ABDUL WODOOD (ROLL NO. 03) ABHYUDAY VARSHNEY (ROLL NO . 04) Case
A 65 years old diabetic patient is brought to the
emergency with gangrene. His pulse rate is 140 beats per minute, respiratory rate is 25 breaths per minute & blood pressure is 80/55 mm of Hg and temperature is 103 degree F. His liver functions are completely deranged and blood lactate levels are markedly higher ,also showing abnormally high WBC count with warm and flushed skin. What’s the likely diagnosis? Explain. Explain the pathogenesis of diagnosed disease. The likely diagnosis is Septic shock. The septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality. Sepsis is defined as life threatening organ dysfunction caused by a dysregulated host response to infection. Pathogenesis of septic shock
Macrophages ,neutrophils, dendritic cells,
endothelial cells and soluble components of innate immune system recognize and are activated by diverse substance derived from microorganisms. After activation these cells, they release various factors that initiate a number of inflammatory and counter-inflammatory responses that interact in complex way to produce septic shock and organ failure. Factors playing major role in pathogenesis of septic shock
Inflammatory and counter inflammatory response
Endothelial activation and injury
Induction of procoagulant state.
Metabolic abnormalities.
Organ dysfunction. Inflammatory and counter-inflammatory responses Toll like receptors recognized microbe derived substances containing PAMPS and G-protein that detect bacterial peptides and C- type lectin receptor such as dectins .Their Ligation leads to increased expression of genes encoding mediators like TNF,IL-1,and IFN-GAMMA and HMGB1. ROS and prostaglandin and PAF are also get elevated. These effectors further leads to increased cytokine and chemokine production. Microbial particles also activate complement cascade resulting in production of anaphylotoxins and opsonins. All these leads to proinflammatory state. This hyperinflammatory state triggers counter inflammatory response i.e immunosupressive response Endothelial activation and injury The pro-inflammatory state and endothelial activation associated with sepsis leads to vascular leakage and tissue edema which have deleterious effects on nutrient delivery and waste removal. Effect of inflammatory cytokines is to loosen endothelial cell tight junction making vessel leaky. Activated endothelial also upregulate production of NO and C3a,C5a, PAF. Another feature is microvascular dysfunction. Induction of procoagulant state Sepsis alters the expression of many factor so as to favor coagulation. Proinflammatory cytokines increases tissue factor production and decrease the production of endothelial anticoagulant factor such as tissue factor inhibitor ,thrombomodulin and protein C. They also dampen fibrinolysis by increasing PAI-1 expression. NETs stimulate both extrinsic and intrinsic pathway of coagulation. Metabolic abnormalities
Septic patients exhibit insulin resistance and
hyperglycemia. Cytokines such as TNF and IL-1, stress -induced hormones and catecholamines all drive gluconeogenesis. Proinflammatory cytokines suppress insulin release and promote insulin resistance ,all this lead to hyperglycemia which decreases neutrophil function thereby decreasing bactericidal activity. Organ dysfunction ➢ Systemic hypotension , interstitial edema, microvascular dysfunction and small vessel thrombosis all leads to cellular hypoxia and improper nutrient delivery. ➢ Mitochondrial damage resulting from oxidative stress impairs oxygen use. ➢ High level of cytokines and secondary mediators diminish myocardial contractility and cardiac output, increased vascular permeability and endothelial injury which lead to acute respiratory distress syndrome ➢ Ultimately ,these factors leads to failure to multiple organs mainly kidney, liver, lungs and heart and at last death. References
Robbins & Cotran Pathologic Basis of Disease
Tenth edition Arizona department of Health services,Arizona USA Wikipedia TREATMENT AND MANAGEMENT OF SHOCK ROLL NO.5-ACHYUT TIWARI ROLL NO.6-ADARSH MISHRA Clinical Case A 65 year old male presents to the emergency department with complaints of severe shortness of breath, chest pain, and light headedness for the past few hours. He has also noticed cold sweat and a sensation of impending doom. The patient has a history of coronary artery disease with a previous myocardial infarction (MI) 3 years ago. He has been compliant with his medications, which include aspirin, a beta-blocker, and a statin. Over the past few weeks, he has experienced occasional chest discomfort, but today the pain became more severe and was accompanied by worsening dyspnea and weakness. He denies nausea or vomiting but feels extremely fatigued. 1. What is the likely diagnosis of the case? 2. What is the pathophysiology of the type of the shock? 3. What is the management plan? The patient is diagnosed with cardiogenic shock secondary to myocardial infarction.
Pathophysiology Cardiogenic shock results from severe impairment of the heart’s ability to pump blood effectively, leading to inadequate tissue perfusion and end organ damage. In this case the large MI has lead to extensive damage to left ventricular myocardium, reducing cardiac output causing hypotension, pulmonary congestion and signs of systemic hypoperfusion. Treatment and Management Plan Signs To Look For- Fast and Weak Pulse Pale, Cold or Calmy skin in cardiogenic and hypovolemic shock Hot and flushed skin in case of septic shock Sweating Fast , Shallow Breathing Management Plan ▪Lie down the patient to maintain blood flow to vital organs. ▪Check patient responsiveness from time to time. ▪Look for the underlying cause , which may be Myocardial Infarction , Ventricular arrhythmias. ▪Managing the underlying cause of shock can prevent the progression of shock into progressive stage. Treatment Plan ▪Vasopressors used to treat low BP, eg dopamine, epinephrine. ▪Inotropic agents to improve pumping function of heart. ▪Aspirin used to reduce blood clotting. ▪Oxygenation to maintain blood saturation levels of oxygen QUESTIONS RELATED WITH EACH TYPE OF SHOCK ROLL NO.7-ADITI AGARWAL ROLL NO.8-ADITRI SINGH Case 1 A 65 years old diabetic patient is brought to the emergency with gangrene. His pulse rate is 140 beats per minute, respiratory rate is 25 breaths per minute & blood pressure is 80/55 mm of Hg and temperature is 103 degree F. His liver functions are completely deranged and blood lactate levels are markedly higher ,also showing abnormally high WBC count with warm and flushed skin. ➢What’s the likely diagnosis? Explain. ➢Explain the pathogenesis of diagnosed disease. ➢Briefly explain the stages of shock. ➢The likely diagnosis is Septic shock. ➢The septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality. ➢Sepsis is defined as life threatening organ dysfunction caused by a dysregulated host response to infection. Pathogenesis of Septic Shock Macrophages ,neutrophils, dendritic cells, endothelial cells and soluble components of innate immune system recognize and are activated by diverse substance derived from microorganisms After activation these cells, they release various factors that initiate a number of inflammatory and counter-inflammatory responses that interact in complex way to produce septic shock and organ failure. • Shock is a progressive disorder that leads to death if the underlying problems are not corrected. • These stages have been documented most clearly in hypovolemic shock but are common to other forms as well:
1- An initial nonprogressive stage during which reflex
compensatory mechanisms are activated and vital organ perfusion is maintained. 2- A progressive stage characterised by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis. 3- An irreversible stage in which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible. Nonprogressive phase: Various neurohumoral mechanisms help to maintain cardiac output and blood pressure. These include:
1-baroreceptor reflex 2-release of catecholamines and antidiuretic hormone 3-activation of renin-angiotensin-aldosterone 4-generalized sympathetic stimulation. Progressive phase: -Characterised by widespread tissue hypoxia Intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. -Arterioles dilate and blood begins to pool in microcirculation. -Peripheral pooling worsens the cardiac output and leads to widespread tissue hypoxia. Irreversible stage:
-Widespread cell injury
-Intestinal flora enters the circulation -Renal failure occurs -Leads to death. CASE 2: A 39 year old male presented to the emergency department with haematemesis ,jaundice and hypotension with blood pressure of 59/22 mmHg. The patient was conscious with a medical history of oesophageal varices secondary to alcoholic hepatitis, previous GI bleed with banding and thrombocytopenia. Haematemesis was preceded by nausea the previous day and EMS reported 1-2 L of blood lost via emesis. Upon arrival, in addition to the severe hypotension, he was in tachycardia with an oxygen saturation of 95% with 3 L of oxygen through a nasal cannula. His arterial blood sample had a pH of 6.60, pCO2 of 103 mmHg, pO2 of 63 mmHg, bicarbonates level of 10.2mEq/L and base excess -28mEq/L. 1. What’s the likely diagnosis? 2. Describe the pathogenesis of the diagnosed disease 3. Briefly describe the classification of shock. ---The likely diagnosis in this case is of hypovolemic shock as there is excessive blood loss via emesis and also patient is in tachycardia.
---In this condition, the cardiac output will be less
due to low blood volume caused by excessive blood loss.
