respiratory Flashcards

Question

why are pigs and cows at higher risk of hypoxic hypertension?

Answer 1

thickest muscular layer of the arteries and little NO secretion by endothelium. hypoxia leads to vasoconstriction, with no NO to counteract it. High mountain disease (brisket disease) is right heart failure due to hypoxic pulmonary hypertension in cattle residing at high altitudes

Answer 2

C- in cows the Mediastinum thick and able to withstand considerable pressure difference between the 2 pleural cavities. No fenestrations Millers: In the dog the tissue in the mediastinum is extremely scanty (small or insufficient), but the pleura that covers it is not fenestrated. Therefore one lung can be collapsed independently of the other. from thrall: In most dogs and cats, the mediastinal pleural layers do not form an anatomic barrier between the left and right pleural spaces, because normal mediastinal pleura contain fenestrations. Thus, unilateral pleural fluid or gas is not usually contained to one side by the mediastinum. For example, 22 of 24 dogs having air injected into one pleural space quickly developed bilateral pneumothorax.1 Pleural fluid or gas may remain unilateral if the mediastinal pleura is not fenestrated; if the normal fenestrations become closed as a result of inflammation or plugging; or if the pleural fluid is too viscid to pass through a normal fenestration.

Answer 3

B https://en.wikivet.net/Avian_Respiration_-_Anatomy_%26_Physiology#:~:text=Avian%20Trachea,-The%20avian%20trachea&text=The%20trachea%20can%20be%20palpated,terminal%20part%20of%20the%20trachea.

Answer 4

Paired: cervical, cranial thoracic, caudal thoracic, abdominal Clavicular: unpaired, located dorsal and caudal to the crop in the thoracic inlet and has intra and extrathoracic components Cervicocephalic air sacs: o Not connected to the lungs but connect to the caudal aspect of the infraorbital sinus lots of bones pneumatized can vary between species- humerus, clavicle, coracoids, vertebrae, ribs femur, + others

Answer 5

clavicular air sac

Answer 6

constriction acetylcholine muscarinic also increases mucus secretion, causes vasodilation of the pulmonary vessels and regulates inflammation bronchoconstriction also occurs in response to inflammatory mediators

Answer 7

tall pseudostratified columnar ciliated respiratory epithelium

Answer 8

PVR is low in the normal resting animal and it decreases even further when pulmonary blood flow and/or pulmonary vascular pressures increase, as occurs during exercise. This is because an increase in pressure recruits previously unperfused vessels. Additionally, pulmonary vascular smooth muscle relaxes during exercise so that small arteries and veins dilate. Together these changes increase the capacity of the pulmonary vasculature. In the systemic circulation, arteries and arterioles provide the primary source of vascular resistance; in the pulmonary circulation, the resistance is more evenly distributed across the arteries or arterioles and capillaries, with smaller contributions from veins (Fig. 46.4). Unlike the arterioles in the systemic circulation, the small arteries in the pulmonary circulation neither provide large resistance nor dampen the arterial pulsations; consequently, pulmonary capillary blood flow is pulsatile.

Answer 9

A Although the pulmonary circulation has both alpha-adrenergic receptors (which cause vasoconstriction) and beta-adrenergic receptors (which cause vasodilation), the net effect of sympathetic activation is vasoconstriction. flight response to move blood to the muscles. during exercise the vessels dilate... This dilation is in part passive as a result of the increase in intravascular pressure, which is a result of the increased blood flow. In addition, flow-induced release of nitric oxide from the endothelium also causes relaxation of smooth muscle and vessel dilation.

Answer 10

20% azygous 80% pulmonary veins about 20% of bronchial venous blood returns to the right atrium by means of the azygous vein. In this manner, deoxygenated blood from the bronchial veins is returned to the right heart, which is typical of the systemic circulation. In contrast, the remaining approximately 80% of deoxygenated bronchial venous blood drains into the pulmonary veins and then the left atrium; this unique and seemingly illogical configuration results in deoxygenated blood from the bronchial veins mixing with the oxygenated blood leaving the lungs in the pulmonary veins and returning to the left heart. Vascular anastomoses between the bronchial capillaries or veins and pulmonary capillaries or veins allow deoxygenated blood from the bronchial circulation to bypass the alveoli and return to the left atrium without having participated in gas exchange. This vascular configuration is one form of an anatomic shunt because the deoxygenated blood leaving the bronchial circulation does not flow past alveoli and become oxygenated but rather is shunted directly into the left side of the heart (left atrium) for distribution in the systemic arterial circulation. The small amount of deoxygenated bronchial blood mixing with the oxygenated blood leaving the lungs contributes to the small difference between the alveolar and arterial O2 partial pressures that occurs under normal conditions

Answer 11

When O2 is high (98% saturated), it combines loosely and reversibly to the heme portion of the hemoglobin - When O2 low (75% saturated), the oxygen is released from hemoglobin - Small amount of O2 (3%) travels dissolved in the blood without hemoglobin - The binding of oxygen and hemoglobin is determined by oxygen tension. - The affinity of hemoglobin for oxygen varies with blood temperature, pH, carbon dioxide tension, and the intracellular concentration of certain organic phosphates.

Answer 12

B - Binding of oxygen with hemoglobin causes displacement of CO2 from the blood into the alveoli. This is because bound hemoglobin is a stronger acid so there is reduction of carbaminohemoglobin, and the excess hydrogen ions reverse the bicarbonate reaction to form CO2 which can diffuse out of the alveolus. This effect doubles the rate of pickup of CO2 in the tissues and release in the lungs.

Answer 13

A is true pH of the blood --> low pH lowers the affinity of hemoglobin for O2. - Alkalosis shifts the curve to the left à increased binding Temperature: An increase in temperature decreases the oxygen binding (shifts the oxygen–hemoglobin dissociation curve to the right). Like increased acidity, increased temperature is a by-product of increased metabolism. 2,3-Bisphosphoglycerate (BPG)- production increases with increased metabolism. PCO2 - increased PCO2 is associated with decreased pH à less oxygen binding

Answer 14

A in 100% oxygen it can be 600mmHg

Answer 15

D CO2 is produced in tissues; therefore tissue PCO2 is higher than the PCO2 of the blood arriving in the capillaries. CO2 diffuses down a concentration gradient from the tissues into the blood. When the blood leaves the tissues, its PCO2 has risen from approximately 40 mm Hg to 46 mm Hg, with exact values depending on the tissue-specific ratio of blood flow to metabolism. This higher CO2 content of deoxygenated blood results from the higher buffering capacity of deoxyhemoglobin, compared with O2-saturated hemoglobin. co2 transported in rbc and dissolved

Answer 16

Under normal circumstances, end tidal CO2 values are very similar to but slightly lower than PaCO2 (up to 5 mm Hg difference). The normal difference between end tidal CO2 and PaCO2 is due to the small amount of alveolar dead space ventilation, in which ventilated alveoli are not perfused so CO2 does not enter the air of the affected alveoli Furthermore, the gradient between end tidal CO2 and PaCO2 can be a useful diagnostic aid for various respiratory and circulatory abnormalities. For example, in uncomplicated hypoventilation where CO2 production exceeds alveolar ventilation, the CO2 increase in the blood results in a similar increase in CO2 in alveolar air; thus the end tidal CO2 to PaCO2 difference remains unchanged. In contrast, the end tidal CO2 to PaCO2 difference is elevated by increases in alveolar dead space ventilation such as result from pulmonary thromboembolism, ventilation to perfusion mismatching, hypovolemia, and decreased cardiac output, among other conditions. Obstructive lung diseases that limit exhalation also increase the end tidal CO2 to PaCO2 gradient

Answer 17

Lung disease accentuates VA/Q mismatching because of obstruction of airways, flooding of alveoli with exudates, and local obstructions to blood flow. This mismatching has a major effect on oxygen exchange but little effect on the exchange of carbon dioxide. - In the case of oxygen, overventilation of some alveoli does not compensate for underventilation of others (due to saturation of Hb). in contrast to oxygen, carbon dioxide is very soluble, and because its dissociation curve is almost linear, the overventilated alveoli can compensate for those that are underventilated. For this reason, hypercapnia (increased PaCO2), rarely occurs in the presence of lung disease.

Answer 18

pH PaCO2 HCO3 base excess

Answer 19

respiratory alkalosis the kidneys take longer to respond to this than the lungs take to compensate for a metabolic acidosis

Answer 20

metabolic alkalosis

Answer 21

metabolic acidosis low HCO3 hyperventilation to release more co2

Answer 22

loss of H+ ions through vomiting hyochloremic metabolic alkalosis

Answer 23

acidosis Increases in K+ cause metabolic acidosis by inhibition of NH3 synthesis and NH4+ excretion.

Answer 24

lymphatic blockage cardiac failur- increased pressure in capillaries and increased transudatation of interstitial fluid, reduced plasma oncotic pressure, any process breaking down the capillary membranes (inflammation, infection)

respiratory Flashcards

(53 cards)