RESPIRATORY Flashcards

1
Q

97% of pneumocytes are of this type – > major role in lungs?

A

Type I pneumocytes

These line the alveoli and are thin as to allow for optimal gas diffusion.

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2
Q

2 major roles of Type II pneumocytes

A

These are the stem cells to both Type I and Type II pneumocytes.
They also secrete pulmonary surfactant to decrease alveolar surface tension, preventing atelectasis.

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3
Q

Which type of pneumocyte proliferates during lung damage?

A

Type II pneumocytes

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4
Q

3 roles of Clara cells

A

Secrete component of surfactant
Degrade toxins
Act as reserve cells

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5
Q

Surfactant synthesis begins around what week of gestation?

A

26

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6
Q

Mature levels of surfactant are not achieved until what week of gestation?

A

35

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7
Q

Law of Laplace

A

Collapsing pressure = 2 (surface tension) / radius

Thus there is an increased tendency to collapse on expiration as the radius decreases.

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8
Q

What amniotic fluid measurement is indicative of fetal lung maturity?

A

Lecithin:sphingomyelin ratio > 2.0

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9
Q

Histological change that occurs in trachea of smoker

A

Metaplasia (ciliated columnar – > squamous)

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10
Q

A patient in the ER is having anaphylaxis. You make an incision beneath the thyroid cartilage to establish airway. Which structure was cut?

A

Cricothyroid membrane

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11
Q

The right pulmonary artery is located where with respect to the bronchus at the lung hilus?

A

Anterior

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12
Q

The left pulmonary artery is located where with respect to the bronchus at the lung hilus?

A

Superior

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13
Q

Which lobe contains the lingula?

A

Left lung lobe (analogous to right middle lobe)

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14
Q

2 structures that perforate the diaphragm at T10

A

Esophagus

Vagus (2 trunks)

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15
Q

3 structures that perforate the diaphragm at T12

A

Aorta
Thoracic Duct
Azygos vein

Hint : At T-1-2 its the red, white, and blue.

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16
Q

By what mechanism does oxygen affect respiration?

A

Chemoreceptors in the carotid body send signals to medulla via glossopharyngeal nerve.
Chemoreceptors in the aortic body send signals to medulla via vagus nerve.

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17
Q

6 drugs known to cause methemoglobinemia

A
Chloroquine, primaquine
Dapsone
Sulfonamides
Local anesthetics
Metoclopramide
Nitroglycerin
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18
Q

If the lung collapses, what happens to the intrathoracic volume?

A

Chest wall is able to expand unopposed by the lungs. The lung volume goes to nearly zero. Intrathoracic volume increases greatly due to chest wall expansion.

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19
Q

Gene mutation and disease associated with Primary Pulmonary Hypertenson

A

Inactivating mutation in BMPR2 (bone morphogenetic protein receptor type II)
Associated with HIV and Kaposi sarcoma (HHV-8)

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20
Q

Equation for physiologic dead space

A

VD=VT x (PaCO2 - PECO2)/PaCO2

Anatomic dead space of conducting airways plus functional dead space in alveoli

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21
Q

3 instances in which compliance is decreased

A

Pulmonary fibrosis
Pneumonia
Pulmonary edema

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22
Q

2 instances in which compliance is increased

A

Emphysema

Normal aging

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23
Q

Form of Hb with low affinity for oxygen

A

Taut – thus this form is favored in tissues where you want to release oxygen.

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24
Q

Form of iron that binds oxygen better

A

Ferrou2 (Fe2+) binds O2 better.

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25
Q

5 things that cause RIGHTward shift in oxygen-hemoglobin dissociation curve

A
CO2
2,3 BPG
Exercise
Acid/altitude
Temperature

In all of these scenarios, hemoglobin has a decreased affinity for oxygen, facilitating unloading of oxygen to tissue.

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26
Q

Characteristic of oxygen that allows for the sigmoidal curve

A

Positive cooperativity – as each oxygen molecule binds to Hb, more and more O2 wants to bind to Hb until all 4 positions available are taken.

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27
Q

Equation for pulmonary vascular resistance

A

PVR =( Ppulm artery - Pleft atrium)/ CO

Pleft atrium = pulmonary wedge pressure

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28
Q

3 pathological characteristics of the arteries in pulmonary HTN

A

Medial hypertrophy
Fibrosis of intima
Atherosclerosis

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29
Q

Changes in oxygen in arterial blood as Hb falls

A

O2 content of arterial blood decreases (less can be carried if you have less Hb)
O2 saturation stays the same (if you have 40% of your normal Hb, it still could be 100% saturated with O2)
Arterial pO2 stays the same because this is the amount of dissolved O2 in the blood and has nothing to do with Hb.

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30
Q

Alveolar gas equation

A

PAO2 = 150 - (PaCO2/0.8)

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31
Q

In hypoxemia (decreased PaO2), which 2 scenarios provide a normal A-a gradient?

A

High altitude
Hypoventilation

You’re just not getting as much oxygen to the alveoli.

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32
Q

In hypoxemia (decreased PaO2), which 3 schenarios provide a high A-a gradient?

A

V/Q mismatch
Diffusion limitation
Right-t-left shunt

There will be an increase in the amount of oxygen in your alveoli vs the amount that reaches your arterial blood.

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33
Q

In hypoxia (decreased O2 delivery to tissues), which 2 scenarios provide a normal A-a gradient?

A

Decreased CO

Hypoxemia

34
Q

In hypoxia (decreased O2 delivery to tissues), which 3 scenarios provide a high A-a gradient?

A

Anemia
CO poisoning
Cyanide poisoning

In these instances, Hb is not carrying as much O2. You’re getting O2 in fine (normal A) but your a is much lower.

35
Q

2 instances in ischemia with a normal A-a gradient

A

Impeded arterial flow

Reduced venous drainage

36
Q

V/Q at the apex

A

3 (wasted ventilation)

37
Q

V/Q at the base

A

0.6 (wasted perfusion)
However, both ventilation and perfusion are greater at the base vs the apex due to gravity causing blood to flow towards base. Capillaries are less distended and less resistant to blood flow. The alveoli are also less inflated and cause less obstruction to blood flow.

38
Q

Area of the lung TB prefers and why?

A

The apex because there is more O2 available for them to eat – blood is not reaching the apex as often, thus not being able to take it away to the rest of the body.

39
Q

V/Q ratio during exercise/increased CO

A

1 due to vasodilation of apical capillaries

40
Q

Changes in O2 and CO2 content of blood in response to exercise

A

No change in PaO2 or PaCO2

Increase in venous CO2 and decrease in venous O2 content

41
Q

3 ways CO2 is transported from the tissues to the lungs

A

Bicarb
Dissolved CO2
Bound to N terminus of Hb as carbaminohemoglobin

42
Q

How does the body compensate for hypoxia at high altitude?

A
Increases ventilation
Make more RBCs
Elevates the erythropoietin levels
Increased 2,3 BPG
Increased mitochondrial tissue
Increase renal excretion of HCO3- (to compensate for the respiratory alkalosis)
43
Q

How does Hct and Hb change in person that has acclimatized to hypoxic environment for weeks?

A

Hct 40-45 – > 60
Hb 15 g/dL – > 20 g/dL

You’re going to want to increase both so that you’re able to deliver more of whatever oxygen you’re receiving to the tissues

44
Q

At what positive G force does visual “black out” occur and why?

A

4-6G

Centrifugal force pooling the blood in the abdomen and legs, causing insufficient blood supply to the heart and brain

45
Q

How is the body affected by a prolonged stay in space at zero gravity?

A
Decreased blood volume
Decreased RBC mass
Decreased muscle strength
Decreased maximum CO
Loss of calcium and phosphate from bones
46
Q

Describe nitrogen narcosis.

A

This is a condition seen in divers and is the result of increased solubility of nitrogen in the blood at an increased depth (Henry’s law). Nitrogen dissolves into the neural membranes causing decreased neuronal excitability. These patients look similar to drunk people.

47
Q

What physiologically is taking place in decompression sickness?

A

Gases composed primarily of nitrogen are dissolved in the blood. At high pressures, the gases begin to escape from the dissolved state, forming bubbles that can occlude BVs.

48
Q

Symptoms of decompression sickness

A

Pain –joint and muscles (UE, LE)
Neurological sx –dizziness, paralysis, syncope
“The chokes” – SOB, pulmonary edema, possible death as air bubbles occlude the pulmonary capillaries

49
Q

Explain the pathophys of acute mountain sickness.

A

Acute cerebral edema due to hypoxia-induced vasodilation.

50
Q

3 components of Virchow’s triad

A

Stasis: post-op, long trips, cast, pregnancy
Hypercoagulability: sickle cell, polycythemia, CHF, estrogen excess, smoking
Endothelial damage: fracture, post-op, post-partum

51
Q

What is Homan’s sign?

A

Pain with ankle dorsiflexion

Seen in DVT – kind of bullshit

52
Q

Characteristic EKG changes seen in pulmonary embolism

A

S1Q3T3 –wide S in lead I, large Q and inverted T in lead III

53
Q

Hallmark of COPD

A

Decreased FEV1:FVC ratio

54
Q

Hallmark of Restrictive Lung disease

A

Decreased total lung capacity

Normal FEV1:FVC ratio

55
Q

Differential dx for eosinophilia

A

Drugs
Neoplasms
Atopic dz (allergy, asthma, Churg-Strauss)
Addison’s dz
Acute interstitial nephritis
Collagen vascular dz
Parasites (Loffler’s eosinophilic pneumonitis: Ascaris, strongyloides, hookworm)

56
Q

Pneumoconioses increase the risk for what 2 syndromes?

A

Cor pulmonale

Caplans syndrome

57
Q

What part of the lung do anthracosis and silicosis affect?

A

Upper lobes

58
Q

Pathogenesis and key histological finding in silicosis

A

Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. IT is thought that silica may disrupt the phagolysosomes and impair macrophages, increasing the susceptibility to TB.

EGGSHELL CALCIFICATION of hilar lymph nodes.

59
Q

Histological features and staining of Asbestosis

A

“Ivory white” calcified pleural plaques
Asbestos bodies –golden-brown fusiform rods resembling dumbbells

Since they are coated with iron, asbestos bodies stain positive with Prussian blue.

60
Q

3 risk factors for neonatal respiratory distress syndrome

A
Prematurity
Maternal diabetes (due to elevated fetal insulin)
Ceserean delivery (decreased release of fetal glucocorticoids)
61
Q

Pathological characteristics of ARDS

A

Diffuse alveolar damage causing increased capillary permeability, allowing for protein-rich exudate to leak into the alveoli.. This causes an intra-alveolar hyaline membrane to form.

62
Q

What causes the damage in ARDS?

A

The release of neutrophilic substances is toxic to the alveolar wall and causes the activation of the coagulation cascade and release of free radicals – > diffuse alveolar damage.

63
Q

Which way does the trachea deviate in spontaneous pneumothorax?

A

TOWARD the side of the lesion (just like atelectasis.)

64
Q

Which way does the trachea deviate in tension pneumothorax?

A

AWAY from the side of the lesion.

65
Q

Only clinical scenario with increased fremitus

A

Consolidation –lobar pneumonia, pulmonary edema, etc.

66
Q

Key manifestations in sarcoidosis

A
GRUELING
Granulomas
Rheumatoid arthritis
Uveitis
Erythema nodosum (tibial)
Lymphadenopathy
Idiopathic
Not TB
Gamma Globulinemia
ACE increase, Vitamin D increase -- > Increased calcium
67
Q

CXR appearance of sarcoidosis

A

Bilateral hilar adenopathy or reticular opacities

68
Q

Patients with silicosis need to be worried about .. ?

A

Increased susceptibility to TB

69
Q

H&E of lung bx from a plumber shows elongated structures with clubbed ends in tissue. What is the dx and what is he at increased risk for?

A

Asbestosis

Increased risk for mesothelioma and bronchogenic CA.

70
Q

Complications that can arise from lung cancer

A

SPHERE
Superior vena cava syndrome
Pancoast tumor
Horner’s syndrome
Endocrine (paraneoplastic syndromes such as PTHrp –> hypercalcemia, ACTH –> Cushings, SIADH –>hyponatremia, Lambert Eaton syndrome)
Recurrent laryngeal sx (hoarseness, dysphagia)
Eeffusions (pleural or pericardial)

71
Q

A 30 y.o. comatose man on ventilatory support in the ICU develops an infection and dies. Autopsy reveals a pus-filled cavity in his right lung. What is the likely etiology?

A

Aspiration – > lung asbcess.

72
Q

A 55 y.o. man who is a smoker and heavy drinker presents with a new cough and flu-like symptoms. Gram stain shows no organisms; silver stain of sputum shows gram negative rods. What is the dx?

A

Legionella pneumophila

73
Q

CXR shows collapse of middle lobe of right lung and mass in right bronchus; patient has history of recurrent pneumonias. What is the dx?

A

Bronchogenic CA

74
Q

Most common lung cancer in non-smokers and females is due to a mutation in what? What is it associated with? Where is it located?

A

Adenocarcinomas are found peripherally and due to activating mutations in k-ras. Associated with hypertrophic osteoarthropathy (clubbing).

75
Q

This subtype of lung cancer grows along alveolar septa.

A

Adenocarcinoma bronchioalveolar subtype – looks like an apparent thickening of alveolar walls

76
Q

Keratin pearls and intercellular bridges seen on histology

-What is it? Where is it found? And what 3 major things is this associated with?

A

SCC of lung

4 Cs: central location, cavitation, cigarettes, hyperCalcemia (produces PTHrP)

77
Q

Histological appearance of small cell lung CA and 4 A’s associated

A

Neoplasm of neuroendocrine Kulchitsky cells –> small dark blue cells with little cytoplasm and huge nuclei
Salt and pepper chromatin
May produce ACTH, ADH, or Abs against pre-synaptic calcium channels (Lambert-Eaton)
Amplification of myc oncogenes

78
Q

Patient comes in with lung mass and flushing, diarrhea, and wheezing. Whats the dx and what is the histological appearance?

A

Bronchial carcinoid tumor -sx due to mass effect (carcinoid syndrome)

Histologically looks like nests of neuroendocrine cells, chromogramin +

79
Q

Histological feature of mesothelioma

A

Psammoma bodies

Hemorrhagic pleural effusions and pleural thickening

80
Q

2 causes of SVC syndrome and what are the complications?

A

Can be caused by malignancy and thrombosis from indwelling catheters which obstruct the SVC, impairing blood drainage from the head, neck, and UE.
If the obstruction is severe, it can raise intracranial pressure leading to headaches, dizziness, and increased risk of aneurysm/rupture of cranial arteries.

81
Q

A 50 y.o. obese man with HTN comes to your clinic to receive care for his chronic fatigue. A CBC shows elevated Hct and Hb. What is the most likely cause?

A

Sleep apnea-induced erythrocytosis (stimulation of Epo due to hypoxia from sleep apnea)