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Physiology & Pathology > Translational Physiology Block 5 > Flashcards

Translational Physiology Block 5 Flashcards

1
Q

What are features of COPD?

A

prolonged expiratory phase (decreased FEV1/FVC), wheezing, increased chest diameter (barrel and breath at higher lung volumes), increased residual volume (air trapping; increased functional residual capacity); decreased elasticity (emphysema), increased airway resistance (bronchitis; decrease in airflow); a cough that produces mucus; reduced mechanical tethering

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2
Q

What is normal FEV1/FVC ratio?

A

0.8 (in first second of expiration)

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3
Q

What are the causes of COPD?

A

Alpha-1-Antitrypson Deficiency (anti inflammatory against neutrophil elastases); smoking

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4
Q

What are the features of fibrosis?

A

decreases residual volume, decreased total lung capacity and decreased functional residual capacity; decreased lung compliance (greater effort needed); normal or elevated FEV1/FVC; rapid shallow breaths

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5
Q

Describe asthma.

A

two forms (intrinsic: exercise and stress; extrinsic: allergens); airways become constricted; can be treated with broncho-dilators and anti-inflammatory agents

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6
Q

What are the five causes of hyoxemia?

A

shunt, V/Q mismatch, inspired air, hypoventilation, and diffusing capacity of the lung (fibrosis)

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7
Q

What is pneumonia? is it restrictive or obstructive?

A

inflammation of the lung caused by infection with bacteria, viruses, and other organisms; restrictive

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8
Q

Describe the fetal circulation.

A

blood enters from the umbilical vein and is shunted by the ductus venosus to the inferior vena cava; blood may then be shunted from the right atrium to the left atrium via the foramen ovale; some blood may enter the right ventricle and is shunted from the the pulmonary artery to the aorta via the ductus arteriosus

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9
Q

How does pulmonary circulation change from fetus to birth?

A

in the fetus, the circulation is not patent (hypoxic vasoconstriction; very high pressures that are greater than the systemic circulation); following birth, the baby may inspire air which opens up the vessels and results in closing of the ducts (resistance and pressure profiles changes to a low pressure system)

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10
Q

What are key events in the development of the baby lung? what complications may arise?

A

resorption of fluid, pulmonary vasorelaxation, and continuous breathing; hyperoxia, apnea, and volutrauma (alveolar distension with mechanical ventilation)

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11
Q

Describe neonatal respiratory distress syndrome.

A

affects premature babies; atelectasis (collapse of alveoli); hypoxemia, hypercapnia (carbia); V/Q mismatch; hypoventilation

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12
Q

Surfactant has a greater effect on smaller or larger alveoli?

A

smaller

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13
Q

What should not be given to a patient with respiratory distress syndrome?

A

oxygen which may cause oxidative stress

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14
Q

How is respiratory distress syndrome treated?

A

exogenous surfactant, endotracheal tube, CPAP device; glucocorticoids (stimulates resorption of fluid if there is an infection)

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15
Q

What are features of chronic neonatal lung injury?

A

(seen at later ages); decreased FEV1 and increased incidence of asthma; etiology: oxidative stress, mechanical stress, or infection causing remodeling of the lung and altered vasculature

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16
Q

Describe a positive pressure ventilator.

A

gas tank with an attached humidifier and pump; two different gas lines close to the body to avoid increased dead-space; soda lime to dilute the expired carbon dioxide

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17
Q

Why would a patient need a ventilator?

A

decreased ventilation caused by CNS depression, structural lung injury, or neuromuscular disease; hypoxemia

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18
Q

What are the goals of a ventilator?

A

increase ventilation (primarily for hypoventilation), restore tidal volume, restore FRC; decrease demand on respiratory muscles; supply necessary oxygen

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19
Q

What is the importance of extrinsic PEEP?

A

Setting a PEEP prevents lungs from continuously collapsing and re-expanding (limiting injury); decreased effort needed for breathing; recruitment of collapsed alveoli

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20
Q

Are settings with higher or lower tidal volumes better for the health of the patient?

A

lower

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21
Q

What settings are important in treating a patient with COPD on a ventilator?

A

reducing auto-peep (prevent air trapping); maximizing respiratory rate (slow); maintain patients lung volumes at midpoint (high compliance)

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22
Q

What is optimal PEEP in respiratory distress syndrome?

A

lower inflection point just above alveolar collapse (+ pressure controlled ventilation to prevent volutrauma)

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23
Q

What is peak pressure on a ventilator wavefrom proportional to?

A

resistance plus reciprocal of compliance

24
Q

What is the plateau pressure on a ventilator waveform proportional to?

A

reciprocal of compliance

25
Q

How do you calculate resistance on a ventilator waveform?

A

pulse pressure - plateau pressure

26
Q

What occurs to hemodynamics of a patient on a ventilator?

A

decreases systemic venous return (increased thoracic pressure); right ventricular afterload is increased; left ventricular preload and afterload are decreased

27
Q

Why is auto-PEEP a negative indicator for respiration?

A

incomplete expiration prior to inspiration and possible alveolar distension

28
Q

What happens to a stationary air-water interface? Why is this relevant to respiration?

A

build up of water vapor (47 mm Hg); upper airways humidify inspired air

29
Q

Does carbon dioxide or oxygen have a higher solubility in blood?

A

carbon dioxide; partial pressure x solubility constant

30
Q

What is BTPS? ATPS? STPD?

A

body temperature and pressure saturated with water (37 degrees Celsius and 760-47 mm Hg); ambient temperature and pressure saturated with water (25 degrees Celsius and 760-24 mm Hg); standard temperature and pressure dry (O degrees and 760 mm Hg; blood)

31
Q

What is the equation to calculate lung volume changes in spirometry?

A

(P1V1/T1) = (P2V2/T2)

32
Q

What are examples of restrictive lung disease?

A

pneumothorax (air); pleural effusion (fluid); edema; spinal diseases; neuromuscular disorders

33
Q

How can hemoglobin be used to monitor diabetic patients?

A

nonenzymatic glycosylation of HbA. HbA 1a , HbA 1b , and HbA 1c form when intracellular glucose 6-phosphate (G6P) reacts with the terminal amino groups of the β chains of HbA.

34
Q

What is the composition of sickle hemoglobin; what are the pathological features?

A

valine replaces glutamate on beta chain; hemolysis and decreased blood flow

35
Q

What is a pulse oximeter?

A

Because oxygenated Hb and deoxygenated Hb absorb red and infrared light differently, the pulse oximeter can calculate Sa O 2 from the ratio of pulsatile light absorbed at the two wavelengths (veins and capillaries do not pulse)

36
Q

How can shunt’s be diagnosed?

A

administering pure oxygen

37
Q

What is A-a gradient?

A

alveolar oxygen partial pressure - arterial oxygen partial pressure

38
Q

What is dyspnea?

A

feeling short of breath; may be caused by increased airway resistance

39
Q

Define eupnea.

A

normal breathing

40
Q

What is a sigh or yawn?

A

A sigh is a slow and deep inspiration, held for just a moment, followed by a longer than normal expiratory period; stimulates release of surfactant; stimulated by hypoventilation (respiratory acidosis and hypoxia)

41
Q

Describe a cough.

A

a forced expiratory effort against a closed glottis raises intrathoracic and intra-abdominal pressures to very high levels. The glottis then opens suddenly, and the pressure inside the larynx falls almost instantaneously to near-atmospheric levels. This sudden drop in luminal pressure produces dramatic increases in the axial (alveolus to trachea) pressure gradient that drives airflow. In the trachea, this pressure drop also decreases the radial transmural pressure difference across the tracheal wall, thereby collapsing the trachea, especially the membranous (i.e., noncartilaginous) part of the trachea.

42
Q

How is a sneeze different from a cough?

A

preceded by deep inspiration; a sneeze involves pharyngeal constriction during the buildup phase and an explosive forced expiration through the nose as well as the mouth. This expiration is accompanied by contraction of facial and nasal muscles, so that the effect is to dislodge foreign bodies from the nasal mucosa.

43
Q

Describe breathing during sleep.

A

During non–rapid eye movement (NREM) sleep, the regularity of eupneic breathing increases; also, the sensitivity of the respiratory system to CO2 decreases compared with wakefulness, and the outflow to the muscles of the pharynx decreases. During rapid eye movement (REM) sleep, the pattern of breathing becomes markedly irregular, sometimes with no discernible rhythm, and the sensitivity of the respiratory system to CO2 decreases further.

44
Q

Describe sleep apnea.

A

airway collapse is due to an exaggeration of the normal decrease in airway tone during sleep, superimposed on the structural problem of reduced airway diameter due to obesity. This is a common disorder associated with severe and excessive snoring, poor and interrupted sleep, daytime somnolence, and behavioral changes, possibly leading ultimately to hypertension and cardiac arrhythmias.

45
Q

What is the effect of cholinergic agonists on bronchioles?

A

bronchoconstriction

46
Q

What is the site of highest airway resistance? Is there a greater effect on inspiration or expiration?

A

medium-sized bronchioles; decreased expiratory airflow

47
Q

What adrenergic receptor causes bronchodilation?

A

beta 2 (also causes vasodilation)

48
Q

What is the cause of wheezing in COPD? asthma?

A

damage to lung parenchyma and increased intrathoracic pressures; bronchoconstriction causes turbulent airflow

49
Q

How does hypoxia alter cellular metabolism? what happens to pH? and what is the compensation for the change in pH?

A

anaerobic respiration; metabolic acidosis; increased ventilation (Kussmal breathing)

50
Q

What is the normal response to hypoxia?

A

hypoxic vasoconstriction; increased EPO; increased muscle capillary density; respiratory alkalosis (hyperventilation; peripheral chemoreceptors) compensating by metabolic acidosis (secreting bicarbonate into urine)

51
Q

What is the acid-base abnormality associated with COPD?

A

decreased ventilation leads to hypercapnia (respiratory acidosis)

52
Q

Is V/Q mismatch present in a patient with COPD?

A

No; alveolar ventilation and perfusion (pulmonary capillary loss) may both be decreased

53
Q

What acid-base abnormality can arise from having to much ventilation on a ventilator?

A

respiratory alkalosis is compensated by metabolic acidosis

54
Q

T/F: Capillary loss is associated with damage to lung parencyhma?

A

T

55
Q

Why do COPD patients hypoventilate?

A

decreased responsiveness to hypercapnia; increased V/Q mismatch (possibly); decreased diaphragm function (muscle fatigue)

56
Q

What is the effect of a chest wound on the thoracic cavity?

A

lungs collapse and chest wall is sprung out

Physiology & Pathology (40 decks)

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