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Medical Physiology I > Block 5 Exam > Flashcards

Block 5 Exam Flashcards

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USMLE® Step 1 flashcards
1
Q

Key components of respiratory system

A

An air pump
Mechanisms for carrying O2 and CO2 in the blood
A surface for gas exchange
A circulatory system
A mechanism for locally regulating the distribution of ventilation and perfusion
A mechanism for centrally regulating ventilation

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2
Q

What does magnitude of inspiratory reserve volume depend on?

A 
Current lung volume
Lung compliance
Muscle strength
Comfort
Flexibility of the skeleton
Posture
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3
Q

Total lung capacity

A

Sum of all four volumes

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4
Q

Functional residual capacity

A

Sum of ERV and RV

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5
Q

Inspiratory capacity

A

Sum of IRV and TV

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6
Q

Vital capacity (VC)

A

Sum of IRV, TV, and ERV

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7
Q

Dalton’s law

A

Total pressure is the sum of the individual partial pressures

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8
Q

Henry’s law

A

The concentration of O2 dissolved in water is proportional to PO2 in the gas phase

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9
Q

BTPS

A

Body temperature and pressure, saturated with water vapor

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10
Q

ATPS

A

Ambient temperature and pressure, saturated with water vapor

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11
Q

STPD

A

Standard temperature and pressure/dry

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12
Q

Bronchi

A

Generations 1-10

Contain cartilage

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13
Q

Bronchioles

A

Begin at generation 11

Cartilage free

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14
Q

Conducting airways

A

Nose and lips to alveoli free bronchioles

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15
Q

Terminal bronchioles

A

Most distal conducting airways

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16
Q

Anatomic dead space

A

Small fraction of total lung capacity

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17
Q

What happens with increasing generation?

A

Cartilage, mucus, and linear velocity decrease

Cross sectional area increases

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18
Q

Lung elastic recoil

A

inward

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19
Q

Chest wall/diaphragm elastic recoil

A

outward

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20
Q

P(AW)

A

Airway pressure

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21
Q

P(TM)

A

Transmural pressure

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22
Q

P(TP)

A

Transpulmonary pressure
Static component
Controls lung volume

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23
Q

P(IP)

A

Intrapleural pressure

Relative vacuum

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24
Q

P(A)

A

Alveolar pressure
Dynamic component
Controls airflow

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25
Q

Primary muscles of inspiration

A

Diaphragm

External and internal intercostal muscles

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26
Q

Most important muscle of inspiration

A

Diaphragm

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27
Q

Secondary (accessory) muscles of inspiration

A

Scalenes
Sternocleidomastoids
Neck and back muscles
Upper respiratory tract muscles

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28
Q

Scalenes

A

Lift the first two ribs

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29
Q

Sternocleidomastoids

A

Lift the sternum outward

Contributing to the water-pump handle effect

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30
Q

Neck and back muscles of inspiration

A

Elevate the pectoral girdle and extend the back

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31
Q

Upper respiratory tract muscles

A

Decrease airway resistance

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32
Q

Primary muscles of expiration

A

NONE

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33
Q

Accessory muscles of expiration

A

Abdominal muscles
Intercostals
Neck and back muscles

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34
Q

Abdominal muscles

A

Increases intra-abdominal pressure and forces the diaphragm upward into the chest cavity
Decreasing the rostral-caudal diameter of the thorax and increasing P(IP)

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35
Q

Intercostals

A

Reduce both the anterior-posterior and the transverse diameters of the thorax
Important for coughing

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36
Q

Neck and back muscles in expiration

A

Lowering of pectoral girdle reduces the cross-sectional area of the thorax, whereas flexion of the trunk reduces the rostral-caudal diameter

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37
Q

Hysteresis

A

Different curves are followed during inspiration and expiration
Harder to open a collapsed airway than to keep an airway open

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38
Q

Static compliance (C)

A

Property of the alveoli

Decreases with increasing lung volumes

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39
Q

Obstructive disease effects

A

More compliance
Less elastic recoil
Increased volume
Can’t exhale

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40
Q

Restrictive disease effects

A

Less compliance
More elastic recoil
Decreased lung volume
Can’t inhale or exhale

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41
Q

Pulmonary surfactant

A

Made by type II pneumocytes

42
Q

Role of pulmonary surfactant

A 
Easier to inhale
Promotes more uniform alveolar diameters
Reduces surface tension
Increases compliance
Minimizes fluid accumulation in alveolus
43
Q

Stages of V(L) during reinflation

A

Stable V(L)
Opening of airways
Linear expansion of open airways
Limit of airway inflation

44
Q

What to optimize during cardiorespiratory transition from fetus to neonate

A

Continuous breathing
Pulmonary vasorelaxation
Resorption of lung fluid

45
Q

What to avoid during cardiorespiratory transition from fetus to neonate

A

Apnea
Pulmonary vasoconstriction
Retention of lung fluid

46
Q

What leads to inhibition of fetal respiratory activity

A 
Hypoxia (through adenosine)
Placental unity (prostaglandin)
Descending pontine inhibition
Hyperthermia
Non-REM sleep
47
Q

What drug is used for late preterm delivery with surfactant therapy

A

Betamethasone

48
Q

Saturated phosphatidylcholine in pulmonary surfactant

A

50%

49
Q

Unsaturated phosphatidylcholine in pulmonary surfactant

A

20%

50
Q

Neutral lipids in pulmonary surfactant

A

8%

51
Q

Phosphatidylglycerol in pulmonary surfactant

A

8%

52
Q

Other phospholipids in pulmonary surfactant

A

6%

53
Q

What causes BPD/CLD

A 
Low gestation
Genetic susceptibility
Low birthweight
Baro/volutrauma
Increased inspired O2
Sepsis/inflammation
Nutritional deficit
54
Q

Neonatal contributors to altered airway function

A

Modulated neural output
Parenchymal (alveolar) injury
Airway dysfunction

55
Q

How does hypoxia affect pulmonary vessel diameter

A

Causes pulmonary vasoconstriction

56
Q

Ductus Venosus

A

Shunts blood from the umbilical vein to the inferior vena cava
Bypasses the liver

57
Q

Foramen Ovale

A

Shunts blood from right atrium to left atrium

Bypasses the lungs

58
Q

Ductus Arteriosus

A

Shunts blood from the pulmonary artery to the aorta

Bypasses the lungs

59
Q

What taste is associated with ENaCs

A

Salt

60
Q

What cells contain ENaCs in the kidney

A

Principal cells in the kidney

61
Q

Release of what endogenous hormone is thought to be associated with the transition of the ENaCs at birth

A

Glucocorticoids/cortisol

62
Q

Why is betamethasone used?

A

Can cross the placental barrier

63
Q

What is considered late preterm infant?

A

34-36 weeks

64
Q

What is the primary component of pulmonary surfactant

A

Saturated phosphatidylcholine

65
Q

Contributing factors to neonatal respiratory distress syndrome

A

Surfactant deficiency

Inefficient fluid absorption (37-38 weeks)

66
Q

Treatment of Neonatal respiratory distress syndrome

A

Glucocorticoids
Artificial surfactant therapy
CPAP
Intubation

67
Q

Impact of C-section on Neonatal respiratory distress syndrome

A

Increases risk of neonate respiratory distress by showing lower SpO2

68
Q

What can happen when you don’t have sufficient surfactant

A

Atelectasis

69
Q

Atelectasis

A

Alveoli collapse

70
Q

What are the two roles of glucocorticoids that were discussed?

A

Promotes resorption of fluid

Increases production of surfactant

71
Q

What leads to a right shift of O2-Hb curve

A 
Increased temp
Increased [H+]
Decreased pH
Increased [CO2]
Increased [2,3-DPG]
72
Q

What leads to left shift of O2-Hb curve

A 
Decreased temp
Decreased [H+]
Increased pH
Decreased [CO2]
Decreased [2,3-DPG]
HbF
73
Q

CO2 transport in blood

A

Dissolved CO2
HCO3 -
Carbamino compounds

74
Q

Spirometer

A

Measures changes in V(L)
Doesn’t measure RV
Can measure FEV1

75
Q

He Dilution

A

Measures absolute volumes
Can measure RV, FRC, TLC
Closed system
Volume of distribution approach

76
Q

N2 washout

A

Measures absolute volumes
Can measure RV, FRC, TLC
Open system
Volume of distribution approach

77
Q

Plethysmograph

A

Air tight telephone booth
Use Boyle’s law
Estimates RV
Measures changes in volume and pressure

78
Q

Aggregate lung volume

A

5-6 L

79
Q

Laplace’s law

A

P= 2T/r

80
Q

What increases R(AW)

A

COPD/Emphysema/Chronic Bronchitis
Vagal tone => parasympathetic activity
Histamine => Bronchoconstriction
Reduced lung volumes

81
Q

Change of 1 unit in pH

A

10x in [H+]

82
Q

Change in 0.3 unit of pH

A

2x change in [H+]

83
Q

Buffering power

A

Amount of OH-/H+ (mM) needed to change the pH by one unit

84
Q

Cause of respiratory acidosis

A

Increased PCO2

85
Q

respiratory acidosis leads to

A

decreased blood pH

86
Q

Clinical causes of respiratory acidosis

A

Decreased alveolar ventilation
Decreased lung diffusing capacity
Ventilation/perfusion mismatch

87
Q

Compensation of respiratory acidosis

A

Metabolic alkalosis

88
Q

Cause of respiratory alkalosis

A

Decreased PCO2

89
Q

respiratory alkalosis leads to

A

increased pH

90
Q

clinical causes of respiratory alkalosis

A

Increased alveolar ventilation
Hypoxia
Anxiety

91
Q

Compensation of respiratory alkalosis

A

Metabolic acidosis

92
Q

Cause of metabolic acidosis

A

Decreased HCO3 -

93
Q

metabolic acidosis leads to

A

Decreased pH

94
Q

Clinical causes of metabolic acidosis

A

Decreased urinary secretion of H+
Ketoacidosis
Lactic acidosis
Severe diarrhea

95
Q

Compensation of metabolic acidosis

A

Respiratory alkalosis

96
Q

Cause of metabolic alkalosis

A

Increased HCO3 -

97
Q

metabolic alkalosis leads to

A

increased pH

98
Q

Clinical causes of metabolic alkalosis

A

Increased HCO3 - load

Severe vomiting

99
Q

Compensation of metabolic alkalosis

A

Respiratory acidosis

100
Q

Intracellular metabolic acidosis response

A

Stimulate acid extruders

Inhibit acid loaders

101
Q

Intracellular metabolic alkalosis response

A

Stimulate acid loaders

Inhibit acid extruders

Medical Physiology I (8 decks)

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