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Resp > 02b: Spirometry, Transport, Hb > Flashcards

02b: Spirometry, Transport, Hb Flashcards

1
Q

Spirometers can be used to measure lung volumes except those that include (X)

A

X = RV

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2
Q

T/F: minute ventilation can be recorded from spirometry.

A

True (VT*f)

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3
Q

ERV + IC

A

VC

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4
Q

IC is measured from end-(inspiration/expiration) of (forceful/relaxed) breathing. And IRV?

A

IC: end-expiration of VT (relaxed breathing)
IRV: end-inspiration of VT (relaxed breathing)

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5
Q

FVC is obtained when subject, following max (inspiration/expiration), immediately (inhales/exhales) as rapidly, forcefully, completely as possible.

A

Inspiration;

Expires/exhales

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6
Q

FEV1 is amount of air (inhaled/exhaled) in first (sec/min) of (X).

A

Exhaled;
Second
FVC

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7
Q

Normal FEV1/FVC ratio:

A

80% (0.8)

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8
Q

In (restrictive/obstructive) ventilatory pattern, FEV1 and FVC are (increased/reduced) proportionately. How does their ratio change? What’s the problem with lung/airways?

A

Restrictive; reduced
Ratio unchanged
Lung volume decreased in these cases

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9
Q

In (restrictive/obstructive) ventilatory pattern, FEV1 and FVC are (increased/reduced) disproportionately. How does their ratio change? What’s the problem with lung/airways?

A

Obstructive (airways obstructed);

FVC decreased or normal; FEV1 decreased to less than 80% normal; ratio decreased to less than 70% normal

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10
Q

T/F: Barometric P varies with altitude.

A

True

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11
Q

Atmospheric air essentially consists of which gases?

A

21% O2 and 79% N2

other gases contribute very little

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12
Q

Partial pressure of gas dissolved in liquid: partial pressure in (gas/liquid/solid) phase at which the liquid (gives/takes) it up.

A

Gas;

Neither gives it up nor takes it up (equilibrated; no net change)

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13
Q

Oxygen carried in blood in which forms? Star the reservoir.

A
  1. Dissolved

2. HbO2*

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14
Q

Henry’s law allows calculation of:

A

Concentration of gas dissolved in liquid = (S*P)

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15
Q

List the Bunsen solubility coefficients of CO2 and O2 at body T.

A

O2: 0.003
CO2: 0.075

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16
Q

CO2 is (more/less) soluble in water than O2 and (more/less) soluble than N2. Why?

A

More soluble than both; interacts with polar H2O molecules

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17
Q

More molecules of (CO2/O2) must be dissolved in water to establish equilibrium.

A

CO2

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18
Q

Gas solubility (increases/decreases) with increasing T.

A

Decreases

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19
Q

Hb normally present in blood at concentration of (X). One gram of Hb realistically binds (Y) O2.

A 
X = 15 g/100 mL blood
Y = 1.34 mL
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20
Q

Hb % saturation is a function of (X). The shape of the plot is (Y) and three key points about it are:

A 
X = PO2
Y = sigmoid
  1. Flat upper portion (constant arterial O2 saturation)
  2. Steep slope under PO2 of 40 (allows release of O2 in tissues)
  3. Arterial blood 98% saturated, only 2% increase available
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21
Q

Hb saturation curve is drawn under specified conditions. List them.

A
  1. Hb concentration
  2. PCO2
  3. T and pH
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22
Q

Increasing PCO2 changes Hb saturation curve in which way? And increasing PO2?

A

Shifts entire curve right (Bohr);

No shift, only move up along sigmoid curve

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23
Q

The Hb P(50) is the (X) at which (Y). What’s the normal, physiological value for blood?

A 
X = PO2
Y = Hb is 50% saturation

26 mmHg

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24
Q

The Mgb P(50) is (X) and the HbF P(50) is (Y).

A 
X = 5 mmHg
Y = 15-20 mmHg

For comparison: HbA P(50) is 26 mmHg

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25
Q

Which mechanisms are in place to ensure delivery of O2 from blood to muscle and placenta?

A

Mgb and HbF have significantly higher affinity for O2 than HbA

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26
Q

CO binds Hb with affinity that is (X) times greater than that of O2. Our body produces CO, as a result of (Y), but only (Z)% of our Hb is occupied by it.

A 
X = 240
Y = porphyrin breakdown
Z = 1-2
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27
Q

T/F: CO not only binds Hb with high affinity, but also shifts dissociation curve right, preventing proper O2 binding.

A

False - shifts curves left (O2 can’t unload properly in tissues)

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28
Q

CO2 carried in blood in which forms? Star the ones found in RBC. Double star the ones found in plasma.

A
  1. Dissolved
  2. Bicarbonate
  3. Carbamino compounds (bound to protein)

All forms found in both RBC and plasma

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29
Q

Carbonic anhydrase catalyzes (formation/breakdown) of (X).

A

Formation of

X = H2CO3 (from H2O and CO2)

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30
Q

(X) enzyme catalyzes formation of carbamino-Hb.

A

None; CO2 reacts non-enzymatically with free amino group to form carbamino compounds

31
Q

Arterial blood: most, (X)% of CO2 is in which form?

A

X = 90

HCO3-

32
Q

T/F: Forms of CO2 contributing to gas exchange is in proportion to their amounts in blood (so 90% contribution by HCO3-).

A

False

33
Q

CO2 a-v exchange: List the three forms and the respective contribution from each.

A
  1. HCO3: 60%
  2. Carbamino-Hb: 30%
  3. Dissolved: 10%
34
Q

The total CO2 concentration is function of (X). The shape of the plot is (Y).

A 
X = PCO2
Y = essentially linear
35
Q

The locus of the CO2 concentration curve depends on which factor(s)?

A

Hb saturation;

Haldane effect: lower HbO2 (deoxygenated blood) shifts curve left (more CO2 content for given PCO2)

36
Q

What’s isohydric shift?

A

Change in H+ load with no change in pH

37
Q

In lungs, uptake of O2 aids in (binding/release) of CO2 by its (uptake/release) of protons. Explain.

A

Release; release;

HbO2 stronger acid than deoxy-Hb, so gives up protons and shifts equation to more CO2 production

38
Q

In terms of H+ buffering, the (X) group of (Y) AA is crucial. This is partly because (Y)’s effective range of buffering is in which pH range?

A 
X = imidazole
Y = histidine

5.7-7.7 (includes physiological pH)

39
Q

T/F: Hb, with its 4 histidines, has buffer capacity that’s 6x greater than other plasma proteins.

A

False - has many histidines, not just 4; other fact is true

40
Q

Quantitative defect in globin subunit production is (SCD/thalassemia).

A

Thalassemia

41
Q

SCD mutation is (X). Most common clinical manifestation of SCD is (Y).

A 
X = missense (Glu to Val) in beta chain of HbA
Y = vaso-occlusive crisis
42
Q

HbSC isoelectric point (lower/higher) than HbA, so at given pH, its net charge above its pI is more (positive/negative) and below its pI is more (positive/negative).

A

Higher;
less negative (closer to 0)
more positive

43
Q

T/F: Thalassemias associated with low level functional Hb, but normal RBC production/turnover.

A

False - decreased RBC production and fast RBC turnover (anemia)

44
Q

(SCD/Thalassemia) associated with marked expansion of ineffective bone marrow.

A

Thalassemia

45
Q

Severity of thalassemia depends on:

A

How many of the 4 alpha or 2 beta genes are missing/silent

46
Q

(Alpha/beta)-globin pathology is symptomatic in utero.

A

Alpha

47
Q

Iron chelation is therapy to treat iron (deficiency/overload).

A

Overload

48
Q

Heinz bodies are:

A

RBC inclusions composed of denatured Hb

49
Q

T/F: In alpha-thal, Hb cannot be assembled at all.

A

False - Hb tetramers formed from only beta-chains

50
Q

Alpha-thal: The Hb is that is formed binds O2 with too (high/low) affinity and no cooperativity.

A

High

51
Q

Thalassemia can also result from abnormally long (alpha/beta) globin molecules due to (X) mutation.

A

Alpha;

X = elimination of stop codon

52
Q

T/F: Both alpha and beta thalassemias cause precipitation in bone marrow.

A

False - alpha-thal doesn’t since the Hb tetramers formed from beta globin are soluble (except in old RBCs)

53
Q

T/F: In beta-thal, Hb cannot be assembled at all.

A

False - Hb tetramers formed from only alpha-chains

54
Q

T/F: In beta-thal, the Hb that’s assembled lack O2 binding cooperativity and precipitates.

A

True

55
Q

What’s the cause for expansion of ineffective bone marrow in beta-thalassemia?

A

Excess alpha chains damages RBCs and precursors (anemia)

56
Q

Major cause of morbidity/mortality in beta-thal is (X) from (increased/decreased) intestinal absorption and transfusions.

A

X = iron deposits in endocrine organs, liver, and heart;

Increased

57
Q

T/F: Hereditary persistence of fetal Hb has no deleterious effects.

A

True

58
Q

Two most important acquired Hb-pathies are (X).

A

X = CO poisoning and methemoglobinemia

59
Q

Smoking can lead to (1o/2o) polycythemia, which is (X). This is a result of chronically (high/low) (Y) levels.

A

2o;
X = hematocrit greater than 55%
High;
Y = carboxyHb

60
Q

T/F: Excess CarboxyHb leads to blue-tinted skin, indicative of cyanosis.

A

False - cyanosis is masked since carboxyHb is cherry-red in color

61
Q

T/F: Excess MetHb leads to blue-tinted skin, indicative of cyanosis.

A

True

62
Q

Congential Methemoglobinemia arises from globin mutations that (X) or (Y).

A 
X = stabilize iron in ferric state
Y = impair reduction enzymes (i.e. MetHb reductase)
63
Q

Acquired Methemoglobinemia arises from toxins that (X), such as (Y).

A 
X = oxidize heme iron
Y = nitrate-containing compounds
64
Q

(X) is a green derivative of Hb and usually induced by (Y). What allows conversion back to normal Hb?

A 
X = sulfHb;
Y = drugs

Can’t be converted back

65
Q

T/F: Sulfhemoglobinemia causes cyanosis at low blood levels.

A

True

66
Q

High-affinity Hb-pathy: you’d expect (rise/fall/no change) in hematocrit and blood viscosity.

A

Rise in both

67
Q

List three clinical tests that are based on Hb.

A
  1. Pulse oximetry
  2. fMRI
  3. HbA1c (glycosylated Hb)
68
Q

Pulse oximeter transmits (X) light, absorbed by (Y).

A 
X = red (660 nm) and IR (940 nm)
Y = deoxyHb (red) and oxyHb (IR)
69
Q

fMRI: There’s a (higher/lower) magnetic field with oxyHb because…

A

Lower; HbO2 is diamagnetic

Fe is highly magnetic and deoxyHb is paramagnetic (weakly magnetic)

70
Q

Glycosylated Hb is (reversibly/irreversibly) formed (quickly/slowly) from (X) reacting with (Y).

A

Irreverisbly; slowly;
X = glucose
Y = N-term of Hb beta chains

71
Q

HbA1c provides an assessment of (chronic/acute) (hyper/hypo)-glycemia.

A

Chronic; hyperglycemia

72
Q

What’s the HbA1c cutoff for diabetes?

A

6.5% glycosylated Hb

73
Q

Pulse oximetry: proportion of HbO2 is calculated

from the ratio of (X).

A

X = 660/940 absorbance

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