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24 Cards in this Set
- Front
- Back
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Chemical control of breathing
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1) Arterial PO2
2) Arterial PCO2 3) Arterial [H+] |
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Where is the center for voluntary control of respiration located?
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Cerebral cortex. Sends impulses to respiratory motor neurons via the corticospinal tracts
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Where is the autonomic center for control of respiration located?
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Pacemaker cells in the medulla, part of the pre-Bötzinger complex
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Exception to the reciprocal inhibition of respiration is due to
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a small amount of activity in phrenic axons shortly after inspiration, working to make breathing more smooth
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Side effect that limits the use of opiods in pain management?
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Depression of respiration. However, treatment with 5-HT4 agonists may block this inhibitory effect
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The rhythmic discharge of neurons in the medulla is spontaneous. However, it can be modulated. By what?
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1) Neurons in the pons. Pneumotaxic center in the medial parabrachial and Kölliker-Fuse nuclei of the dorsolateral pons.
2) Afferents in the vagus from receptors in the airways and lungs. |
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Factors that increase the level of respiratory neuron activity in the medulla
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1) Rise in PCO2
2) Rise in [H+] 3) Rise in PO2 |
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Type I cells of aoartic and carotid bodies are excited by
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Hypoxia. Predominantly release dopamin, acting on D2 receptors.
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Nonchemical control affecting the respiratory center (4)
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1) Vagal afferents from receptors in airways and lungs
2) Afferents from the pons, hypothalamus, and limbic system 3) Afferents from proprioceptors 4) Afferents from baroceptors; arterial, atrial, ventricular, and pulmonary |
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Effect of hypoxia on Type I cells ([...]bodies)
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O2 sensitive potassium channels are activated; conduction reduced proportionally to the degree of hypoxia, leading to transmitter release by means of increased calcium influx through L-type channels
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Contrast between pulmonary and systemic artery response to hypoxia
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1) Pulmonary response is vasoconstriction (O2 sensitive K+-channels)
2) Systemic response is vasodilation (ATP-dependent K+-channels) |
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Effects of denervation of carotid and aortic bodies
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1) Little change in ventilation at rest
2) Ventilatory response to hypoxia is lost 3) Ventilatory response to CO2 is reduced by 30% |
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Chemoreceptors in the brainstem are located
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1) On the ventral surface of the medulla
2) In the vicinity of the solitary tract nuclei 3) The locus ceruleus 4) Hypothalamus |
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The effects of CO2 on respiration are mainly due to
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1) Its movement into CSF and brain interstitial fluid
2) It increases [H+] and stimulate H+-sensitive receptors |
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What is the technical term for accumulation of CO2 in the body, and what are the effects?
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1) It is called hypercapnea
2) Depress the CNS 3) Headache 4) Confusion 5) Coma (CO2 narcosis) |
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Two reasons the increase in ventilation due to hypoxia rises only slightly, until the O2 pressure falls below 60 mmHg
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1) Hb is a weaker acid than HbO2, and thus there is a decrease in H+, inhibiting respiration
2) The increase in respiration that does occur, lowers the PCO2, which also inhibit respiration |
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Effect of hypoxia on the CO2 response curve
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Hypoxia makes the individual more sensitive to increases in arterial PCO2
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Effects of H+ on the CO2 response curve
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1) Stimulatory effects of H+ and CO2 are additive
2) For every nmol rise in H+, the curve shifts 0.8mmHg to the left 3) Accounts for about 40% of the ventilatory response |
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What is the Hering-Breuer inflation and deflation reflexes?
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1) An increase in duration of expiration produced by steady inflation of the lungs
2) A decrease in duration of expiration due to marked deflation of the lung |
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Response to activation of rapidly acting fibers
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1) Hyperpnea
2) Cough 3) Bronchoconstriction 4) Mucus secretion |
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Response to activation of slowly adapting fibers
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1) Inspiratory time-shortening
2) Hering-Breuer reflexes 3) Bronchodilation 4) Tachycardia |
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Response to activation of pulmonary and bronchial C fibers
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1) Apnea, followed by rapid breathing
2) Bronchoconstriction 3) Bradycardia 4) Hypotension 5) Mucus secretion |
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Pathway for voluntary control of respiration
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Pass from the neocortex to motor neurons that innervate the respiratory muscles, bypassing the medullary neurons. Thus, it is possible to live without autonomous regulation of breathing. This condition is called Ondines curse
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The hyperventilation in shock is due to
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Chemoreceptor stimulation caused by acidosis and hypoxia,secondary to local stagnation of blood flow, and is not baroreceptor mediated.
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