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PARASCI_L3
Shock at the cellular level
| Question | Answer |
|---|---|
| diffusion of oxygen from lungs into blood | oxygenation |
| 760mHg | atmospheric pressure at sea level |
| total exchange of gases between atmosphere and lungs | pulmonary ventilation |
| exchange of gases in the alveoli | alveolar ventilation |
| derangement of oxygen delivery and consumption at a cellular level | shock |
| stronger faster heartbeat, vessel dilation, vessel constriction to nonessential organs | sympathetic response |
| located in carotid arteries and aortic arch, respond to changes in stretch of the vessel walls | baroreceptors |
| monitor O2, CO2 &H+ in carotid bodies | chemoreceptors |
| responses associated with pain/cold factors | extrinsic reflexes |
| detects vasoconstriction | alpha receptors |
| detects increase in heart rate and force of contraction | beta 1 receptors |
| vasodilation of skeletal muscle and relaxation of bronchioles | beta 2 receptors |
| neural response: hypothalamus releases | corticotropin |
| neural response: corticotropin stimulates pituatary gland to release | adrenocorticotropin hormone |
| ACTH stimulates adrenal gland to release | cortisol (hyperglycaemic hormone) |
| elevates blood sugar level and stimulate Na and water retention | hyperglycaemic hormone |
| when kidney perfusion decreases | arterial bp drops |
| in response to bp drop, kidneys release what from the juxtaglomerular apparatus? | renin |
| renin does what to produce angiotensin II | catalyses the reaction |
| angiotensin II acts on blood vessels causing | vasoconstriction |
| angiotensin II acts on which gland to cause aldosterone release | adrenal gland |
| causes kidney tubules to increase sodium reabsorption, which causes water retention | angiotensin II |
| causes vascular blood volume and arterial bp to increase | water retension |
| in response to bp drop, osmoreceptors in the hypothalamus stiumulate what to release ADH | posterior pituatary gland |
| decrease in blood volume, pressure and increase in osmolality of bodily fluids is triggers what? | osmoreceptors |
| directly vasoconstricts and causes water reabsorption | anti-diuretic hormone |
| when only glycolysis is functioning to produce ATP, respiration is said to be | anaerobic |
| when both glycolysis and the krebs cycle are functioning to produce ATP, respiration is said to be | aerobic |
| in anaerobic respiration, pyruvate converts to | lactic acid |
| in aerobic respiration, pyruvate converts to | 2 acetyl CoA |
| lactic acid accumulation impairs the | Na+/K+ pump |
| impairment of the Na+/K+ pump results in | excess intracellular Na+ |
| excess intracellular sodium causes | cellular oedema and increased membrane permeability |
| cellular oedema results in | cell lysing |
| anaerobic cell lysing results in | lactic acid in the extracellular space |
| impaired cellular metabolism releases | vasoactive inflammatory mediators |
| impaired cellular metabolism increases production of | oxygen free radicals |
| impaired cellular metabolism results in excessive | lactic acid and H+ ions |
| diminished blood volume resulting in inadequate vascular filling | hypovolaemic shock |
| how much blood loss for hypovolaemic shock | 15-20% |
| how much blood volume per kilo of a human being | 70ml |
| heart pumps blood insufficiently to meet body's demands | cardiogenic shock |
| increase LV end systolic volume | increase in preload |
| increase in end systolic volume and preload when paired with decreased myocardial contractility | increase in afterload |
| coronary artery impairment | both increase in preload and afterload |
| Decreased CO, HOTN, hypoperfusion, tissue hypoxia despite adequate intravascular volume. | cardiogenic shock definition |
| MI, arrhythmia, valve defect, ventricular aneurysm | intrinsic factors of cardiogenic shock |
| Pulmonary embolism, tension pneumothorax, cardiac tamponade | extrinsic factors of cardiogenic shock |
| due to mechanical obstruction of blood flow through central circulation | obstructive shock |
| PE, dissecting aortic aneurysm, pneumothorax, hameothorax, atrial myxoma, hemidiaphragm | factors of obstructive shock |
| myocardium contracts against high afterload | p1 obstructive shock |
| sympathetic activation causes vasoconstriction to maintain bp | p2 obstructive shock |
| normal BP maintained but organ perfusion decreased | p3 obstructive shock |
| increased pressure causes venous congestion | p4 obstructive shock |
| vasculature expands until normal blood volume doesnt fill circulatory system | distributive shock |
| loss of vessel tone, enlarged vascular compartment, displaced vascular vol from central circulation | signs of distributive shock |
| decreased sympathetic control, excessivevasodilatory substances released | causes of distributive shock |
| brain injury, CNS depressing drugs, general anaesthesia, hypoxia or lack of glucose | causes of neurogenic shock |
| hypotension, warm skin due to loss of cutaneous control | symptoms of neurogenic shock |
| loss of sympathetic control above T6 causing loss of vasomotor tone | neurogenic shock |
| an inflammatory response initiated by presence of organism in normally sterile tissue | infection |
| presence of live bacteria in bloodstream | bacteraemia |
| presence of pathogen in bloodstream leading to sepsis | septicaemia |
| syndrome comprising of set clinical signs in response to systemic inflammation | Systemic inflammatory response syndrome |
| orignially defined as SIRS triggered by a primary localised infection | Sepsis |
| bacterial, fungal, viral or parasitic infection | causes of sepsis |
| pathogen invasion | p1 sepsis |
| pathogen binds to toll-like receptors on monocytes | p2 sepsis |
| release of pro inflammatory cytokines to control infection | p3 sepsis |
| macrophages release TNF-A, IL-B1, IL-2, IL-6 | increases NO release from endothelial cells, vasodilation, and cellular permeability, and initiated compliment pathway` |
| stimulate hypothalamus to incrs temp | IL-1 and IL-6 |
| IL-4, IL-10, IL-1, IL-13 | anti-inflammatory cytokines |
| failure to balance pro and anti-inflammatory mechanisms | altered coagulation, endothelial cell damage, vasodilation, increased capillary permeability and abnormal blood flow (perfusion). |
| can develop with hypoperfusion and hypoxia widespread, resulting in lactic acid build up and change of metabolism | Multiple organ dysfunction syndrome |
| 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 |
| multiple small thrombi/emboli form in small blood vessels resulting in occlusion | thrombotic phase |
| fribrinolysis of thrombi occurs, suppressing thrombin and further aggravating bleeding | fibrinolytic phase |
| life threatening organ dysfunction caused by disregulated host response to infection | septic shock |
| RR>22/min, change in GCS, systolic blood pressure </= 100mmHg | Quick Sequential Organ failure Assessment |
| 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 |
| 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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