Unit 4 - Diffusion/perfusion Physio

Front 1

The order of structures 02 msut pass in diffusing from surfactant liquid surface in alveolar lumen to hemoglobin

Back 1

Surfactant containing liquid -> alveolar membrane -> basement membrane -> capillary endothelium -> plasma > erythrocyte membrane

Front 2

Is viscocity involved in determining diffusion rate?

Back 2

No; area, thickness, moelcularw eight, driving pressure, and solubility however do determine diffusion rate

Front 3

Which gas has the least solubility: C02, C0, 02, N20

Back 3

CO is .047 times as soluble in body fluids as N20

Front 4

How would blood flow through an aleveolar capillary that is 1/4 the legnth affect 02 diffusion

Back 4

P02 of the blood leaving the pulmonary capillary would be lower than P02 of the alveolus served by the capillary

Front 5

Which gases are diffusion limited: C02, CO, 02, N20

Back 5

C0; quantity of Co being carried from lungs does not increase with blood flow; i.e. transfer is not perfusion limited but diffusion limited

C02, 02 and N20 transfer in a healthy subject is not diffusion limited but perfusion limited

Front 6

Oxygen diffusion vs C02

Back 6

Oxygen diffuses through barriers about 1/20th as readily as C02

Front 7

Characteristic findings of a moderate diffusion block

Back 7

Hypoxia without hypercapnea bc C02 diffuses muche easier than 02 through barriers

Front 8

Can a severe diffusion block cause hypercapnea

Back 8

Yes; but moderate or mild diffusion blocks will not

Front 9

Will a pt with reduced diffusing capacity remain cyanotic at 100% 02

Back 9

No

Front 10

Will a pt with a right to left shunt due to tetralogy of fallot remain c yanotic at 100% 02

Back 10

Yes

Front 11

In an erect individual, where is lung perfusion highest

Back 11

Base of the lungs; it is here that V/Q is loweest bc of big perfusion denominator

Front 12

Wheer is V/Q ratio highest

Back 12

Superior part of the lung; while both ventilation and perfusion increase at the superior part, ventilation increases more than perfusion

Front 13

A transection at what vertebral point would stop respiration

Back 13

C3,4,5 keep the diaphragm alive

Front 14

Where does stimuli for the contraction of the diaphragm originate

Back 14

Floor of fourth ventricle; medulla; when depressed may become dependent upon impinging stimuli from peripheral chemoreceptors to continue functioning

Front 15

A cat has 9th/10th CN severed bilaterally and a section is made just above the apneustic center. How does this modulate the respiratory pattern

Back 15

Decerebrate rigidity and long inspiratory gasps (apneustic center is the only one firing)

Front 16

Location of the major central chemoreceptor area

Back 16

Medulla

Front 17

What does the apneustic center cause when separated from the rest of the brain

Back 17

Long inspiratory gasps

Front 18

Location of the pneumotaxic center

Back 18

Pons

Front 19

Function of the pneumotaxic center

Back 19

Inhibits inspiratory activity

Front 20

What structure is most important for increasing respiratory minute volume in response to small increases in PC02 of body fluids

Back 20

Medullary chemoreceptors/central chemoreceptors

Front 21

To what change are peripheral chemoreceptors most sensitive to

Back 21

Decreases in P02 in the arterial blood

Central chemoreceptors most sensitive to PC02

Front 22

Can H+ pass readily through the BBB?

Back 22

No

Front 23

Why would chemoreceptors in the carotid and aortic bodies respond faster to increases in arterial PC02

Back 23

Takes longer for blood to reach central chemoreceptors in the medulla; they produce a rapid increase in ventilation in response to increased PC02

Front 24

Resting conditions; sensitivity of peripheral receptors to P02 decreases from 500 to 100 mmHg

Back 24

Small change in ventilation; low sensitivity

Front 25

Resting conditions; sensitivity of peripheral receptors to P02 decreases from 70 to 40 mmHg

Back 25

Doubling of ventilation; high sensitivity

Front 26

decentralized peripheral receptors (cut 9th, 10th CN) will no longer respond to...

Back 26

hypoxia by causing an increased respiratory minute volume

Front 27

Why would CO poisoning or anemia not cause an increased frequency of impulses in afferent neurons from the carotid bodies

Back 27

Arterial P02 is independent of Hb concentration and wont be registered by peripheral chemoreceptors; there is still a reduction of oxygen content in the blood but not in the P02 of blood

Front 28

What TWO things would be detected by peripheral chemoreceptors

Back 28

Cyanide or low arterial P02

Front 29

Are peripheral chemoreceptors sensitive to reductions in blood flow

Back 29

No; there is a high blood flow rate anyways that also makes them insensitive to reductions in oxyhemoglobin concentrations

Front 30

It has been noted in breath holding experiments that lung distension increases the tolerance of the body for C02 and hypoxia. What is the mechanism of action?

Back 30

Inhibition of sensory neurons in the hypoglossal nerve; when lung distension inhibits inspiration this is the Hering-Breuer reflex; neither the hypoglossal nerve nor the diaphragm is involved in this mechanism

Front 31

Adaptations to high altitude

Back 31

1. Hyperventilation: increased respiratory rate, arterial P02, and arterial pH; decreased arterial PC02
2. Polycythemia: increased hemoglobin concentration in the blood; increased 02 carrying capacity of the blood; increased blood volume
3. Increased concentration of systemic capillaries; increased efficiency during exercise
4. 02 dissociation curve shifts to the right: increased conc. of 2,3DPG; hb releases more 02 at a P02 of 40 mmHg

Front 32

What two factors would increase arterial pressure in individuals who have lived at altitudes of 12K ft for a week

Back 32

Increased hematocrit (increased blood viscocity) = increased pressure
Low alveolar P02 = vasoconstriction (hypoxic shunting) = increased pressure

Front 33

Lecithin: spingomyelin ratio greater than 2:1 in amniotic fluid

Back 33

Adequate surfactant

Front 34

What happens in RDS in premature infants

Back 34

The small alveoli collapse into larger ones bc of lack of surfactant

Front 35

Effect on hypoxemia on coronary circulation

Back 35

Vasodilation

Front 36

Effect of hypoxemia on pulmonary circulation

Back 36

Vasoconstriction

Front 37

Which lung volume remains in the lungs after a tidal volume is expired?

Back 37

functional residual capacity

Front 38

A person has a vital capacity of 5L, a tidal volume of .5 L, an inspiratory capacity of 3.5L and a functional residual capacity of 2.5L. What is hsi expiratory reserve volume?

Back 38

1.5L; ERV = VC - IC (which is TV + IRV)

Front 39

Why is blood flow highest at the base?

Back 39

Gravity affects arterial hydrostatic pressure; blood flow is highest at the base, where arterial hydrostatic pressure is greatest and the difference between arterial and venous pressure is also greatest. This pressure difference drives blood flow.

Front 40

Which site along the bronchial tree is the site of highest resistance?

Back 40

Medium sized bronchi;

alveoli are arranged in parallel so their resistance is not the highest

Front 41

If am embolism blocked blood flow to the left lung, how would it effect alveolar P02 in the left lung relative to the P02 of inspired air

Back 41

They would be equal because there is no gas exchange occuring

Front 42

In a maximal expiration, the total volume expired is the same as which lung volume

Back 42

(Forced) vital capacity

Front 43

V/Q ratio in a shunt

Back 43

V/Q = 0

Front 44

V/Q ratio in dead space

Back 44

V/Q = infinity (no blood flow to dead space)

Front 45

Significant of an increased A-a gradient

Back 45

Signifies lack of 02 equilibrium between alveolar gas (A) and systemic arterial blood (a).

Front 46

Is bp lower in pulmonary caps or systemic caps

Back 46

Pulmonary

Front 47

Is the interstitial lower in the pulm caps or systemic caps

Back 47

Bc the thoracic cavity has a negative pressure, the interstitia lfluid is more engative in pulm circulation

Front 48

Which has the higher interstitial conc of proteins; skeletal muscle caps or pulm caps

Back 48

PUlm caps; they are more permeable to proteins than skeletal muscles

Front 49

How does an increase in p ulmonary blood flow during exercise affect pulmonary arterial resistance

Back 49

Decrease; increased blood flow dilates bc pulm arteries are very compliant

Front 50

End P02 in capillaries draining from the apices compared to the base

Back 50

At the apices, high V/Q ratio = higher P02
At the bases, low V/Q ratio = lower P02

Front 51

Why does the nonlinearity account for the normal differenc between alveolar and arterial oxygen tension (A-a) gradient?

Back 51

You cant just average end capillary P02

Front 52

Why do pts with in adequate surfactant or restrictive lung diseases have a normal FEV1/FVC ratio

Back 52

They cant expand as much to get air in to blow out and then there is increased elastic recoil so they can blow out a normal seeming amount

Front 53

Diffusion limited transport process

Back 53

Alveolar gas does not equilibrate with end pulmonary capillary concentrations

CO is an example of this; bc it strongly binds hemoglobin its partial pressure is almost zero

Front 54

02, N2, C02, N20 are alle xamples of gases limited by whta in ventilation

Back 54

Perfusion limited; diffuse easily across the membrane but limited by blood flow

Front 55

How is blood flow to the brain affected by PC02

Back 55

Low PC02 vasoconstricts
High PC02 vasodilates (to get more 02 to brain being depressed by the low pH)

Front 56

Hwo are long chain fatty acids coming into muscle cells initially processed

Back 56

they are activated as acyl coenzyme A and transported as acyl carnitine across the inner mitochondrial membrane into the matrix

Front 57

where is carnintine synthesized

Back 57

liver; this deficiency can be observed in preterm babies with lvier problems or dialysis patients

Front 58

blockage of transport of LCFA into the mitochondria deprives pt of energy; what will show in a muscle biopsy

Back 58

disrupts the muscle cell w accumulation of lipid droplets

Deficiencies in carnitine acyltransferase enzymes I and II can cause similar symptoms

Front 59

Which hormones stimulate the release of fatty acids into the blood

Back 59

glucagon, epinephrine and NE; these all activate adipocyte membrane adenylate cyclase

Front 60

Which is a prominent lipid enzyme activated by cAMP during fasting?

Back 60

Lipoprotein lipase

Front 61

What enzyme malfunctions in diseases associated w symptoms of high blood triacylglyceride levels and steatorrhea?

Back 61

Liporpotein lipase

Front 62

What must occur in fatty acids before they can be oxidized

Back 62

They must be activated by thiokinase (also known as acyl CoA synthase)

ATP is hydrolyzed to AMP plus pyrophosphate in this reaction. In contrast, the enzyme thiolase cleaves off acetyl CoA units from B-ketoacyl CoA, while it forms thioesters during B oxidation

Front 63

Where are ketone bodie synthesized?

Back 63

B-hydroxybutyrate and aceotacetate are synthesized in liver mitochondria; liver produces ketonebodies under conditions of asting associated with high rates of fatty acid oxidation


Higher amounts of B-hydroxyutyrate than acetoacetate produced, since high liver levels of NADH lead to the dehydrogenation of acetoacetate