Usmle Step 1 Fa Respiratory-Anatomy And Physiology

Front 1

In the lungs you have pseudostratified ciliated epithelium to what point?

Back 1

Respiratory bronchioles

Front 2

In the lungs you have goblet cells until what point?

Back 2

Terminal bronchioles

Front 3

Where is a foreign object most likely going to be lodged if upright? If supine?

Back 3

Upright: Lower portion of R inferior lobe
Supine: upper portion of R inferior lobe

Front 4

What structures perforate the diaphragm and at what vertebral levels?

Back 4

C8-IVC
C10: esophagus and vagus
C12: aorta, thoracic duct, azygous vein

Front 5

Innervation to lung

Back 5

Phrenic (C3-5)

Front 6

Muscles of inspiration/expiration during quiet breathing

Back 6

Inspiration: diaphragm
Expiration: passive

Front 7

Muscles of inspiration/expiration during exercise

Back 7

Inspiration: diaphragm, external intercostals, scalene, SCM
Expiration: rectus abdominus, int/ext obliques, transversus abdominis, internal intercostals

Front 8

Important lung products

Back 8

Surfactant
Prostaglandins
Histamine
Angiotensin converting enzyme
Kallikrein

Front 9

Surfactant
(a) source
(b) composition
(c) function

Back 9

(a) type II pneumocytes
(b) dipalmitoyl phophaticholine
(c) decrease surface tension of alveoli; increases compliance and decreases work of breathing

Front 10

Histamine effect on bronchi

Back 10

Bronchoconstriction

Front 11

Angiotensin convertin enzyme fct

Back 11

Converts angI to angII; also inactivates bradykinin

Front 12

Kallikrein fct

Back 12

Activates bradykinin

Front 13

Methemoglobin

Back 13

Oxidized HgB (ferric Fe3+) that does not bind O2 as readily. It has increased affinity for CN-

Front 14

Treatment for CN- poisoning (mechanism)

Back 14

Nitrites oxidize HgB to metHbB which binds to CN- and allows cytOxidase to fct; forms thiocyanate which is renally excreted

Front 15

Which gases are perfusion limited?

Back 15

O2 (in normal health), CO2, N2O

Front 16

Which gases are diffusion limited?

Back 16

O2 (pulmonary fibrosis) and CO

Front 17

Etiology of primary pulmonary HTN

Back 17

Inactivation in BMPR2 (normally inhibits vascular smooth muscle proliferation)

Front 18

Etiology of secondary pulmonary HTN (pathophys)

Back 18

(1) COPD (destruction of lung parenchyma)
(2) recurrent thromboemboli (decrease cross sectional area of pulmonary vascular bed)
(3) mitral stenosis (increased resistance equals increased pressure)
(4) autoimmune dz (inflammation leads to intimal fibrosis and medial hypertrophy)
(5) L to R shunt
(6) sleep apnea or living at high altitudes (hypoxic vasoconstriction)

Front 19

Cor pulmonale

Back 19

Pulmonary HTN leads to RVH and eventual death from decompensation

Front 20

Hypoxemia
(a) definition
(b) major causes (A-a gradient in each)

Back 20

(a) decrease in arterial P02
(b)(1) high altitude (normal A-a)
(2) hypoventilation (normal A-a)
(3) V/Q mismatch (increased A-a)
(4) diffusion limitation (incr A-a)
(4) R to L shunt (incr A-a)

Front 21

Hypoxia
(a) definition
(b) major causes

Back 21

(a) decreased oxygen delivery to tissue
(b) decreased cardiac output
Hypoxemia
Anemia
Cyanide poisoning
CO poisoning

Front 22

Ischemia
(a) definition
(b) causes

Back 22

(a) loss of blood flow
(b) reduced venous drainage

Front 23

Shunt
(a) V/Q=?
(b) effect of 100% O2 on PaO2

Back 23

Shunt is airway obstruction V/Q=0
Giving 100% O2 will not improve oxygenation

Front 24

Dead space
(a)V/Q=?
(b) effect of 100% O2 on PaO2

Back 24

Dead space is blood flow obstruction; V/Q approaches infinity; assuming <100% dead space, giving oxygen will improve PO2

Front 25

Response to high altitude
(a) acute ventilation
(b) chronic ventilation
(c) epo/hct/hgb
(d) 2,3DPG
(e) cellular changes
(f) renal
(g) pulmonary vasculature

Back 25

(a) acute incr in ventilation
(b) chronic increase in ventilation
(c) incr Epo incr Hct and Hgb due to chronic hypoxia
(d) Incr 2,3 DPG (binds Hgb so that it releases more O2)
(e) increased mitochondria
(f) incr renal exfretion of bicarb to compensate for resp alkalosis
(g) chronic hypoxic pulmonary vasoconstriction results in RVH

Front 26

Response to exercise
(a) CO2 production
(b) O2 consumption
(c) ventiltion
(d) V/Q ratio in lung
(e) pulmonary blood flow
(f) pH
(g) PaO2, PaCO2, venous CO2 content

Back 26

((a) incr CO2 production
(b) increased O2 consumption
(c) incr ventilation rate to meet O2 demand
(d) V/Q from apex to base becomes more uniform
(e) incr pulmonary blood flow due to incr cardiac output
(f) decr pH during strenuous exercise (secondary lactic acidosis)
(g) no change in PaO2, PaCO2, but increase in venous CO2 content