Shock at the cellular level
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| diffusion of oxygen from lungs into blood | oxygenation
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| 760mHg | atmospheric pressure at sea level
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| total exchange of gases between atmosphere and lungs | pulmonary ventilation
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| exchange of gases in the alveoli | alveolar ventilation
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| derangement of oxygen delivery and consumption at a cellular level | shock
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| stronger faster heartbeat, vessel dilation, vessel constriction to nonessential organs | sympathetic response
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| located in carotid arteries and aortic arch, respond to changes in stretch of the vessel walls | baroreceptors
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| monitor O2, CO2 &H+ in carotid bodies | chemoreceptors
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| responses associated with pain/cold factors | extrinsic reflexes
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| detects vasoconstriction | alpha receptors
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| detects increase in heart rate and force of contraction | beta 1 receptors
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| vasodilation of skeletal muscle and relaxation of bronchioles | beta 2 receptors
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| neural response: hypothalamus releases | corticotropin
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| neural response: corticotropin stimulates pituatary gland to release | adrenocorticotropin hormone
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| ACTH stimulates adrenal gland to release | cortisol (hyperglycaemic hormone)
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| elevates blood sugar level and stimulate Na and water retention | hyperglycaemic hormone
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| when kidney perfusion decreases | arterial bp drops
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| in response to bp drop, kidneys release what from the juxtaglomerular apparatus? | renin
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| renin does what to produce angiotensin II | catalyses the reaction
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| angiotensin II acts on blood vessels causing | vasoconstriction
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| angiotensin II acts on which gland to cause aldosterone release | adrenal gland
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| causes kidney tubules to increase sodium reabsorption, which causes water retention | angiotensin II
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| causes vascular blood volume and arterial bp to increase | water retension
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| in response to bp drop, osmoreceptors in the hypothalamus stiumulate what to release ADH | posterior pituatary gland
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| decrease in blood volume, pressure and increase in osmolality of bodily fluids is triggers what? | osmoreceptors
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| directly vasoconstricts and causes water reabsorption | anti-diuretic hormone
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| when only glycolysis is functioning to produce ATP, respiration is said to be | anaerobic
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| when both glycolysis and the krebs cycle are functioning to produce ATP, respiration is said to be | aerobic
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| in anaerobic respiration, pyruvate converts to | lactic acid
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| in aerobic respiration, pyruvate converts to | 2 acetyl CoA
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| lactic acid accumulation impairs the | Na+/K+ pump
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| impairment of the Na+/K+ pump results in | excess intracellular Na+
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| excess intracellular sodium causes | cellular oedema and increased membrane permeability
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| cellular oedema results in | cell lysing
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| anaerobic cell lysing results in | lactic acid in the extracellular space
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| impaired cellular metabolism releases | vasoactive inflammatory mediators
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| impaired cellular metabolism increases production of | oxygen free radicals
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| impaired cellular metabolism results in excessive | lactic acid and H+ ions
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| diminished blood volume resulting in inadequate vascular filling | hypovolaemic shock
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| how much blood loss for hypovolaemic shock | 15-20%
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| how much blood volume per kilo of a human being | 70ml
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| heart pumps blood insufficiently to meet body's demands | cardiogenic shock
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| increase LV end systolic volume | increase in preload
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| increase in end systolic volume and preload when paired with decreased myocardial contractility | increase in afterload
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| coronary artery impairment | both increase in preload and afterload
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| Decreased CO, HOTN, hypoperfusion, tissue hypoxia despite adequate intravascular volume. | cardiogenic shock definition
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| MI, arrhythmia, valve defect, ventricular aneurysm | intrinsic factors of cardiogenic shock
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| Pulmonary embolism, tension pneumothorax, cardiac tamponade | extrinsic factors of cardiogenic shock
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| due to mechanical obstruction of blood flow through central circulation | obstructive shock
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| PE, dissecting aortic aneurysm, pneumothorax, hameothorax, atrial myxoma, hemidiaphragm | factors of obstructive shock
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| myocardium contracts against high afterload | p1 obstructive shock
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| sympathetic activation causes vasoconstriction to maintain bp | p2 obstructive shock
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| normal BP maintained but organ perfusion decreased | p3 obstructive shock
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| increased pressure causes venous congestion | p4 obstructive shock
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| vasculature expands until normal blood volume doesnt fill circulatory system | distributive shock
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| loss of vessel tone, enlarged vascular compartment, displaced vascular vol from central circulation | signs of distributive shock
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| decreased sympathetic control, excessivevasodilatory substances released | causes of distributive shock
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| brain injury, CNS depressing drugs, general anaesthesia, hypoxia or lack of glucose | causes of neurogenic shock
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| hypotension, warm skin due to loss of cutaneous control | symptoms of neurogenic shock
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| loss of sympathetic control above T6 causing loss of vasomotor tone | neurogenic shock
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| an inflammatory response initiated by presence of organism in normally sterile tissue | infection
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| presence of live bacteria in bloodstream | bacteraemia
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| presence of pathogen in bloodstream leading to sepsis | septicaemia
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| syndrome comprising of set clinical signs in response to systemic inflammation | Systemic inflammatory response syndrome
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| orignially defined as SIRS triggered by a primary localised infection | Sepsis
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| bacterial, fungal, viral or parasitic infection | causes of sepsis
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| pathogen invasion | p1 sepsis
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| pathogen binds to toll-like receptors on monocytes | p2 sepsis
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| release of pro inflammatory cytokines to control infection | p3 sepsis
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| macrophages release TNF-A, IL-B1, IL-2, IL-6 | increases NO release from endothelial cells, vasodilation, and cellular permeability, and initiated compliment pathway`
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| stimulate hypothalamus to incrs temp | IL-1 and IL-6
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| IL-4, IL-10, IL-1, IL-13 | anti-inflammatory cytokines
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| failure to balance pro and anti-inflammatory mechanisms | altered coagulation, endothelial cell damage, vasodilation, increased capillary permeability and abnormal blood flow (perfusion).
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| can develop with hypoperfusion and hypoxia widespread, resulting in lactic acid build up and change of metabolism | Multiple organ dysfunction syndrome
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| activated endothelial cells release pro-thrombotic factors to compensate for blood loss (factor VII), but then attempts to break down the clots, causing widespread bleeding,tissue ischaema. | disseminated intravascular coagulation
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| multiple small thrombi/emboli form in small blood vessels resulting in occlusion | thrombotic phase
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| fribrinolysis of thrombi occurs, suppressing thrombin and further aggravating bleeding | fibrinolytic phase
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| life threatening organ dysfunction caused by disregulated host response to infection | septic shock
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| RR>22/min, change in GCS, systolic blood pressure </= 100mmHg | Quick Sequential Organ failure Assessment
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| hypoperfusion causes alveolar and capillary wall damage, incrs surfactant, leaky tissues, gas exchange impaired, decreased organ/tissue perfusion, and organ failure | Acute Respiratory Distress Syndrome
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| Sudden interruption of renal function, decreased glomerular filtration rate, and reabsorption of Na and H2O resulting in renal necrosis | Acute Renal Failure
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