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Step 1 > Pulm > Flashcards

Pulm Flashcards

1
Q

Respiratory Distress, Neuro impairment (confusion), upper body petechial rash (thrombocytopenia)

A

Fat Emboli (long bone fracture)…microvascular occlusion

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2
Q

Acute Onset Resp failure, bilateral lung opacities, decreased Pa02/Fi02

A

Acute Respiratory Distress Syndrome

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3
Q

Causes of Acute Respiratory Distress Syndrome

A

Trauma, Sepsis, Shock, Gastric Aspiration, Acute Pancreatitis, Uremia

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4
Q

Intra-alveolar hyaline membranes

A

Acute Respiratory Distress Syndrome. Initial damage from Neutrophils, coag cascade, and free radicals

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5
Q

Normal value in Acute Respiratory Distress Syndrome

A

PCWP!!!
due to protein exudate into alveoli due to increased alveolar capillary permeability (so you basically have protein fluid build up in alveoli and so 02 doesnt go through. so its an example of a shunt)

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6
Q

Non cardiogenic pulmonary edema vs cardiogenic

A

noncardio: normal PCWP
cardiogenic: increased PCWP

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7
Q

Lung compliance in ARDS

A

decreased

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8
Q

Sudden onset dyspnea, chest pain, tachypnea with leg swelling

A

Pulmonary Embolism

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9
Q

FATBAT = Types of PE’s

A

Fat, Air, Thrombus, Bacteria, Amniotic Fluid, Tumor

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10
Q

V/Q mismatch: Hypoxemia and Respiratory Alkalosis

A

PE (my impulse is Respiratory Acidosis because CO2 doesnt get it out. this is wrong)

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11
Q

Respiratory Alkalosis in PE

A

PE causes hypoperfusion of affected pulm parenchyma -> redist. of pulm blood flow and V/Q mismatch -> intrapulmonary R-L shunting -> Hypoxemia

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12
Q

Normal A-a gradient hypoxemia

A

High Altitude, Hypoventilation (opiods/narcotics)

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13
Q

V/Q mismatch causes

A

COPD, Pulmonary Fibrosis, Pulmonary Embolism, Pneumonia, Pulmonary Hyptertension, Asthma

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14
Q

Increased A-a gradient

A

V/Q mismatch, Diffusion Limitation (fibrosis), R-L shunt.
Note: Diffusion limitation i.e. fibrosis DOES RESPOND to 100% 02.
Shunt does NOT respond to 100% 02

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15
Q

CF (sweat glands)

A

Decreased NaCl absorption = hypertonic sweat

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16
Q

CF (respiratory and gastric glands)

A

Decreased Cl secretion =
increased Na and H20 absorption =>
Dehydrated (thick) mucus and negative transepithelial potential (i.e. nasal mucosal surface)

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17
Q

CF path

A

Auto Rec.
Decreased H20 in epithelial secretions = thick viscous mucus =
1. chronic airway obstruction, impaired respiratory bacteria clearance (CHRONIC PRODUCTIVE COUGH)
2. GI maldigestion/absorption (STEATORHHEA)

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18
Q

CF clinical features

A

Chronic Productive Cough
Steatorrhea and FTT
Recurrent Sinopulmonary Infections/Sinusitis (Pseudomonas and Staph Aureus)
Male Infertility (BILAT ABSENCE OF VAS DEFERENS)

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19
Q

Normal CFTR f(x) - Sweat glands

A

Sweat Glands: CFTR (CL- channel) absorbs Cl-, and also activates ENaC (Na channel) to increase Na reabsorption

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20
Q

Normal CFTR f(x) - Respiratory and Gastric Glands

A

Resp/Gastric Glands: CFTR (CL- channel) secretes Cl-, and limit ENaC (Na channel) from absorbing Na

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21
Q

CFTR Mneumonic

A

ClENaC Sap GRsi

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22
Q

Pneumothorax clinical signs

A
  • Unilat chest pain and dyspnea
  • unilat chest expansion
  • Hyperresonance
  • decreased Tactile Fremitus
  • decreased breath sounds
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23
Q

Rupture of apical (subpleural) blebs. Tall, thin young male

A

Primary Spontaneous Pneumothorax

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24
Q

ATP-Gated Cl- Channel

A

CFTR

In CF, the misfolded PROTEIN retained in RER. Misfolded so abnormal post-translational modification.

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25
Q

Last two features to disappear (conducting/respiratory zone)

A

Cilia and Smooth muscle –> Respiratory Bronchioles

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26
Q

Cartilage and goblet cells extend to end of ____

A

bronchi

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27
Q

Type 1 pneumocytes are _____ cells

A

squamous

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28
Q

Type 2 pneumocytes are ______ cells

A

cuboidal

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29
Q

F(x) of Lamellar bodies?

A

Store and transport Surfactant

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30
Q

Conducting zone

A

Pseudostrat ciliated columnar
Warm, Humidify, and Filter air
End of Terminal Bronchiole

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31
Q

Respiratory Zone

A

Respiratory bronchioles = Cuboidal

Alveoli = Squamous

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32
Q

R or L Left has fewer lobes?

A

Left has Less Lobes

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33
Q

Aspirate to which lobe?

A

AspiRate to R Lobe (angle is less oblique)

Standing: lower Inferior R Lobe
Supine: superior Inferior R Lobe

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34
Q

Diaphragm structures (which level)

A

T8: IVC
T10: Esophagus, Vagus
T12: Aorta, Thoracic Duct, Azygous Vein

I Ate - 10 Egg Vites - ATA 12

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35
Q

Vital Capacity

A

TLC - RV
Tidal Volume + IRV + ERV
Max V that can be expired after a max inspiration

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36
Q

Volume of gas present in lungs after a maximal inspiration

A

Total Lung Capacity

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37
Q

Physiologic Dead Space

A

Anatomic Dead Space (Respiratory Zone) + Alveolar Dead Space

Apex of lung = biggest contributor of alveolar dead space (poor perfusion)

V of inspired air that doesn’t participate in gas exchange

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38
Q

Minute Ventilation vs Alveolar Ventilation equation

A 
Minute = Tidal Volume x Resp Rate
Alveolar = (Tidal V - Dead space) x Resp Rate
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39
Q

Pressures at FRC

A

Airway and alveolar P = 0

Intrapleural = -5

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40
Q

Explain Fetal Hb higher 02 affinity

A

lower affinity for 2,3-BPG (stabilizes Taut)

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41
Q

Drugs that Cause this:

Fe2+ —> Fe3+ (methemoglobin)

A

Nitrites and benzocaine

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42
Q

Methemoglobin

A

Has increased affinity for Cyanide.

Induced methemoglobinemia using nitrites + thiosulfate to treat Cyanide Poisoning

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43
Q

Chocolate-colored blood + Cyanosis

A

Methemoglobinemia

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44
Q

Carboxyhemoglobin

A

Left shift in O2-Hb curve = decrease O2 unloading in tissues

CO decreased O2 carrying capacity and O2 content of blood but NOT O2 in plasma (PaO2)

45
Q

Normal value in CO poisoning

A

PaO2 (doesnt change plasma content)

46
Q

Decreased O2 content of blood with no change in O2 saturation or PaO2 (arterial PO2)

A

Decreased Hemoglobin

47
Q

Dissolved O2 aka PaO2 changes in CO poisoning, Anemia, Polycythemia?

A

No change….stays normal in all 3

48
Q

Normal O2 levels

A

Inspired air: 160
Trachea: 150
Alveolar (-47): 104
Venous: 40

49
Q

(P-pulmartery - P-leftatrium)/CO

A

Pulmonary Vascular Resistance

Pleftatrium aka pulm wedge pressure

50
Q

Response to Exercise

A

Arterial system stays in homeostasis, Venous fluctuates:

No change in PaO2 or PaCO2. Increased venous CO2, decreased venous O2

V/Q ratio from base to apex becomes more uniform

51
Q

DVT Prophylaxis/Acute treatment

A

HEPARIN DOG (unfractionated) or LMW Heparin (enoxaparin)

52
Q

DVT Treatment/Long-term prevention

A

Oral anticoagulants = Warfarin, Rivaroxaban

53
Q

V/Q mismatch
Hypoxemia
Respiratory Alkalosis

A

Pulmonary Embolism
In order to decrease hypoxemia, ventilation increases
With Hyperventilation you get resp alk

54
Q

Sudden onset dyspnea, chest pain, tachypnea, tachycardia

A

Pulmonary Embolism

55
Q

Fat Emboli Triad

A 
Hypoxemia
Neuro sx (confusion/seizures/lethargy)
Petechial Rash (head, neck, thorax, axilla, etc)

Associated with long bone fracture and liposuction

56
Q

Imaging test of choice for PE

A

CT Pulmonary Angiography

57
Q

Does PE cause hemorrhagic or ischemic infarct?

A

Hemorrhagic (wedge shaped)–> lung has dual blood supply

58
Q

Decreased FEV1/FVC

A

Obstructive

59
Q

Hyperplasia of mucus-secreting cells (increased Reid Index)

A

Chronic Bronchitis

60
Q

MQs and neutrophils release proteases (i.e. elastase)

A

Emphysema

61
Q

Barrel-shaped Chest

A

Emphysema

62
Q

Enlargement/dilation of air spaces

A

Emphysema

63
Q

Obstructive lung disease that causes Pulsus Paradoxus

A

Asthma

64
Q

Shed epithelium that forms whorled mucus plugs, leading to occlusion of bronchi/bronchioles and small airway destruction

A

Asthma

65
Q

Reversible bronchoconstriction caused by bronchial hyperresponsiveness

A

Asthma

66
Q

Bronchiectasis associations

A

Bronchial obstruction
Poor ciliary motility (smoking, Kartagener)
Cystic Fibrosis
Allergic Bronchopulmonary Aspergillosis

67
Q

Allergic Triad

A

Allergic Rhinitis
Atopic Dermatitis
Asthma

68
Q

Chronic necrotizing infection of the bornchi

A

Bronchiectasis

69
Q

Hemoptysis, Recurrent infections, permanently dilated airways

A

Bronchiectasis

70
Q

Most frequent cause of Pulsus Paradoxus in absence of pericardial disease

A

Asthma/COPD

71
Q

Increased ACE and Ca2+, noncaseating granuloma, bilateral hilar lymphadenopathy

A

Sarcoidosis

72
Q

Drugs causing Restrictive lung disease

A

Bleomycin, Busulfan, Amiodarone, methotrexate

73
Q

FEV1/FVC > 80%

A

Restrictive

74
Q

Rheamatoid Arthritis + Pneumoconioses with intrapulmonary nodules

A

Caplan syndrome

75
Q

Ivory white, calcified PLEURAL and SUPRDIAPHRAGMATIC PLAQUES

A

Asbestosis –> PARIETAL PLEURA

76
Q

Lower lobe pneumoconiosis

A

Asbestosis

77
Q

Upper lobe pnemoconiosis

A

Berylliosis, Coal workers pneumoconiosis, Silicosis

78
Q

Iron in alveolar septum

A

Ferruginous body = asbestosis

79
Q

macrophages with carbon

A

Coal workers pneumoconiosis (black lung disease)

80
Q

pneumoconiosis with increased suceptibility to TB

A

Silicosis

Silica disrupts phagolysosomes and imparis macrophages

81
Q

Eggshell calcification(around the rim) of hilar lymph node

A

Silicosis

82
Q

birefringent particles surrounded by collagen (pneumoconiosis)

A

Silicosis

83
Q

Alveolar collapse/ground-glass appearance of lung fields

A

NRDS

84
Q

Cardiac anomaly risk in NRDS

A

Persistently low O2 –> risk of PDA

85
Q

toxicity of supplemental 02 for NRDS patient

A

RIB

Retinopathy, Intraventricular hemorrhage, Bronchopulmonary dysplasia

86
Q

Risk factors for NRDS

A

Prematury
Maternal diabetes (causes increased fetal insulin, which decreases surfactant levels)
C-section

87
Q

Tx for NRDS

A

articifical surfactant, maternal steroids before birth

88
Q

2 risks increased in Pneumoconiosis

A

Cor Pulmonale and Caplan

89
Q

noncaseating granuloma (thus responsive to steroid) + industrial exposure

A

Berryliosis

90
Q

Normal Pa02 during day, hypoxia at night

A

Sleep Apnea

91
Q

Increased PaCO2 during waking hours and sleep, decreased PaO2 during sleep

A

Obesity Hypoventilation Syndrome

92
Q

Nerve relevant to OSA

A

Hypoglossal

93
Q

Daytime somnolence, morning headaches, RHF

A

OSA

94
Q

Lungs hyperresonant to percussion

A

Pneumothorax (simple or tension)

95
Q

Increased tactile fremitus, egophony

A

Consolidation (Lobar pneumonia, pulmonary edema)

96
Q

Tracheal Deviation toward side of lesion

A

Atelectasis –> Bronchial obstruction

97
Q

Tracheal Deviation away from lesion

A

Tension pneumothorax (hyperresonant percussion) or Pleural effusion (dull percussion)

98
Q

Fluid in pleural layers

A

Pleural effusion. Tx with thoracentesis

99
Q

Air in pleural layers

A

Pneumothorax

100
Q

unilateral chest pain, dyspnea, expansion. Hyperresonance

A

Pneumothorax

101
Q

dyspnea in tall, thin, young male (esp a smoker)

A

Primary spontanous pneumothorax –> rupture of SUBPLEURAL APICAL BLEBS

102
Q

air fluid levels on CXR (almost looks like a fungus ball)

A

Abscess

103
Q

Tx for lung abscess

A

Clindamycin

104
Q

Carcinoma in apex of the lung

A

Pancoast tumer (aka superior sulcus tumor)

105
Q

Sx of Pancoast tumor

A

Invades cervical sympathetic chain (autonomic ganglia) = Horner’s. SVC syndrome, hoarseness, sensorimotor deficits. Shoulder/upper extremity pain from compression of brachial plexus

106
Q

Causes of SVC syndrome

A

malignancy (Pancoast tumor) and thrombosis from indwelling cathethers

107
Q

keratin pearls and intercellular bridge

A

Squamous cell carcinoma

108
Q

Inactivating mutation of bmpr2 = ____________. Pathology = _____________ (because bmpr2 usually inihibits it)

A

Pulmonary Arterial Hypertension

Vascular smooth muscle proliferation
–>Ultimately get intimal fibrosis and thickening

109
Q

What effect does pulmonary artery hypertension have on cardiac heart sounds?

A

Accentuated (louder) pulmonary component of second heart sound (P2)…“Loud second heart sound at the upper sternal border” (all Patients take meds)

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