RECALL MED UNIVERSITY
🌟 Altitude-related disorders
🎯 Pathology
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the partial pressure of oxygen decreases at high altitudes —> hypoxia
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peripheral chemoreceptors are stimulated (due to hypoxia) —> increased rate and depth of breathing —> respiratory alkalosis as too much CO2 is blown off —> reduced respiratory drive
💡 Types
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acute mountain sickness (AMS)
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high altitude cerebral oedema (HACE)
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high altitude pulmonary oedema (HAPE)
🩺 Acute mountain sickness
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pathology
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self-limiting, and it’s due to the body’s reaction to the reduced partial pressure of oxygen in the atmosphere which leads to hypoxia
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clinical features
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mainly headache
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nausea, vomiting, loss of appetite, fatigue
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diagnosis
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clinical
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prevention
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ascend slowly (max 500 m/day) —> to give the body enough time to adjust physiologically to the reduced partial pressure of oxygen
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acetazolamide —> carbonic anhydrase inhibitor that speeds up the acclimatisation process by inducing a metabolic acidosis which helps increase the respiratory drive
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descend if symptoms persist
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🩺 High altitude cerebral oedema
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pathology
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life-threatening complication associated with high altitudes
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occurs 2 days above altitudes > 4000 m
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pathophysiology
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hypoxia —> reduced ATP in neurons and glia —> reduced activity of Na+/K+/ATPase pumps —> high Na+ in neurons —> water enters by osmosis —> neurons swell —> raised intracranial pressure —> compression of cerebral vasculature —> reduced blood supply to neurons —> death of neurons by apoptosis
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clinical features
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earliest clinical finding = ataxia
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headache, papilloedema, focal neurological deficits, seizures
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diagnosis
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clinical
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management
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descent with assistance (at least 1000 m or until symptoms improve) to keep physical exertion to a minimum
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dexamethasone
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portable hyperbaric chamber or supplemental oxygen if descent is not an option
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🩺 High altitude cerebral oedema
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pathology
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most common cause of death associated with high altitudes
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affects un-acclimatised people at altitudes between 2500-3000 m
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non-cardiogenic
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pathophysiology
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hypoxia —> reduced production of nitric oxide in the pulmonary circulation —> pulmonary hypertension —> increased capillary hydrostatic pressure —> pulmonary oedema
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clinical features
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early
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non-productive cough
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exertional dyspnoea
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later
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dyspnoea at rest
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orthopnoea
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pink frothy sputum
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diagnosis
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clinical
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prevention
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slow ascent
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management
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supplemental oxygen or hyperbaric chamber
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nifedipine
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⛰ Mechanisms of acclimatisation
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Metabolic acidosis
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the initial increased hypoxic drive increases the rate and depth of ventilation leading to respiratory alkalosis as a result
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the kidneys compensate for this by increasing the excretion of bicarbonate leading to a metabolic acidosis
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Increased erythropoiesis
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hypoxia increases the production of erythropoietin to speed up the maturation of red blood cells, thereby increasing the oxygen-carrying capacity of the blood
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although a high plasma viscosity increases pulmonary vascular resistance
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Reduced pulmonary vascular resistance
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due to collateral circulations opening up between pulmonary arteries and veins
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