occlusions. If death from
pulmonary air embolism is suspected, the heart and pulmonary artery should be opened in situ under waterso thatescaping froth orfoam formedbymixtureofairandbloodcan bedetected.
or cerebral arterialairembolismmay cause sudden death by much smaller amounts of air than in the venous air embolismn.
PredisposingFactors A number of primary (genetic) and secondary (acquired) factors favour thrombosis Primary (Genetic) factors: i) Deficiency of antithrombin ii) Deficiency of protein C or 5 iii) Defects fibrinolysis iv) Mutation in factor VSecondary (acquired)factors: a) Risk factors: i) Advanced age ii) Prolonged bed-rest iii) Immobilisation iv) Cigarette smoking b) Clinical conditions predisposing to thrombosis: i) Heart diseases (e. myocardial infarction, CHF, rheumatic mitral stenosis, cardiomyopathy) il) Vascular diseases (e. atherosclerosis, aneurysms of the aorta and other vessels, varicosities of leg veins) iii) Hypercoagulable conditions (e. polycythaemia, dehydration, nephrotic syndrome ,disseminated cancers) iv) Shock v) Tissue damage e g. Trauma, fractures, burns, surgery vi) Late pregnancy and puerperium vii) Certain drugs (e. anaesthetic agents, oral contraceptives).
ClinicalEffects These depend upon the site of thrombi, rapidity of formation, and nature of thrombi. 1. Cardiac thrombi. Large thrombi in the heart maycause sudden death bymechanical obstruction of blood flow or through thromboembolism to vital organs. 2. Arterial thrombi. These cause ischaemic necrosis of the deprived part (infarct) which may lead to gangrene. Sudden death may occur following thrombosis of coronary artery. 3. Venous thrombi (Phlebothrombosis). These may cause following effects: i) Thromboembolism ii) Oedema of area drained iii) Poor wound healing iv) Skin ulcer v) Painful thrombosed veins(thrombophlebitis) vi) Painful white leg(phlegmasia albadolens) due toileofemoral venous thrombosis in postpartum cases vii) Thrombophlebitis migrans in cancer. 4. Capillary thrombi. Microthrombi in microcirculation may give rise to disseminated intravascular coagulation (DIC).
Thromboembolism A detached thrombus or part of thrombus constitutes
Embolism. These may arise in the arterial or venous circulation (Fig. 5): the Arterialmost (systemic)common type of
Thromboembolism, aortic heart (80-85%):valves, prosthetic TheseArterial are heart muralemboli valves thrombimay and becardiomyopathy. Inderived the leftfrom atriumthe or B. Following Causes left aneurysms, ventricle,within sources: vegetations pulmonarythe A. Arteries: Causes veins on These within the andmitral includetheor
Emboli developing in relation to atherosclerotic plaques, aortic paradoxical upon arterial siteemboli from the systemnic venous of collateralcirculation. Circulation. Theeffects If the ofvascular arterial emboli occlusiondepend
Their size, of lodgement, and adequacy occurs, the following ill-effects may result: i] Infarction of the organ or its affected part e. ischaemic necrosis in the lower limbs (70-75%), spleen, kidneys, brain, intestine. Ii) Gangrene following infarction in the lower limbs if the collateral circulation is inadequate. In) Arteritis and mycotic aneurysm formation from bacterialresultendocarditis. From coronary iv) Myocardial embolism infarction may occur followingcerebral coronary artery. Venousv) Sudden
Death may or embolism in the middle
Thromboembolism, Venous emboli may arise from the following sources: i) Thrombi in the veins of the lower legs are the most common cause of venous emboli. It) Thrombi in the pelvic veins iii) Thrombi in the veins ofthe upperlimbs. Iv) Thrombosis in cavernous sinus of the brain. V) Thrombi inthe right side of heart. The most significant effect of venous embolism is obstruction of pulmonary arterial circulation leading to pulmonary embolism. > PULMONARYTHROMBOEMBOLISM <
Pulmonary Thromboembolism
DEFINITION. Pulmonary embolism is the most common and fatal form of venous thromboembolism in which there is occlusion of pulmonaryarterial tree by thromboemboli. Pulmonary thrombosis as such is uncommon thrombosis and may occur from in pulmonary pulmonary thromboembolism atherosclerosis and is pulmonary tabulated in hypertension. Table S. ETIOLOGYDifferentiation of pulmonary
Pulmonary emboli are more common in hospitalised or bed-ridden patients, though they can occur in ambulatory patients as well. The causes are as follows: i) Thrombi originating from large veins of lower legs (such as popliteal, femoral and iliac) are the cause in 95%of pulmonary emboli ii) Less common sources include periovarian, thrombi in uterine varicositiesand broad of superficialligamentveins veinsof the legs, and pelvic veins such as periprostatic,
General Pathology 3
Course: Introduction to pathology
University: Rajiv Gandhi University of Health Sciences
- Discover more from:
