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Questions and Answers
Chemoreceptors monitor blood levels of CO2 and O2 and stimulate the adrenal medulla to release catecholamines.
Chemoreceptors monitor blood levels of CO2 and O2 and stimulate the adrenal medulla to release catecholamines.
True
Angiotensin II reduces blood pressure by causing peripheral vasodilation.
Angiotensin II reduces blood pressure by causing peripheral vasodilation.
False
Shock can lead to multisystem failure, affecting organs such as the heart, brain, and kidneys.
Shock can lead to multisystem failure, affecting organs such as the heart, brain, and kidneys.
True
In acute tubular necrosis, the kidneys appear grossly swollen and exhibit blurred architectural markings.
In acute tubular necrosis, the kidneys appear grossly swollen and exhibit blurred architectural markings.
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Widespread cell injury in the context of shock leads to increased myocardial contractility.
Widespread cell injury in the context of shock leads to increased myocardial contractility.
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Shock is solely due to an increase in cardiac output.
Shock is solely due to an increase in cardiac output.
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The transition from aerobic to anaerobic metabolism during shock leads to lactic acid production.
The transition from aerobic to anaerobic metabolism during shock leads to lactic acid production.
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Cardiogenic shock can occur without any loss of blood volume.
Cardiogenic shock can occur without any loss of blood volume.
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Septic shock is a subtype of hypovolemic shock.
Septic shock is a subtype of hypovolemic shock.
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Severe burns can be a cause of hypovolemic shock.
Severe burns can be a cause of hypovolemic shock.
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Cellular metabolism is impaired during shock, leading to potential cell death.
Cellular metabolism is impaired during shock, leading to potential cell death.
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Deficient filling in the heart can be caused by cardiac tamponade.
Deficient filling in the heart can be caused by cardiac tamponade.
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Septic shock can be initiated by certain microbial constituents.
Septic shock can be initiated by certain microbial constituents.
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Histamine release from mast cells decreases capillary permeability.
Histamine release from mast cells decreases capillary permeability.
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Nitric oxide is responsible for vasodilation during septic shock.
Nitric oxide is responsible for vasodilation during septic shock.
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Pro-inflammatory cytokines like TNF-α and IL-1 have no impact on endothelial cell adhesiveness.
Pro-inflammatory cytokines like TNF-α and IL-1 have no impact on endothelial cell adhesiveness.
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The complement cascade is activated by microbial components.
The complement cascade is activated by microbial components.
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In sepsis, there is a shift from anti-inflammatory (TH2) to pro-inflammatory (TH1) cytokines.
In sepsis, there is a shift from anti-inflammatory (TH2) to pro-inflammatory (TH1) cytokines.
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Endothelial cell tight junctions become tighter during the inflammatory response in sepsis.
Endothelial cell tight junctions become tighter during the inflammatory response in sepsis.
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Activated immune cells produce reactive oxygen species that contribute to vascular injury.
Activated immune cells produce reactive oxygen species that contribute to vascular injury.
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Septic shock leads to decreased tissue edema and vascular leakage.
Septic shock leads to decreased tissue edema and vascular leakage.
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Menstrual blood aids the growth of staph aureus organism.
Menstrual blood aids the growth of staph aureus organism.
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Reduced effective circulating blood volume is a feature of shock.
Reduced effective circulating blood volume is a feature of shock.
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Spinal cord injury does not influence vascular tone.
Spinal cord injury does not influence vascular tone.
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The irreversible stage of shock is characterized by recovery.
The irreversible stage of shock is characterized by recovery.
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Baroreceptors are located in the aortic arch and carotid sinuses.
Baroreceptors are located in the aortic arch and carotid sinuses.
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Neurohumoral mechanisms are inactive during hypotension.
Neurohumoral mechanisms are inactive during hypotension.
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Catecholamines such as epinephrine increase heart rate and vasodilation.
Catecholamines such as epinephrine increase heart rate and vasodilation.
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In the early stage of shock, vital organs receive priority for blood supply.
In the early stage of shock, vital organs receive priority for blood supply.
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Organ tissue hypoperfusion occurs due to normal sympathetic control of vascular tone.
Organ tissue hypoperfusion occurs due to normal sympathetic control of vascular tone.
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Chemoreceptors monitor blood levels of nutrients and hormones.
Chemoreceptors monitor blood levels of nutrients and hormones.
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Activated endothelium decreases the production of nitric oxide and other vasoactive inflammatory mediators.
Activated endothelium decreases the production of nitric oxide and other vasoactive inflammatory mediators.
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Proinflammatory cytokines increase the production of anti-coagulant factors in endothelial cells.
Proinflammatory cytokines increase the production of anti-coagulant factors in endothelial cells.
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Sepsis can lead to systemic activation of thrombin causing the deposition of fibrin-rich thrombi.
Sepsis can lead to systemic activation of thrombin causing the deposition of fibrin-rich thrombi.
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Adult Respiratory Distress Syndrome can result from endothelial injury and increased vascular permeability.
Adult Respiratory Distress Syndrome can result from endothelial injury and increased vascular permeability.
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Insulin resistance and hyperglycaemia are not observed in septic patients.
Insulin resistance and hyperglycaemia are not observed in septic patients.
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In disseminated intravascular coagulation (DIC), excessive coagulation factors and platelets lead to decreased bleeding.
In disseminated intravascular coagulation (DIC), excessive coagulation factors and platelets lead to decreased bleeding.
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Systemic hypotension is characterized by increased blood pressure in the body.
Systemic hypotension is characterized by increased blood pressure in the body.
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The collective actions of bacterial constituents and chemical mediators can cause fever and systemic vasodilatation.
The collective actions of bacterial constituents and chemical mediators can cause fever and systemic vasodilatation.
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Exotoxins produced by staph aureus are not linked to septic shock.
Exotoxins produced by staph aureus are not linked to septic shock.
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The use of absorbent tampons during menstruation is associated with septic shock.
The use of absorbent tampons during menstruation is associated with septic shock.
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Study Notes
Pathology of Shock
- Shock is defined as systemic tissue hypoperfusion due to reduced cardiac output and/or reduced effective circulating blood volume.
- Hypoperfusion of cells and tissues leads to insufficient oxygen (cellular hypoxia) and nutrient supply. Waste product clearance is inadequate and metabolism shifts from aerobic to anaerobic.
- Widespread cellular metabolism impairment/dysfunction occurs.
- Prolonged shock state causes irreversible tissue injury resulting in multi-organ damage and potential patient death.
Pathophysiology of Shock
- Cells switch from aerobic to anaerobic metabolism, producing lactic acid.
- Cell function ceases and the cell swells.
- Cell membranes become more permeable, leading to electrolyte and fluid leakage in and out of the cells.
- The Na+/K+ pump, essential for maintaining cell function, is impaired.
- Mitochondria are damaged, leading to cell death.
Aetiology and Classification of Shock
-
Types of shock:
- Cardiogenic shock
- Hypovolaemic shock
- Distributive shock
- Shock associated with systemic inflammation (e.g., septic shock)
- Neurogenic shock
- Anaphylactic shock
Cardiogenic Shock
- Acute circulatory failure with a sudden fall in cardiac output without a reduction in blood volume.
- Caused by myocardial pump failure.
- Causes include:
- Deficient emptying (e.g., myocardial infarction, papillary muscle rupture, ventricular rupture, acute myocarditis, cardiac arrhythmias, cardiomyopathies)
- Deficient filling (e.g., cardiac tamponade from haemopericardium)
- Obstruction to outflow (e.g., pulmonary embolism, tension pneumothorax, dissecting aortic aneurysm)
Hypovolaemic Shock
- Results from loss of blood or plasma volume.
- Causes include:
- Severe haemorrhage
- Fluid loss (severe burns, diarrhoea, vomiting, extensive injury, uncontrolled diabetes mellitus, diabetes insipidus, diuretic overdose)
Shock Associated with Systemic Inflammation (e.g., Septic Shock)
- Caused by various insults such as microbial infections, burns, trauma, or pancreatitis.
- Characterized by a massive outpouring of inflammatory mediators causing arterial vasodilation, vascular leakage, and venous blood pooling.
- Widespread endothelial cell activation and injury often leading to a hypercoagulable state (DIC - Disseminated Intravascular Coagulation).
- Several microbial constituents initiate the process of septic shock.
Neurogenic Shock
- Less common, caused by loss of vascular tone and peripheral pooling of blood.
- Common causes include spinal cord injury and anaesthesia.
Anaphylactic Shock
- Initiated by generalized IgE-mediated hypersensitivity reaction.
- Characterized by widespread systemic peripheral vasodilation and increased vascular permeability.
- Leads to tissue hypoperfusion and hypoxia.
Two Basic Features of Shock Pathogenesis
- Reduced effective circulating blood volume
- Reduced oxygen supply to cells and tissues (resultant anoxia)
Stages of Shock
- Initial non-progressive phase
- Progressive stage
- Irreversible/intractable stage
Initial Non-Progressive Stage
- The body attempts to maintain adequate cerebral and coronary blood supply by redistribution.
- This involves mechanisms like baroreceptor reflexes, chemoreceptor reflexes, and the renin-angiotensin-aldosterone system (RAAS).
- These mechanisms lead to tachycardia, peripheral vasoconstriction, and fluid conservation.
Progressive Stage
- Widespread tissue hypoxia occurs, with anaerobic glycolysis and lactic acidosis.
- Tissue pH lowers, reducing effectiveness of vasomotor response and leading to pooling in microcirculation.
- Decreased cardiac output, anoxic injury, and progression to DIC are common.
Irreversible/Intractable Stage
- Widespread cell damage (with lysosomal enzyme leakages).
- Decreased myocardial contractility
- Renal shutdown (acute tubular necrosis)
- Ischemia of the bowel might introduce intestinal bacteria into the blood, causing or worsening septic shock.
Morphology of Shock
- Characterised by multisystem failure due to hypoxia causing extensive degeneration and necrosis in numerous organs.
- Major affected organs: heart, brain, kidneys, lungs, GIT, and adrenals.
- Specific organ-level structural changes are described in detail.
Clinical Manifestation of Shock
- Clinical findings like hypotension, weak rapid pulse, tachypnea, cool clammy/warm flushed skin, and oliguria (a decreased amount of urine output) are presented
- The presence of any of the aforementioned symptoms could indicate shock.
Diagnosis of Shock
- A detailed history coupled with a physical examination (including vital signs assessment) is critical
- Various laboratory investigations (e.g., blood culture, blood count, biochemistry panel, C-reactive protein, ECG, blood lactate, arterial blood gases, and clotting profile) are essential to confirm shock.
Management of Septic Shock
- Treat infection with broad-spectrum antibiotics.
- Establish an intravenous line for fluid resuscitation, monitoring blood pressure.
- Administer oxygen.
- Provide nutritional support when needed.
- Use vasoconstrictors and inotropes when needed.
- Manage hyperglycemia with insulin therapy as required.
Toxic Shock Syndrome
- Similar to septic shock, caused by toxins produced by Staphylococcus aureus.
- Associated with the use of absorbent tampons during menstruation, which facilitates staph aureus growth in the menstrual blood.
Neurogenic Shock
- Due to loss of vascular tone leading to peripheral pooling of blood.
- Common causes are spinal cord injury and anaesthesia.
Anaphylactic Shock
- Initiated by IgE-mediated hypersensitivity reaction.
- Characterized by widespread vasodilation and increased vascular permeability resulting in tissue hypoperfusion and hypoxia.
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Description
This quiz covers the pathology and pathophysiology of shock, focusing on systemic tissue hypoperfusion and its consequences. It includes an overview of the different types of shock, cellular responses, and the implications of prolonged shock states. Test your understanding of these critical concepts in shock management.
