03b: Buffers, Immuno, Perfusion Flashcards

1
Q

Normal arterial blood pH is (X), meaning there’s (Y) concentration of H+.

A
X = 7.4
Y = 40 nM
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2
Q

Normal body pH range is (X), meaning normal H+ range is (Y).

A
X = 7.38-7.42
Y = 42-38 nM
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3
Q

Tolerated pH range in our body is (X), meaning tolerated H+ range is (Y).

A
X = 6.8-7.8
Y = 158-16 nM
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4
Q

List the sources of acids in our body.

A
  1. Oxidation of fuel (CO2 production forms H2CO3)

2. Metabolism (H2SO4, H3PO4, uric acid)

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5
Q

Body produces volatile and fixed acids. What’s the difference?

A

Volatile (respiratory) acids can be excreted via lungs; non-volatile are products of metabolism and are “fixed” in body until kidney excretion

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6
Q

Optimal buffering occurs when pH value is (smaller/larger) than pKa.

A

Equal!

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7
Q

List some good body buffers, with pKa near (X).

A

X = 7.4;

  1. Phosphate buffer system (6.8)
  2. Proteins, esp with His (7-7.8); Hb
  3. H2CO3 system (6.1)
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8
Q

Buffer is substance that (minimizes/maximizes) change in (X) by doing what?

A

Minimizes;
X = pH

Donating/accepting protons

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9
Q

Acids (donate/accept) protons and bases (donate/accept) protons.

A

Donate; accept

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10
Q

Isohydric principle states that:

A

when several buffers are in solution, they’re all in equilibrium with the H+

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11
Q

Isohydric principle: the (X) of each buffer will dictate (Y) ratio.

A
X = pKa
Y = base concentration to weak acid concentration
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12
Q

At pH 7.4, your H+ concentration is (X). If you drop to 6.4, how does that concentration change?

A

X = 40 nM

One pH drop means H+ conc increased by factor of 10, so 400 nM is new conc

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13
Q

Under normal circumstances, based on Davenport Diagram with PaCO2 of (X), pH of (Y), and H+ conc of (Z), what’s the concentration of HCO3- ?

A
X = 40 Torr
Y = 7.4
Z = 40 nM

24 mM

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14
Q

Most common cause of community acquired pneumonia is infection via:

A

Streptococcus pneumoniae (Gram positive bac)

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15
Q

Innate immune defense against respiratory pathogens: first line of defense consists of:

A
  1. Intact epithelium within lung

2. Alveolar macrophages

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16
Q

T/F: We inhale bacterial pathogens on a regular basis.

A

True

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17
Q

T/F: Complement is part of humoral innate immune system, crucial to lung protection from bacteria.

A

Partially false - it is humoral, but complement levels within normal lung fluid are not sufficiently high

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18
Q

List the three actions of alveolar macrophages, when encountering bacterial pathogen.

A
  1. Ingest/kill bacteria
  2. Secrete pro-inflamm cytokines
  3. Secrete mediators to recruit neutrophils
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19
Q

T/F: Neutrophils are not present in normal lung.

A

True

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20
Q

Phagocytic cells that combat bacterial infection such as pneumonia.

A

Macrophages and neutrophils

21
Q

T/F: During pneumonia, macrophages and monocytes act as phagocytic cells, combating bacteria in lung.

A

False - not monocytes (which are only in peripheral blood)

22
Q

NETS are formed when neutrophil extrudes (X). Which functions do these NETS serve?

A

X = its DNA

  1. Engulf/trap pathogens
  2. Proteins (associated with nucleic acid) have antimicrobial activity
23
Q

Aside from neutrophils, a(n) (X)-staining material is found in the alveoli during inflammatory response. It’s composed of (Y) from (blood/air/ISF). List the pros/cons of it.

A
X = pink
Y = proteins; blood

Pros: Ab to bacteria (opsonization)
Cons: fluid interferes with normal gas exchange (hypoxia, dyspnea)

24
Q

List the mechanisms of immune system that may lead to lung injury following infection.

A
  1. Excess cytokines
  2. Excess ROS/RNS production
  3. Proteolytic enzyme release
  4. Epithelial barrier disruption (excess inflammation)
  5. NET attacks normal cells
25
Q

T/F: Excess production of ROS shouldn’t cause damage if the mediators stay within the phagolysosome.

A

True

26
Q

Exchange of O2 and CO2 in lungs is determined by which 4 things?

A
  1. V/Q
  2. RER
  3. Gas tensions (in inspired air and mixed venous blood)
  4. Chemical processes in blood
27
Q

Hypoxemia is defined as (X). At sea level, it can be a result of which four things?

A

X = Low arterial PO2

  1. Shunt
  2. Inadequate (hypo-) ventilation
  3. Diffusion issue
  4. V/Q mismatch
28
Q

Hypoventilation is simply defined as (X). What’s the most common causes for it?

A

X = reduced/deficient alveolar ventilation

Usually diseases outside lung (i.e. neuromuscular disorders)

29
Q

Give some diseases/scenarios that cause diffusion impairment, leading to hypoxemia.

A

Thickening of blood-gas barrier (i.e. fibrosis, asbestosis, infection)

30
Q

An example of a natural shunt is from coronary venous blood to (X), via (Y) (arteries/veins).

A

X = LV
Y = Thebesian
veins

31
Q

Intrapulmonary shunt differs from extra pulmonary shunt in which way?

A

Intrapulm: blood perfuses unventilated alveoli
Extrapulm: Blood completely bypasses lung

32
Q

Patent ductus arteriosus is example of (intra/extra)-pulmonary shunt. Give example of the other kind of shunt.

A

Extrapulmonary;

Pulmonary edema (fluid-filled alveoli) could cause intrapulmonary shunt

33
Q

T/F: Breathing 100% O2 doesn’t significantly raise PaO2.

A

False - it does, but the CONTENT of O2 is only raised minimally

34
Q

Normal blood flow to lung is (X) and resting alveolar ventilation is (Y). Thus, normal V/Q ratio is (Z).

A
X = CO = 5 L/min
Y = 4 L/min
Z = 4/5 = 0.8
35
Q

T/F: There’s a fairly homogenous V/Q ratio in each alveolus.

A

False - non-homogeneity (regional differences)

36
Q

Blocked respiratory tube would result in (low/high) V/Q ratio.

A

Low (low V)

37
Q

In (low/high) V/Q ratio, you’d except alveolar gas P to reflect composition of inspired gas. Why?

A

High;

Not enough perfusion to deplete O2 or enrich alveolar gas with CO2

38
Q

Gravity causes (less/more) negative IP pressures at apex of lung. And (smaller/greater) alveolar distending pressures.

A

More; greater

39
Q

T/F: Alveoli at apex of lung have greater distending P, thus greater compliance.

A

False - greater distending P, so larger volumes, so decrease in compliance/distensibility

40
Q

(Ventilation/perfusion) greatest at apex of lung. And base?

A

Both greatest at base

41
Q

Mean pulmonary artery pressure is (X), with (increasing/decreasing) BP at lower levels of arterial tree.

A

X = 15 mmHg (or 20 cm H2O)

Increasing (increase hydrostatic P due to gravity)

42
Q

In severe disease states, such as (high/low) (X) P, zone (1/2/3) of lung is useless for gas exchange and considered part of (Y) dead space.

A

Either high Alv P or low arterial P (hemorrhage);
Zone 1
Y = alveolar

43
Q

In Zone (1/2/3) of lung, (X) behaves like starling resistor.

A

2;

Pulmonary venues

44
Q

Greatest distending pressures for vessels in Zone (1/2/3) of lung. Vascular resistance and perfusion here is (high/low)

A

Zone 3;

Lowest resistance, highest perfusion

45
Q

High V/Q ratio at (apex/base) of lung. Low V/Q ratio at (apex/base) of lung.

A

Apex; base

46
Q

You’d except higher PCO2 levels in areas with (low/high) V/Q ratio, such as (apex/base).

A

Low; base

47
Q

You’d except higher PO2 levels in areas with (low/high) V/Q ratio, such as (apex/base).

A

High; apex

48
Q

You successfully correct your patient’s hypoxemia with 100% O2. If you notice a large increase in the A–a difference, it is indicative that hypoxemia is caused by:

A

R to L shunt