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USMLE > DIT X: Pulmonary > Flashcards

DIT X: Pulmonary Flashcards

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0
Q

Tracheoesophageal fistula: definition, most common type

A

Abn connection between esoph + trachea Most common Type C (85%): upper esoph ends in blind pouch, lower esoph connects to trachea

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1
Q

Rx tiotropium

A

Inhaled anticholinergic relaxes airway, opposes bronchospasm COPD

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2
Q

TE fistula: types

A

A: esoph atresia w/o fistulas (no connection) B: upper esoph connects C: lower esoph connects D: upper & lower both connect E: fistula but no esoph atresia (“H type”)

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3
Q

What type of epithelium lines trachea, and what metaplasia is seen in smokers?

A

Ciliated columnar epithelium –> squamous metaplasia in smokers

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4
Q

Kartagener syndrome: alternate name, what is the defect?

A

Primary ciliary dyskinesia, due to non-functional dynein

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5
Q

Kartagener syndrome: clinical triad, other S&S

A

Triad: situs inversus, bronchiectasis, chronic sinusitis Others: infections, infertility, hearing loss

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6
Q

4 embryologic structures making up diaphragm

A

Septum transversum, pleuroperitoneal membranes, dorsal mesentery of esoph, abdo wall muscles

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7
Q

Congenital diaphragmatic hernia: presentation and complications

A

Presentation: flattened abdo, cyanosis, inability to breathe, most often on L side, assoc w polyhydramnios Complications: compression of thorax –> lung hypoplasia

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8
Q

Hiatal hernia: types

A

Sliding: most common, GEJ displaced, “hourglass stomach” Paraesophageal: cardia moves into thorax, GEJ stays in place

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9
Q

Innervation of diaphragm, to where does pain refer?

A

Phrenic nerve (C3, 4, 5) –> pain refers to neck and shoulder

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10
Q

Conducting zone vs respiratory zone

A

Conducting zone: nose to terminal bronchioles, no gas exchange, anatomic dead space Respiratory zone: resp bronchioles to alveolar sacs, gas exchange

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11
Q

Which lung is most common location for inhaled foreign body and why?

A

Right lung; right mainstem bronchus wider and more vertical than left

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12
Q

How many bronchopulmonary segments in each lung?

A

10 in right: 3 RUL, 2 RML, 5 RLL 8-10 in left: 4-5 LUL, 4-5 LLL

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13
Q

Respiratory muscles used in quiet respiration

A

Inspiration: diaphragm Expiration: relaxation

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14
Q

Accessory muscles of inspiration and expiration

A

Insp: SCM, ext intercostals, scalene muscles Exp: transversus abdominus, rectus abdominus, int & ext obliques, int intercostals

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15
Q

Type I pneumocytes

A

simple squamous epith, >97% alveolar surface, gas exchange, unable to replicate

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16
Q

Type II pneumocytes

A

large cuboidal, at alveolar-septal junctions, secrete pulmonary surfactant, can replace type I pneumocytes in lung damage

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17
Q

Surfactant: composition and function

A

Dipalmitoyl phosphatidylcholine; decreases alveolar surface tension

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18
Q

Lecithin:Sphingomyelin Ratio

A

from amniotic fluid sample, used to determine if premature lung is mature enough (ratio >2.0)

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19
Q

How to mature premature baby’s lungs pre-delivery?

A

Give mom corticosteroids

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20
Q

Chronic sinusitis + infertility + situs inversus

A

Kartagener Syndrome (Primary Ciliary Dyskinesia)

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21
Q

Structures traversing the diaphragm, and at which vertebral levels?

A

T8: IVC T10: esoph + vagus nerve T12: aorta, azygos vein, thoracic duct

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22
Q

Anatomical dead space vs functional dead space

A

Anatomical: air in airways Functional: capable of gas exchange, but none occurs

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23
Q

Eqn: Physiologic dead space

A

Vd = Vt x (PaCO2 - PeCO2) / PaCO2

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24
Eqns: Pulmonary vascular resistance
(delta)P = Q x R
25
Relationship between functional residual capacity and chest wall dynamics
FRC: point at which outward force of chest wall and inward force of lung is perfectly balances, differs from person to person (compliance)
26
Normal pulmonary artery pressure and Dx of pulm HTN
Normal: 10-15 mmHg Pulm HTN: pulm artery pressure \>25 mmHg during rest, or \>35 during exercise
27
Pathological changes seen in pulmonary HTN + consequences
Arteriosclerosis, media hypertrophy, fibrosis of intima Consequences: cor pulmonale, right heart failure
28
Causes of secondary pulmonary HTN
Chronic lung disease (COPD, pulm fibrosis), mitral stenosis, recurrent TE, autoimmune, L to R shunts (VSD), sleep apnea, high altitude
29
Tx for pulmonary HTN
Bosentan / ambrisentan, prostaglandin analogue, sildenafil, dihydropyridine CCB
30
MOA of bosentan & ambrisentan
competitively antagonize endothelin-1 receptors --\> decrease pulm vasc resistance
31
Primary pulmonary HTN: mutation, epidemiology, 2 disease associations
* abnormalities in BMPR2 (Bone Morphogenetic Protein Receptor type II) --\> excessive vasc smooth muscl prolif * esp women, avg age 36 * assoc w HIV and Kaposi sacroma (HHV-8)
32
If a lung collapses, what happens to intrathoracic volume?
Intrathoracic vol increases (chest wall expands)
33
What gene mutation causes primary pulmonary HTN?
BMPR2 (Bone Morphogenetic Protein Receptor Type II)
34
HbA: composition and 2 forms
* 2 alpha globins + 2 beta globins + 4 heme * T form (taut): low affinity for O2, favours tissues * R form (relaxed): high affinity for O2
35
How is fetal Hb different from adult Hb?
* 2 alpha globins + 2 gamma globins * lower affinity for 2,3-DPG = higher affinity for O2
36
Normally, Hb has which form of iron?
Ferrous (Fe 2+)
37
Methemoglobin has which form of iron?
Oxidized --\> ferric
38
Clinical use of methemoglobin
Higher affinity for cyanide, can use in cyanide poisoning (give nitrates to oxidize Hb)
39
Tx for cyanide poisoning
* amyl nitrite, sodium nitrite: to oxidize Hb to methemoglobin --\> pick up cyanide * thiosulfate: binds cyanide to be excreted renally
40
What is carboxyhemoglobin, and what effect does it have on the oxygen dissoc curve?
* Hb bound to CO * Left shift
41
Substances causing methemoglobinemia
* nitrates & nitrites * antimalarial drugs (eg chloroquine, primaquine) * dapsone * sulfonamides * local anaesthetics (eg lidocaine) * metoclopramide
42
Tx for methemoglobinemia
* **methylene** blue * vit C * cimetidine (H2 blocker)
43
Eqn: total blood O2 content
Total Blood O2 content = dissolved O2 + (Hb binding capacity x O2 sat)
44
How does anemia affect O2 sats and arterial PaO2?
Does not change either
45
How does exercise change arterial and venous O2 content?
no change in arterial O2, decreased venous O2 (due to increased O2 demand)
46
Alveolar gas equation
PAO2 = 150 - PaCO2/0.8 | (See DIT p. 386)
47
A-a gradient: normal value, what would increase it?
* Normally small (10-15) * Increase: shunting or V/Q mismatch, pulm fibrosis, increased FiO2, age
48
PaO2 : FiO2 ratio; normal and abnormal values
* normal: 300-500 mmHg * \<300: gas exchange deficit * \<200: severe hypoxia
49
V/Q ratios in lung apex vs lung base
* apex: V/Q \> 1 , decreased perfusion * base: V/Q \< 1 (shunting), decreased ventilation
50
How is CO2 transportedd from tissues to lungs? (3 ways)
1. as bicarb 2. bound to N-terminal of Hb (as carbaminoHb) 3. dissolved in blood
51
V/Q in airway obstruction vs in blood flow obstruction
* Airway obstruction: V/Q --\> 0 * Blood flow obstruction: V/Q --\> infinity
52
Acute mountain sickness: S&S
headache, fatigue, acute cerebral edema, acute pulm edema
53
Compensatory mechs for hypoxia at high altitude
* increased ventilation, EPO, 2,3-DPG, mitochondria, O2 efficiency, renal excr of bicarb
54
How much does the Hb & hematocrit change in a person that has acclimatized to a hypoxic environment for weeks?
* Hb: 15 gL --\> 20 * hematocrit: 40-45 --\> 65
55
At what positive G-force does visual blackout occur and why?
4-6 Gs; blood pools in abdo and legs, lack of flow to brain
56
What G force is ahceived during spacecraft liftoff?
8-9 Gs
57
Nitrogen narcosis
Nitrogen dissolves into neural memb --\> reduced neuronal excitability Becomes jovial / careless, drowsy, loss of strenght & coord, like EtOH intoxication
58
Pathophys of decompression sickness
Nitrogen bubbling out of solution
59
Decompression sickness: S&S, Tx
* pain in joints and muscles of arms & legs, neurologic problems (dizziness, paralysis, syncope), "chokes" (bubbles cuase SOB, pulm edema, death) * Tx: hyperbaric therapy
60
By what mechanism does acute mountain sickness cause cerebral edama and acute pulmonary edema?
* cerebral edema: hypoxia-induced vasodilation * pulmonary edema: hypoxia-induced vasoconstriction
61
Primary spontanous pneumothorax: epidemiology and etiology
* tall, thin young males * due to rupture of apical blebs
62
Dx of pneumothorax
decreased breath sounds on affected side, CXR, CT
63
Virchow's triad
Stasis + hypercoagulability + endothelial damage
64
Homan's sign
* pain with ankle dorsiflexion * may indicate DVT but not specific
65
DVT: S&S
unilateral swollen foot/ankle, +/- pain, +/- Homan's sign, +/- palpable cord
66
Dx of DVT
D-dimer, compression U/S
67
D-dimer: what is it, how is it used?
* fibrin degradation product, used in Dx of DVT but not very specific * if -ve: DVT ruled out * if +ve: follow with compression U/S
68
How to prevent DVT
subcut heparin bid-tid, SCDs / compression stockings
69
Tx of DVT
heparin until warfarin (coumadin) therapeutic
70
PE: S&S
pleuritic chest pain, SOB, hemoptysis (rare), fever, tachypnea, tachycardia, altered mental status (AMS), confusion
71
Classic ECG changes in PE
* S1Q3T3 (only in 20% cases) * wide S in Lead I * large Q & inverted T in Lead III
72
Dx of PE: gold std and others
* Gold std: pulmonary angiogram * Others: D-dimer, DVT in lower extremity, large Aa grad, ECG changes, CT, V/Q scan
73
Tx of PE
* heparin / warfarin * consider thrombolysis if massive PE
74
Causes of emboli
* fat, amniotic fluid, tumour, bacterial, air, thrombus
75
FEV1/FVC in normal vs obstructive vs restrictive lung disease
* normal: ~0.8 * obstructive: \< 0.8 * restrictive: normal/increased
76
Curshmann's spirals
spiral-shaped mucus plugs & desquamated epithelium, found in asthma
77
Charcot-Leyden crystals
assoc w eosinophilic inflamm, found in asthma
78
Asthma: 2 histological findings
Curschmann's spirals, Charcot-Leyden crystals
79
DDx for eosinophilia
* "DNAAACP" * Drugs * Neoplasm * Atopic diseases: allergy, asthma, Churg-Strauss * Addison disease * Acute interstitial nephritis * Collagen vascular disease * Parasites
80
Reid Index
* thickness of glands making up lung wall * \>0.5 in chronic bronchitis
81
Chronic bronchitis: definition and Dx
* hyperplasia of goblet cells and submuscosal glands * Dx: daily productive cough for \>3 mths, for at least 2 consecutive years
82
"Blue bloaters": which disease and why?
* Chronic bronchitis * cyanosis and periph edema, from poor oxygenation and pulm HTN
83
Emphysema: CXR findings
barrel-chest, flattening of diaphragm, blunting of costophrenic angles
84
Types of emphysema, locations, and causes (2)
* Centriacinar: smoking, upper lobes & superior segments of lower lobes * Panacinar: alpha 1-antitrypsin deficiency, lower lobes
85
"Pink puffers": which disease?
Emphysema; due to dyspnea and hyperventilation
86
Name 2 causes of bronchiectasis
CF, Kartagener syndrome
87
Function of alpha 1-antitrypsin
Protects against elastase
88
Most common cause of pulmonary HTN
COPD
89
N-acetylcysteine: uses (3)
* acetaminophen OD * mucolytic * prevents contrast-induced nephropathy
90
Inhaled Tx of choice for chronic asthma
inhaled steroid
91
Inhaled Tx of choice for acute exacerbations of asthma
b2 agonist (albuterol, levalbuterol)
92
Asthma drug: narrow therapeutic index, drug of last resort
Theophylline (methylxanthine)
93
Asthma drug: blocks conversion of arachidonic acid to leukotriene
Zileuton
94
Asthma med: inhibits mast cell release of mediators, used for prophylaxis only
Cromolyn
95
Asthma med: inhaled Tx that blocks muscarinic receptors
Muscarinic antagonists (eg ipotropium, tiotropium)
96
Asthma: inhaled long-acting b2 agonist
Salmeterol
97
Asthma med: blocks leukotriene receptors
Zafirlukast, montelukast
98
What meds if taken long term can result in rebound nasal congestion?
alpha agonists (nasal decongestants), eg psuedoephedrine & phenylephrine
99

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