shock & types ,pathogenesis of shock.pptx

shock is a condition where tissue in the body didnt receive enough oxygen and nutrients to allow cell to function.here the document discusses about type and pathogenesis of shock

1. shock DR. ARCHANA NIKAM DEPT. OF PATHOLOGY AND MICROBIOLOGY

2. SHOCK- DEFINATION Clinical syndrome that result from poor tissue perfusion In this condition tissue in the body do not receive enough oxygen & nutrients to allow cell to function. This ultimately leads to cellular death may progress to organ failure finally to hole body failure ( death)

3. classification 1. hypovaemic shock 2. cardiogenic shock 3.septic ( toxaemic ) nshock 4. other type- a.traumatic hock B.neurogenic shock C. hypoadrenal shock

4. Hypovolaemic shock Result from inadequate circulatory blood volume by various etiologic factors that may my be either from theclo of whole blood ( red cell and plasma ) from haemorrhage or the loss of plasma volume alone ETIOLOGY- Acute haemorrhage Dehydration from excess vomiting or dirrhoea Burn Excessive use of diuretics Acute pancreatitis

5. pathogeneis Inadequate circulating blod volume Decrteased cardiac output , low intracardiac pressure inadequate oxygen, nutritional supply to all tissue/ organ Shock

6. types 1.≤ 1000ml : compensated 2.1000- 1500ml : mild 3. 1500- 2000ml: moderate 4.> 2000ml : severe c/c Tachycardia Hypotension Oligiuria Alt. mental sate- cofuion to lethargic

7. Cardiogenic shock Acute circulatory failure with sudden fall in cardiac output from acute disease of the heart without actual reduction of blood volume ( normovolaemia ) results in cardiogenic shock ETIOLOGY- 1. deficient emptying Eg. MI, cardiomyopathies, rupture of heart or ventricle or papillary muscle , cardiac arrthemias 2. deficient filling- Cardiac tamponade from haemopericardium 3. obstruction to outflow- pul . Embolim , dissecting aortic aneurysm, ball valve thrombus

8. Pathogenesis- Lt. ventricular dysfunction c/c- dyspnoea , tachycardia, increased heart rate Decreased cardiac output Descreased tissue perfusion pulmonary oedema alveolar pulmonary oedema shock

9. Septic shock Severe bacterial infection or septicaemia induces septic shock. Tit may be the result of gram negative septicaemia ( endotoxic shock) or from gram positive septicaemia ( exotoxic shock) ETIOLOGY- GRMA NEGATIVE BACTERIA( 62%)- Psedomonas , e. Coli, haemophilus GRAM POSITIVE BACTERIA ( 47%)- staphylococcus aureus, enterococci, streptococcus pneumoniae FUNGI( 19%)- most common candida species

10. Pathophysiology of septic shock Bacterial infection Endotoxin & other microbial products Binds to LPS binding protein in serum Binds to CD14 receptors on mononuclear cells CD14 binds to TLR4 RELEASE OF CHEMICAL MEDIATORS

11. Pathophysiology of septic shock In septic shock systemic vasodilatation and pooling of blood in the periphery leads to tissue hypoperfusion and though the cardiac output is preserved this is accompanying widespread endothelial cell actvation and often leads to hypercoagulable state that can manifest DIC . Septic shock is associated with change in metabolism that can directly suppress cellular function. The net is hypo- perfusion and dysfunction of multi- organ.

12. Major factors contributing to the pathophysiology of septic shock are following Inflammatory mediators : Various microbe cell wall contains LPS( - tive bact.)AND LTG( + tive bact.( lipotheichoic acid)) these are released bind to free LPS& LTG this complex then to cell surface receptor CD14 on macrophage, mononuclear phagocytic cell. Endothelial cell CD14 binds to the signal transducing protein TLR-4 UPON ACTIVATION CASCADE OF CYTOKINES MEDIATORS TNF, TL-1 , IL-8, INF. The compliment cascade are actvated directly or through proteolytic activity of plasmin resulting in production of anaphylotoxins c3a & c5a, chemotactic factor c5a causes vasodilatation& increased vascular permeability. Activated endothelial cell and macrophages release NO contribute to pro- inflammatory state

13. Endothelial cell activation and injury: Endothelial cell activation by microbial products or inflammatory mediators produced by leukocytes. Has 3 major sequel- thrombosis, increase vascular permeability, vasodilatation. Pro- inflammatory cytokines result in increased tissue factor production by endothelial cell and monocyte the production of endothelial anti- coagulant factor –tissue factor pathway inhibitor, thrombomodulin and protein c reduced. Reduced blood flow at the level of small vesssels produce stasis that reduce the wash out activated thrombi in small vessels, that lead to tissue hypoperfusion .

14. In DIC increase consumption of coagulation factor & platelet leads to bleeding Increase vascular permeability leads exudation of fluid in to interstitium causing oedema Endothelium increase the release of NO

15. Metabolic abnormalities : septis pt. exhibit insulin resistance and hypoglycemia. Cytokines such as TNF & IL-1, stress induced hormone (glucagon, catecholamine) all drive gluconeogenesis. At the same time the pro inflammatory cytokines suppress insulin release while simultenously promoting insulin resistance in the liver and other tissue, by surface expression of glucose transporter . Hyperglycemia reduced neutrophil function & bactericidal activity. Sepsis also related with adrenal insufficiency & functional deficiencyof glucacordicoid .

16. Immunosupression : Hyperinflammatory state activate immunosuppression mechanism which involves both innate & adaptive immunity by production of anti- inflammatory mediators ( soluble TNF receptors, IL-receptor antagonist & IL -10) Organ dysfunction Systemic hypotension , interstitial oedema , small vessel thrombosis reduce the delivery of oxygen & to the tisue

17. High level of cytokines , sec. mediators reduces myocardial contractility & CO. increase vascular permeability & endothelial injury acute respitory distress syndrome ultimately cause multiple organ failure.

18. Traumatic shock Resulting from trauma initially due to hypovolaemia , but afterwads suffer from plasma volume loss ETIOLOGY- severe inury , surgery with marked blood loss, obstretrical trauma

19. Neurogenic shock Results from causes of interruption of ympathetic vasomotor supply. ETIOLOGY- High cervical spinal cord injury, accidental high spinal anaesthesia , severe head injury

20. Hypoadrenal shock Unknown adrenal insufficiency in which pt. fails respond to normally stress of vtrauma , surgery , illness ETIOLOGY- administration of high doses of glucocorticoids sec,. Adrenal insufficiency ( in tb)

21. stages of shock 1. compensated shock- a. widespread vasoconstriction- by activation of neuronal, humoural fctors g. baroreceptors, chemoreceptors, catecholamines, enin , angiotensin---increased pheripheral resistance- increased heart rate and cold clammy skin. B. fluid conservation by kidney- release of aldosterone from hypoxix kidney by actvation of RAA Mechanism – release of ADH due to decrased effective circulating blood volume – reduced glomerular fitration rate due to arteriolar constriction - shifting of tiue fluid into the plasma due to lowered capillary hydrostatic pressure C. stimulation of adrenal medulla- in response to low crdiac output adrenal medulla timulated ( epinephrine and nor pinphrin ) result in increase cardic output and increased heart rate

22. 2. progressive decompansted shock – if the compensatory mechanism fails to restore circulation, vital organ shows the effects of hypoxia. Persistent oxygen deficiency leads to intra cellular anaerobic glycolysis with lactic acidosis, thus reduce tissue Ph and vasomotor response resulting reduce cardiac output and anoxic injuryto endothelial cell leads to DIC

23. 3.irreversible decompensated shock – When thre is failure to restoration o circulation by compensatory mechanism or by therapeutic intervention, the process of shock enters the irreversible stage. Widespread cell injury is reflected in lyssomal enzyme leakage , nitric oxide reduced myocardial contractability , acute tubular necrosis ultimately death.

24. Clinical presentation of shock Alt. mental status Restless, confusin , stupor, coma, agitation Pt. may unconscious or semi- conscious Pallor Icrease sweating Cold clammy skin, warm in septic shock Tachycardia Low BP Temp. may or may not be raised Dehydration Oligouria

25. Morphology of shock Characteristic feature is multisystem failure Due to prolonged hypoxia resulting in degeneration and necrosis in various organs. Basicaly major organ affected are the brain, heart, lungs, and kidney. Morphologic changes also noticed in the adrenal gland, git , liver, and other organ.

26. Hypoxic encephalopathy Occurs Due to cerebral ischaemia followedby alt. state of consciousness . BP falls 50mmhg causes Hypotension in prolonged shock and cardiac arrest, brain get suffers from ischaemic damage with loss of cortical functions, coma and a vegetative state Gross- severe ischaemic necrosis esp. at border zone between the ant. And middle cerebral arteries Microscopically- noticeable changes occurs if ischaemia prolonged for 12 to 24 hrs. neurons, particularly purkinje cells, are more prone to develop the effects of ischaemia . The cytoplasmof the affected neurons is intensely eosinophilic and nucleus small pyknotic . Dead and dying nerve cells are replaced by gliosis

27. Heart in shock More vulnerable to the effects of hypoxia Heart is affected in cardiogenic as well as in other forms of shock. There are 2 types of morphologic changes in heart in all types of shock 1) haemorrhage and necrosis- there may be small or large ischaemic areas or infarct, particularly located in the subepicardial and subendocardial region. 2) zonal lesion- these are opaque transverse contraction bands in the myocytes near the intercalated disc

28. Shock lung Lungs due to dual blood supply are generally not affected by hypovolaemic shock but septic shock the morphologic changes in lungs are quite prominent termed shock lung Gross- lungs are heavy and wet Microscopically- ards brifly changes include congestion , interstitial and alveolar oedema , interstitial lymphocytic infiltrate, alveolar hyaline membranes, thickening and fibrosis of alveolar septa, and fibrin and platelet thrombi in the pulmonary microvasculature.

29. Shock kidney Grossly- kidneys are soft and swollen. Section surface shows blurred architectural markings Microscopically- Tubular lesions are seen at all levels of nephron and are referred to as acute tubular necrosis(ATN) which can occur following other causes besides shock If extensive muscle injury or intravascular haemolysis Peculiar brown tubular casts are seen

30. Liver in shock Grossly- faint nutmeg appearance Microscopically- depeding upon the time gap between injury and cell death, ischaemic shrinkage, hydropic change, focal necrosis or fatty change may be seen, liver function may impaired

31. Haemorrhagic gastroentropathy Mucosal and mural infarctionthe non- occlusive ischaemic injury of bowel must be distinguished from full fledged infarction in which deeper layers of gut( muscularis and serosa) are also damaged In shock due to burns acute stress ulcers of the stomach or duodenum may occur and are known as curlings ulcers Grossly- the lesions are multifocal and widely distributed throughout bowel. The lesion are superficial ulcers , reddish purple in colour . The adjoining bowel mucosa is oedematous and haemorrhagic . Microscopically- bowel surface shows dilated and congested vessels and haemorrhagic necrosis of the mucosa and sometimes submucosa , sec. infection may supervene and condition may progress into pseudomembranous enterocolis .

32. Complication of shock ARDS- acute respiratory distress syndrome DIC- desseminated intravascular coagulation ARF- acute renal failure MODS- multiple organ dysfunction syndrome. With progression of the condition , pt. may develop stupor, coma, and death.

33. Adrenals in shock The adrenals show stress response in shock. This includes release of aldosterone in response to hypoxic kidney, relase of glucocorticoids from adrenal cortex and catecholamines like adrenaline from adrenal medulla. In severe shock , acute adrenal haemorrhagic necrosis may occur.