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USMLE STEP 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What makes up the Conducting Zone?

A

Large airways: Nose, Pharynx, Trachea, Bronchi

Small airways: Bronchioles and Terminal Bronchioles

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2
Q

Function of Conducting Zone

A

Warms and humidifies air but does not participate in gas exchange
Anatomical Dead Space

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3
Q

Cartilage extends until

A

Bronchi

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4
Q

Goblet cells extend until

A

End of Bronchi

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5
Q

Pseudostratified, ciliated, columnar cells extend until

What is the cilia’s function?

A

End of Terminal Bronchioles to beat mucus up and out of lung

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6
Q

Smooth muscle in airway wall extends until

A

terminal bronchioles

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7
Q

What makes up the respiratory zone?

A

= Lung Parenchyma. Respiratory bronchioles, alveolar ducts and alveoli
participates in gas exchange

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8
Q

What kind of cells are in the Respiratory zone?

A

Cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli

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9
Q

Type I Pneumocytes
Percentage of alveolar surface
Kind of cell
Function

A

97% of alveolar surface. Squamous cells optimal for gas diffusion

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10
Q

Type II Pneumocytes
Kind of cell
Function

A

Clustered cuboidal cells. Secrete surfactant and act as precursors

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11
Q

Collapsing Pressure Formula

A

P = 2 (surface Tension) / Radius

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12
Q

When are alveoli most likely to collapse?

A

On Expiration

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13
Q

Function of surfactant

A

Decreased alveolar surface tension to prevent atelectasis

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14
Q

Composition of surfactant

A

Complex mix of lecithins. The most important of which is dipalmitoylphasphatidylcholine

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15
Q

When does surfactant production begin in the fetus? When does it reach mature levels? What indicates maturity?

A

Begins at week 26. Mature by week 35. Mature when Lecithin/Sphingomyelin > 2

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16
Q

Clara Cells:
Location
Appearance
Function

A

In Terminal and Respiratory Bronchioles. Non ciliated columnar cells with secretory granules. Secrete components of surfactant, degrade toxins and act as reserve cells

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17
Q

of lobes in each lung?

A

R: 3, L: 2 + Lingula

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18
Q

Foreign body most likely to be lodged in

A

R lung because R mainstem bronchus is wider and more vertical than L

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19
Q

Aspirate a peanut:
While upright?
While supine?

A

Upright: Lower Portion of R Inferior Lobe
Supine: Superior Portion of R Inferior Lobe

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20
Q

Relationship bet Pul Artery to the Bronchus?

A

RALS

Right: Anterior, Left Superior

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21
Q

Structures perforating the Diaphragm

A

I ate 10 eggs at 12
T8: IVC
T10: Vagus and Esophagus
T12: Aorta, Azygous, Thoracic duct (Red White and Blue)

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22
Q

What innervates the Diaphragm? Where is pain from the Diaphragm referred?

A

C3, 4, 5 keeps you alive

Pain referred to shoulder (C5) and Trapezius ridge (C3, C4)

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23
Q

Muscles of respiration (quiet and exercise)

A

Inspiration: Quiet –> Diaphragm, Exercise –> SCM, Scalene, External Intercostals
Expiration: Quiet –> Passive, Exercise –> Obliques (Internal and External), Abdominis (Rectus and Transversus) Internal Intercostals

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24
Q

Inspiratory Reserve Vol

A

Air that can be breathed in after normal inspiration

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25
Q

Tidal Vol

A

500mL. Air that moves into the lung on quiet inspiration

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26
Q

Expiratory Reserve Vol

A

Air that can still be breathed out after a normal expiration

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27
Q

Reserve Volume

A

Air left in lung after maximal expiration

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28
Q

Inspiratory capacity

A

TV + IRV

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29
Q

Function Residual Capacity

A

RV + ERV

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30
Q

Vital Capacity

A

TV + IRV + ERV

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31
Q

Total Lung Capacity

A

IRV + TV + ERV + RV

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32
Q

Physiological Dead Space
Definition
Calculation

A

Vol of inspired air that does not participate in gas exchange
VD = Anatomical Dead Space of conducting airways + functional dead space in alveoli
VD = TV [(PaCO2 -PECO2)/PaCO2] Taco Paco Peco Paco

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33
Q

Largest contributor to functional dead space?

A

Apex of Lung

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34
Q

The tendency is for the lung to … and for the chest wall to …

A

Lung wants to collapse, Chest wall wants to spring outward

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35
Q

@ FRC: What is happening with the lung - chest wall system? What is the P in the alveoli and airway? What is the P in the Intrapleural space?

A

@ FRC: Inward pull of lung = outward pull of chest wall and system pressure is atmospheric. P in the alveoli and airway = 0. P in the Intrapleural space is negative to prevent pneumothorax

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36
Q

Alveolar transmural pressure is …

A

Always positive. Meaning always tending to collapse

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37
Q

What determines the elastic properties of both the chest wall and lungs?

A

Their combined volume

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38
Q

What is compliance?
What increases compliance?
What decreases compliance?

A

Change in lung vol for a given change in pressure
Increases in emphysema and normal aging
Decreases in fibrosis, pneumonia and edema

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39
Q

Hemoglobin
Composed of
Exists in 2 forms
Exhibits

A

Composed of 2 alpha and 2 beta subunits
Exists in Taut form in tissues (low affinity) and Relaxed form in lungs (high affinity)
Exhibits positive cooperativeity and negative allostery

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40
Q

What shifts Hemoglobin dissociation curve to the R (towards T form)

A

CADET! Turn R!

CO2 and Cl, Acidosis and Altitude, BPG, Exercise, Increased Temp

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41
Q

Fetal Hemoglobin
Consists of
Different affinities?

A

Consists of 2 alpha and 2 gamma subunits

Lower affinity for BPG = higher affinity for O2 –> curve shifted to the L

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42
Q 
Methemoglobin
What is it ?
Change in affinity?
Shift in curve?
Treat with
A

Oxidized Iron 3+ (ferric) instead of Iron 2+ (ferrous)
Lower affinity for O2, Higher affinity for cyanide
Shifts curve to R
Treat with Methylene Blue

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43
Q

Nitrite poisoning causes

A

Oxidization of Fe2+ to Fe3+

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44
Q

How to treat cyanide poisoning?

A

Use nitrites to oxidize Hemoglobin to methemoglobin. MetHem with bind cyanide and allow cytochrome oxidase to function. Then use Thiosulfate to bind cyanide –> forms thiocynate which is renally excreted

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45
Q

Carboxyhemoglobin
What is it
Affect on O2 binding curve

A

Hemoglobin bound to CO

Shifts curve to L –> decreased O2 unloading in tissues

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46
Q

Appearance of Hemoglobin O2 binding curve?

A

Sigmoidal because of cooperativity

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47
Q

Pulmonary Circulation Re Resistance and Compliance

A

Low Resistance and High Compliance

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48
Q

How does a decrease in PA02 (= increase in PACO2) affect pulmonary circulation?

A

Vasoconstriction to shift blood away from poorly ventilated areas

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49
Q

Which gases are perfusion limited? What does that mean?

A

O2 (normally), CO2, N2O. Diffusion Increases if Blood Flow Increases

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50
Q

Which gasses are diffusion limited? What does that mean?

A

O2 (in fibrosis or emphysema), CO. Gas does not equilibrate by the time the blood reaches the end of the capillary.

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51
Q

Gas diffusion equation
What happens in Emphysema?
What happens in Fibrosis?

A

Vgas = (A/T) x D(P1-P2)
Emphysema –> Area decreases
Fibrosis –> Thickness increases

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52
Q

Pulmonary artery pressure: Normal? PHTN?

A

Normal: 10-14mmHg, PHTN: >/= 25 (rest) or >/= 35 (exercise)

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53
Q

PHTN affect on pulmonary artery

A

Arteriosclerosis, Medial Hypertrophy, Intimal Fibrosis

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54
Q

Cause of Primary PHTN

A

Inactivation of BMPR2 gene which normally functions to inhibit vascular smooth muscle proliferation

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55
Q

What causes secondary PHTN? What is the course of the disease?

A

COPD (destruction of lung parenchyma), Mitral Stenosis (Increased resistance –> increased P), Recurrent thromboemboli (decreased cross sectional area of pulmonary vascular bed), autoimmune disease, L –> R shunt (increased sheer stress –> endothelial injury), Sleep Apnea, Living at high altitude
Respiratory distress –> Cyanosis and RVH –> cor pulmonale –> death

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56
Q

Pulmonary Vascular Resistance formula

A

PVR = (P pulmonary artery - P left atrium) / CO

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57
Q

O2 content of blood formula

What is normal O2 binding capacity?

A

O2 binding capacity x saturation + dissolved O2

O2 binding capacity normally 20ml/dL

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58
Q

1g Hb can bind how much O2?
How much Hb is normally in blood?
When does cyanosis occur?

A

1.34mL
15 g Hb/dL
Cyanosis occurs when deoxygenated Hb > 5g/dL

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59
Q

What happens to O2 content of blood, O2 sat and PaO2 when Hb decreases?

A

O2 content decreases but O2 sat and PaO2 remain the same

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60
Q

Formula for oxygen delivery to tissues

A

CO x O2 content of blood

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61
Q

Alveolar gas equation

A 
PAO2 = PIO2 - PaCO2/R
PAO2 = 150 - PaCO2/.8
R = CO2 produced/O2 consumed
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62
Q

A-a gradient
Normal value
Increased in?
Causes?

A

Normal A-a gradient = 10-15mmHg
Increased in hypoxemia due to lesion in Lung
Causes: Shunting, V/Q mismatch, Fibrosis

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63
Q

Causes of hypoxemia with normal A-a gradient?

A

High altitude, hypoventilation

64
Q

What causes hypoxemia with increased A-a gradient?

A

V/Q mismatch, Diffusion limitation, R-L shunt

65
Q

Causes of Hypoxia

A

Decreased cardiac output, Hypoxemia, Anemia, CO poisoning

66
Q

What can cause ischemia?

A

Arterial flow or venous drainage blocked

67
Q

V/Q at apex? base?

A

apex = 3 (wasted ventilation). base = .6 (wasted perfusion)

68
Q

Where in the lung is ventilation greatest? Where is perfusion greatest?

A

Both at base

69
Q

What happens to V/Q during exercise?

A

Vasodilation of apical capillaries –> V/Q approaches 1 at apex

70
Q

What kind of organisms thrive in the apex of the lung?

A

Those that thrive on high O2 like TB

71
Q

V/Q = 0

A

Shunt (airway obstruction). 100% O2 wont help

72
Q

V/Q = infinity

A

Blood flow obstruction (physiological dead space) Assuming <100% dead space, O2 will help

73
Q

PAO2, PaO2, and PvO2 in apex, middle and base

A

Apex: PA>Pa>Pv
Middle: Pa>PA>Pv
Base: Pa>Pv>PA

74
Q

In what forms is CO2 transported in the blood?

A

Bicarb: 90%, CarbaminoHb (binds at N terminus and binding favors T form): 5%, Dissolved CO2: 5%

75
Q

How does oxygenation of Hb affect CO2 in blood?

A

Oxygenation –> dissociation of H from Hb. H + bicarb = CO2 thus more CO2 is released from RBC
Haldane Effect

76
Q

Bohr Effect

A

Increased H in periphery –> Hb O2 curve shifted to R and O2 unloading favored

77
Q

Response to high altitude?

A

Increased Mito, Increased renal excretion of bicarb (to combat alkalosis) Increase in ventilation, decreased PO2 + PCO2, Increased EPO –> Increased Hb and Hc, Increased BPG, RVH
“Mr. V. Deb”

78
Q 
Response to exercise
CO2 production
O2 consumption
Ventilation
V/Q
Pulmonary blood flow
pH
PaO2, PaCO2, venous CO2, venous O2
A

CO2 production increases, O2 consumption increases, Ventilation increases, V/Q becomes more uniform, Pulmonary blood flow increases, pH decreases (lactic acidosis), PaO2 NC, PaCO2 NC, venous CO2 increase, venous O2 decreases

79
Q 
DVT
What predisposes to it?
What can it lead to?
Physical Exam sign?
Treatment and prevention?
A

Virchow’s triad of Vascular damage (exposed collagen), Increased coagulability (defect in coagulation cascade, most commonly factor V Leiden), Reduced flow [VIR]
Leads to Pul embolus
Homan’s Sign –> Dorsiflexion of foot –> calf pain
Heparin for prevention and acute management. Warfarin for long-term prevention of recurrence

80
Q

Sudden onset of dyspnea, chest pain, and tachypnea

A

Pulmonary embolism

81
Q

Types of PE?

A

FAT BAT

Fat, Air, Thrombus, Bacteria, Amnionic fluid, Tumor

82
Q

Fat embolus associated with…

Presents as…

A

Long bone fracture and liposuction

Presents as hypoxemia, neurological abnormalities, petechial rash

83
Q

Major risk with Amnionic fluid embolus?

A

Can lead to DIC especially post partum

84
Q

Imaging test of choice for PE?

A

CT pulmonary angiography

85
Q

Where do most PEs arise from?

A

95% from deep leg veins

86
Q

Most dangerous location for PE?

A

Saddle Embolus of Pulmonary Artery

87
Q

Histology of thromboembolus formed premortem?

A

Lines of Zahn: interdigitating areas of pink (platelets, fibirn) and red (RBCs)

88
Q

Obstructive Lung Disease: Names, RV, FVC, PFTs, V/Q, PO2, PCO2

A

Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis
RV: Increases, FVC: Decreases
FEV1 decrease, FVC decreases, FEV1/FVC decreases
V/Q decreases, PO2 decreases, PCO2 increases

89
Q

Chronic Bronchitis: Clinical definition

A

Productive Cough for >3 months (not necessarily consecutive) for >2 years

90
Q

Chronic Bronchitis: Pathology and Physical Findings

A

Harry Reid Won 50% Securing Complete Democratic Control
Hypertrophy of Mucus secreting glands in bronchi, Reid Index > 50%, Wheezing, Small airway disease, Crackles (early) Dyspnea (late), Cyanosis (early onset hypoxemia due to shunting)

91
Q

Emphysema: pathology and findings

A

PERCE
Pursed lip breathing (increased airway pressure prevents collapse), Enlarged airspace, Recoil decreased, Compliance increased, Elastase activity increased

92
Q

Two types of emphysema

A 
Centriacinar = smoking 
Panacinar = alpha-1-antitrypsin deficiency
93
Q

Alpha Agonists
Names
Uses
Tox

A

Pseudoephedrine, Phenylephrine
Reduce hyperemia, edema, nasal congestion.
Open up Eustachian tube.
Pseudoephedrine is a stimulant. Can cause HTN. Pseudoephedrine can cause CNS stimulation/anxiety

94
Q 
Dextromethorphan
Class
MoA
Uses
Risk
Antidote
A 
Opioid (synthetic codeine analog)
Antagonizes NMDAR
Antitussive
Mild abuse potential
Naloxone treats OD
95
Q

Bosentan
MoA
Uses

A

Competative antagonist of endothelin 1 receptor
Decreases Pulmonary Vascular Resistance
Used to treat Pulmonary Arterial HTN

96
Q

N Acetylcysteine
Type of drug
Action
Uses

A

Mucolytic expectorant
Loosens mucus plugs in CF
Antidote for acetaminophen OD

97
Q

Guaifenesin
Type of drug
Action

A

Expectorant that thins the respiratory secretions but does not suppress the cough reflex

98
Q

Molecules that cause bronchoconstriction?

A

Adenosine, ACh

99
Q

Molecules that cause Bronchodilation

A

cAMP

100
Q

Ab Asthma therapy
Name
MoA
Uses

A

Omalizumab
Monoclonal IgE Ab that binds up serum IgE
Used in allergic asthma resistant to steroids and long acting beta2 agonists

101
Q

Anti Leukotrienes
Names
MoA
Uses

A 
Montelukast, Zafirlukast 
--/ leukotriene receptor. 
Especially good in aspirin induced asthma
Zileuton --/ 5 lipoxygenase pathway. 
Blocks arachidonic acid --> leukotrienes
Both used to treat Asthma
102
Q

Corticosteroids used to treat Asthma
Names
MoA

A

Beclomethasone, Fluticasone

  • -/ cytokine production
  • -/ NFkB (NFkB –> TNF alpha)
103
Q

Antimuscarinics
Name
MoA
Uses

A

Ipratropium (short), Tiotropium (long)
–/ muscarinic receptors thereby preventing bronchoconstriction
Asthma and COPD

104
Q 
Methylxanthines
Names
MoA
Use
Tox
Metabolism 
Blocks actions of
A

Theophylline–/ PDE leading to increased cAMP
Asthma treatment
Narrow therapeutic index –> cardiotoxic, neurotoxic
P450 metabolism
Blocks actions of Adenosine

105
Q

Pneumothorax presentation

A

PTHORAX
Pleuritic pain, Tracheal deviation, Hyperresounant, sudden Onset, Reduced breath sounds, Absent Fremitus, XR –> Collapse

106
Q

Beta 2 agonists
Short
Long (uses, tox)

A

Short: Albuterol –> Beta2 –> SM relaxation
Long: Salmeterol, Formoterol.
Used for prophylaxis.
Can cause tremors and arrhythmias

107
Q

Asthma drug targets

Classes of drugs

A

Antiinflammation + Anti parasympathetic tone
First Line Therapy: Corticosteroids
Beta 2 agonists, Methylxanthines, Anti Muscarinic, Antileukotrienes, Abs

108
Q

H1 Blockers 2nd Gen
Names
Use
Tox

A

Loratadine, Fexofenadine, Desloratadine (adine)
Allergy
Much less sedating because do not enter CNS

109
Q

H1 Blockers, 1st Gen
Names
Use
Tox

A

Diphenhydramine, dimenhydrinate, chlorpheniramine (en/ine, en/ate)
Allergy, motion sickness, sleep aid
Sedation, antimuscarinic, anti alpha adrenergic

110
Q

Kinds of antihistamines used in the lung?

A

H1 blockers

111
Q

Pleural Effusion: Lymphatic
Name
Due to
Appearance

A

Chylothorax. Due to thoracic duct injury from trauma or malignancy.
Appears milky with high triglyceride content

112
Q

Pleural Effusion: Exudate
Caused by
Action that must be taken?

A

High Protein content, appears cloudy
“CAPTAIN”
Due to Collagen Vascular Disease, Abdominal pathology, Pneumonia, TB, Trauma (occurs in states of increased vascular permeability), Asbestos, Infection (Pneumonia), Malignancy
Must be drained to prevent infection

113
Q

Pleural Effusion: Transudate

Caused by

A

Low protein content
“CHEMN”
Due to CHF, Hepatic cirrhosis (Hypoalbuminia), Embolism, Meig Syndrome, Nephrotic syndrome

114
Q

Hypersensitivity Pneumonitis
Type of Rxn
Presentation
Seen in what kind of pt?

A

Mixed Type III/IV hypersensitivity rxn to environmental antigen
“Holding Down Tough Cows on a Farm”
Presents with headache, dyspnea, tight chest, cough
Seen in farmers and bird owners

115
Q 
Interstitial (atypical) pneumonia
Organisms
Characteristics 
Distribution
Course
A

Viruses (influenza, RSV, adenovirus), Mycoplasma, Legionella, Chlamydia
Diffuse, patchy inflammation in interstitial areas
Involves ≥ 1 lobe.
Indolent course

116
Q 
Bronchopneumonia 
Organisms
Characteristics
Histo 
Distribution
A

S pneumoniae, S aureus, H influenzae, Klebsiella
Acute inflammatory infiltrates from bronchioles into adjacent alveoli
Neutrophils in alveolar spaces
Patchy distribution involving ≥ 1 lobe

117
Q

Lobar Pneumonia
Organisms
Characteristics

A

S. pneumoniae, KlebsiellaIntra
alveolar exudate –> consolidation
May involve entire lung

118
Q 
SVC syndrome 
Def
Presentation
Causes
Can lead to...
A

Obstruction of SVC impairs blood drainage from Head (Facial Plethora) Neck (JVD) and Arms (Edema)
Caused by malignancy, thrombosis (from indwelling catheters)
Can lead to Increased ICP –> headache, dizziness, aneurysm, cranial artery rupture

119
Q

Pancoast Tumors

A

Carcinomas in apex of lung affect cervical sympathetic plexus resulting in Horner’s Syndrome (Ipsilateral Miosis, Anhidrosis, Ptosis)

120
Q 
Mesothelioma 
Location
Associated with
Results in
Histology
A

Pleural. Associated with asbestosis.
Results in Hemorrhagic pleural effusions and pleural thickening.
Psommoma bodies

121
Q 
Bronchial Carcinoid Tumor 
Prognosis
Metastasis
Symptoms due to
Can lead to
Histology
A

Excellent Prognosis.
Metastasis: rare.
Symptoms due to mass effect
Can lead to CARCinoid syndrome (5HT release –> Cutaneous flushing, Asthmatic wheezing, Right valve lesions, Cramps, Diarrhea, Salivation)
Nests of neuroendocrine cells. Chromogranin +

122
Q 
Large Cell Carcinoma 
Location
Differentiation
Prognosis
Treatment 
Histology
A 
Peripheral, highly anaplastic undifferentiated tumor
Poor Prognosis
Surgery. 
Poor response to chemo 
Pleomorphic giant cells
123
Q 
Small Cell (Oat Cell) Carcinoma
Location
Differentiation
May produce 
Genetics 
Treatment
Histology
A

Central, undifferentiated, aggressive
May produce ACTH, ADH, Abs against presynaptic Ca channels (Lambert Eaton)
Genetics: amplification of myc oncogenes
Chemotherapy.
Inoperable
Kulchitsky cells (small dark blue cells). Salt and Pepper neuroendocrine chromatin

124
Q 
Squamous Cell Carcinoma 
Location
Arise from 
Characteristics
Histology
A

Central
Hilar mass arises from bronchus
Cavitation, Cigarettes, hyperCa (produces PTH)
Dysplastic squamous cells with Keratin Pearls and Intracellular Bridges

125
Q

Lung Abscess
Definition
Caused by
CXR

A

Localized collection of pus within parenchyma
Caused by bronchial obstruction (cancer), aspiration of oropharyngeal contents (pts predisposed to LOC i.e. alcoholics), infection of S aureus or anaerobes (Bacteroides, Fusobacterium, Peptostretococcus)
Air-Fluid levels often seen on CXR

126
Q 
Bronchioloalveolar adenocarcinoma 
Derived from
CXR
Histology
Prognosis
A

Derived from Clara Cells
Hazy infiltrates similar to pneumonia
Grows along alveolar septa –> apparent thickening of alveolar walls
Excellent prognosis

127
Q 
Adenocarcinoma
Can present as...
Location
Most common lung cancer in
Genetics
Physical Exam Findings
A

Can present as pneumonia
Peripheral.
Develops in scars (old Tuberculous Granulomas)
Most common lung cancer in nonsmokers and females
Activating k-ras mutation
Osteoarthropathy (clubbing)

128
Q

Where do Lung Cancers metastasize to?

A

Brain, Liver (jaundice, hepatomegaly), Adrenals, Bone (pathologic fracture)

129
Q

Most common cause of Lung Cancer?

A

Metastasis from Breast, Bladder, Colon, or Prostate

130
Q

Lung Cancers Not Associated with Smoking?

A

Bronchioloalveolar and bronchial carcinoid

131
Q

Complications of Lung Cancer

A

SPHERE
SVC syndrome, Pancoast tumor, Hornerns, Endocrine (paraneoplastic), Recurrent laryngeal symptoms (hoarseness), Effusions (pleural or pericardial)

132
Q

Lung Cancer Presentation

A

ABCDE
Avalanche, Bloody cough, Cough, Coin Lesions on XR, nonCalcified nodules on CT, Disrupted bronchi (bronchial obstruction), whEezing

133
Q 
Consolidation (Lobar Pneumonia, Pulmonary Edema)
Breath sounds
Percussion
Fremitus
Tracheal deviation
A

Breath sounds: Bronchial, Late inspiratory Crackles
Percussion: dull
Fremitus: increased
Tracheal deviation: none

134
Q 
Tension Pneumothorax
Presentation
Pathology
Breath sounds
Percussion
Fremitus
Tracheal deviation
Most common pt
A 
Unilateral chest pain, dyspnea, unilateral chest expansion
Air enters pleural space but cannot exit
Breath sounds: decreased
Percussion: hyperresonant
Fremitus: decreased 
Tracheal deviation away from lesion
Trauma or lung infection
135
Q 
Spontaneous Pneumothorax 
Presentation
Pathology
Breath sounds
Percussion
Fremitus
Tracheal deviation
Most common pt
A

Unilateral chest pain, dyspnea, unilateral chest expansion
Rupture of apical bleb –> accumulation of air in pleural space
Breath sounds: decreased
Percussion: hyperresonant
Fremitus: decreased
Tracheal deviation towards side of lesion
Tall thin young male

136
Q 
Atelectasis (Bronchial Obstruction)
Breath sounds
Percussion
Fremitus
Tracheal deviation
A

Breath sounds: decreased
Percussion: dull
Fremitus: decreased
Tracheal deviation toward side of lesion

137
Q 
Pleaural Effusion 
Breath sounds
Percussion
Fremitus
Tracheal deviation
A

Breath sounds: decreased
Percussion: dull
Fremitus: decreased
Tracheal deviation: none

138
Q

Obstructive Sleep Apnea
Description
Associations

A

Respiratory effort against airway obstruction. Associated with obesity, snoring, HTN, PHTN, Arrhythmias, Sudden Death

139
Q 
Sleep Apnea
Definition
Types
Results in
Treatment
A

Cessation of breathing for >10 sec
Central (no respiratory effort) vs Obstructive
Results in Hypoxia –> EPO release –> Erythropoiesis
Wt loss, CPAP, Surgery

140
Q 
ARDS
Causes
Pathology
Initial damage caused by
Histology
A

Caused by Aspiration, Acute pancreatitis, Air or Amnionic emboli, Radiation, DIC, Drugs, Dialysis, Diffuse Infection, Sepsis, Shock, Trauma, Uremia
Diffuse alveolar damage –> Increased capillary permeability –> protein rich exudate into alveoli –> Intraalviolar hyaline membane
Initial damage caused by release of substances toxic to alveolar wall by neutrophils, activation of coagulation cascade, ROS
Histo: Alveolar fluid and hylaline membranes

141
Q 
NRDS 
Pathology
Lechithin/Sphingomyelin ratio
Because of low O2 tension -->
Therapeutic O2 --> 
Risk factors 
Treatment
A

Surfactant deficiency –> Increased Surface Tension –> alveolar collapse
L/S < 1.5 predictive
Because of low O2 tension –> risk of PDA
Therapeutic O2 –> ROP and Bronchopulmonary Dysplasia
Risk factors: Prematurity, Maternal Diabetes, Cesarean delivery (decreased release of glucocorticoids)
Treatment: maternal steroids before birth. Artificial surfactant for the infant

142
Q 
Asbestosis
Associated with what kind of jobs?
Associated with what other diseases 
Histology?
Appearance?
A

Associated with shipbuilding, roofing, plumbing
Associated with Bronchogenic Carcinoma and Mesothelioma
Asbestos bodies are golden brown fusiform rods (dumbbells) in Macs Ivory White calcified pleural plaques are pathognomonic but not precancerous

143
Q 
Silicosis 
Associated with what kind of jobs?
Pathology
Increased risk for
Affects which lobes?
Appearance?
A

Associated with foundries, sandplansting, mines
Si –> Macs –> release fibrogenic factors
Increased risk for TB because Si –/ phagolysosomes thereby –/ macs.
Also increased risk for Bronchogenic Carcinoma
Affects Upper Lobes
Eggshell calcifications on hilar lymph nodes

144
Q

Anthracosis
Associated with what kind of pt?
Which lobes are affected?

A

Coal Miners Lung. Affects Upper Lobes

145
Q

Names of Pneumoconioses

A

Anthracosis, Silicosis, Asbestosis

146
Q

Pneumoconioses + RA

A

Caplan Syndrome which can lead to Cor Pulmonale

147
Q

Drugs that cause restrictive lung disease

A

Bleomycin, Busulfan, Amiodarone, Methotrexate

148
Q

Interstitial Restrictive Lung Disease
Characterized by
Names

A

Decreased Diffusion Capacity and Increased A-a Gradient
“A Good Physician Would Never Speak Hateful, Disgusting Epithets Intentionally”
ARDS, Goodpasture, Pneumoconioses, Wegeners (granulomatosis with polyangiitis), NRDS (hyaline membrane disease), Sarcoidosis (bilateral hilar lymphadenopathy, noncaseating granulomas, Increased ACE and Ca), Hypersensitivity pneumonitis, Drugs, Eosinophilic Granulomas (Langerhans cell histiocytosis), Idiopathic (repeat injury with collagen deposition)

149
Q

Extra-pulmonary restrictive lung disease

A

Muscles: Polio, MG.
Structural: Scoliosis, Morbid Obesity

150
Q

Restrictive Lung Disease: Lung Volumes, PFTs

A

FVC: decreased, TLC: decreased, FEV1/FVC > 80%

151
Q

Bronchiectasis Pathology and Associations

A

“No Hot Days Post September, Onto KA”

chronic Necrotizing infection of bronchi, Hemoptasis, permanently Dilated airways, Purulent Sputum, Smoking (poor ciliary motility), bronchial Obstruction, Kartageners’s (Dynein arm), Allergic bronchopulmonary Aspergillosis, CF

152
Q

Asthma physical exam findings:

A

“His Majesty Coughed and Wheezed In Excruciating Pain ‘Till Dawn”

Hypoxia, Mucus plugging, Cough, Wheeze, I/E ratio decreased, Pulsus Paradoxus (decrease in Systolic Pressure), Tachypnea, Dyspnea

153
Q

Test given to prove asthma

A

Methacholine challenge. Muscarinic agonist

154
Q

Asthma pathological causes and course

A

Bronchial hyper-responsiveness causes reversible Bronchoconstriction + Smooth Muscle hypertrophy
Antigen –> IgE on mast cell. Mast cell releases inflammatory mediators (leukotrienes, histamine, etc.)
Early response to inflammation = bronchoconstriction
Late response to inflammation = Bronchial hyper-reactivity

155
Q

Asthma triggers

A

URI, stress, allergens

156
Q

Asthma histology

A

Cushmann’s Spirals (shed epithelium from mucus plugging). Charcot-Leyden Crystals (Formed from breakdown of eosinophils in sputum)

USMLE STEP 1 (25 decks)

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