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USMLE > DIT X: Pulmonary > Flashcards

DIT X: Pulmonary Flashcards

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USMLE® Step 1 flashcards
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
Q

Eqns: Pulmonary vascular resistance

A

(delta)P = Q x R

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25
Q

Relationship between functional residual capacity and chest wall dynamics

A

FRC: point at which outward force of chest wall and inward force of lung is perfectly balances, differs from person to person (compliance)

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26
Q

Normal pulmonary artery pressure and Dx of pulm HTN

A

Normal: 10-15 mmHg

Pulm HTN: pulm artery pressure >25 mmHg during rest, or >35 during exercise

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27
Q

Pathological changes seen in pulmonary HTN + consequences

A

Arteriosclerosis, media hypertrophy, fibrosis of intima

Consequences: cor pulmonale, right heart failure

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28
Q

Causes of secondary pulmonary HTN

A

Chronic lung disease (COPD, pulm fibrosis), mitral stenosis, recurrent TE, autoimmune, L to R shunts (VSD), sleep apnea, high altitude

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29
Q

Tx for pulmonary HTN

A

Bosentan / ambrisentan, prostaglandin analogue, sildenafil, dihydropyridine CCB

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30
Q

MOA of bosentan & ambrisentan

A

competitively antagonize endothelin-1 receptors –> decrease pulm vasc resistance

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31
Q

Primary pulmonary HTN: mutation, epidemiology, 2 disease associations

A
  • 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)
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32
Q

If a lung collapses, what happens to intrathoracic volume?

A

Intrathoracic vol increases (chest wall expands)

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33
Q

What gene mutation causes primary pulmonary HTN?

A

BMPR2 (Bone Morphogenetic Protein Receptor Type II)

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34
Q

HbA: composition and 2 forms

A
  • 2 alpha globins + 2 beta globins + 4 heme
  • T form (taut): low affinity for O2, favours tissues
  • R form (relaxed): high affinity for O2
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35
Q

How is fetal Hb different from adult Hb?

A
  • 2 alpha globins + 2 gamma globins
  • lower affinity for 2,3-DPG = higher affinity for O2
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36
Q

Normally, Hb has which form of iron?

A

Ferrous (Fe 2+)

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37
Q

Methemoglobin has which form of iron?

A

Oxidized –> ferric

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38
Q

Clinical use of methemoglobin

A

Higher affinity for cyanide, can use in cyanide poisoning (give nitrates to oxidize Hb)

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39
Q

Tx for cyanide poisoning

A
  • amyl nitrite, sodium nitrite: to oxidize Hb to methemoglobin –> pick up cyanide
  • thiosulfate: binds cyanide to be excreted renally
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40
Q

What is carboxyhemoglobin, and what effect does it have on the oxygen dissoc curve?

A
  • Hb bound to CO
  • Left shift
41
Q

Substances causing methemoglobinemia

A
  • nitrates & nitrites
  • antimalarial drugs (eg chloroquine, primaquine)
  • dapsone
  • sulfonamides
  • local anaesthetics (eg lidocaine)
  • metoclopramide
42
Q

Tx for methemoglobinemia

A
  • methylene blue
  • vit C
  • cimetidine (H2 blocker)
43
Q

Eqn: total blood O2 content

A

Total Blood O2 content = dissolved O2 + (Hb binding capacity x O2 sat)

44
Q

How does anemia affect O2 sats and arterial PaO2?

A

Does not change either

45
Q

How does exercise change arterial and venous O2 content?

A

no change in arterial O2, decreased venous O2 (due to increased O2 demand)

46
Q

Alveolar gas equation

A

PAO2 = 150 - PaCO2/0.8

(See DIT p. 386)

47
Q

A-a gradient: normal value, what would increase it?

A
  • Normally small (10-15)
  • Increase: shunting or V/Q mismatch, pulm fibrosis, increased FiO2, age
48
Q

PaO2 : FiO2 ratio; normal and abnormal values

A
  • normal: 300-500 mmHg
  • <300: gas exchange deficit
  • <200: severe hypoxia
49
Q

V/Q ratios in lung apex vs lung base

A
  • apex: V/Q > 1 , decreased perfusion
  • base: V/Q < 1 (shunting), decreased ventilation
50
Q

How is CO2 transportedd from tissues to lungs? (3 ways)

A
  1. as bicarb
  2. bound to N-terminal of Hb (as carbaminoHb)
  3. dissolved in blood
51
Q

V/Q in airway obstruction vs in blood flow obstruction

A
  • Airway obstruction: V/Q –> 0
  • Blood flow obstruction: V/Q –> infinity
52
Q

Acute mountain sickness: S&S

A

headache, fatigue, acute cerebral edema, acute pulm edema

53
Q

Compensatory mechs for hypoxia at high altitude

A
  • increased ventilation, EPO, 2,3-DPG, mitochondria, O2 efficiency, renal excr of bicarb
54
Q

How much does the Hb & hematocrit change in a person that has acclimatized to a hypoxic environment for weeks?

A
  • Hb: 15 gL –> 20
  • hematocrit: 40-45 –> 65
55
Q

At what positive G-force does visual blackout occur and why?

A

4-6 Gs; blood pools in abdo and legs, lack of flow to brain

56
Q

What G force is ahceived during spacecraft liftoff?

A

8-9 Gs

57
Q

Nitrogen narcosis

A

Nitrogen dissolves into neural memb –> reduced neuronal excitability

Becomes jovial / careless, drowsy, loss of strenght & coord, like EtOH intoxication

58
Q

Pathophys of decompression sickness

A

Nitrogen bubbling out of solution

59
Q

Decompression sickness: S&S, Tx

A
  • pain in joints and muscles of arms & legs, neurologic problems (dizziness, paralysis, syncope), “chokes” (bubbles cuase SOB, pulm edema, death)
  • Tx: hyperbaric therapy
60
Q

By what mechanism does acute mountain sickness cause cerebral edama and acute pulmonary edema?

A
  • cerebral edema: hypoxia-induced vasodilation
  • pulmonary edema: hypoxia-induced vasoconstriction
61
Q

Primary spontanous pneumothorax: epidemiology and etiology

A
  • tall, thin young males
  • due to rupture of apical blebs
62
Q

Dx of pneumothorax

A

decreased breath sounds on affected side, CXR, CT

63
Q

Virchow’s triad

A

Stasis + hypercoagulability + endothelial damage

64
Q

Homan’s sign

A
  • pain with ankle dorsiflexion
  • may indicate DVT but not specific
65
Q

DVT: S&S

A

unilateral swollen foot/ankle, +/- pain, +/- Homan’s sign, +/- palpable cord

66
Q

Dx of DVT

A

D-dimer, compression U/S

67
Q

D-dimer: what is it, how is it used?

A
  • 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
Q

How to prevent DVT

A

subcut heparin bid-tid, SCDs / compression stockings

69
Q

Tx of DVT

A

heparin until warfarin (coumadin) therapeutic

70
Q

PE: S&S

A

pleuritic chest pain, SOB, hemoptysis (rare), fever, tachypnea, tachycardia, altered mental status (AMS), confusion

71
Q

Classic ECG changes in PE

A
  • S1Q3T3 (only in 20% cases)
  • wide S in Lead I
  • large Q & inverted T in Lead III
72
Q

Dx of PE: gold std and others

A
  • Gold std: pulmonary angiogram
  • Others: D-dimer, DVT in lower extremity, large Aa grad, ECG changes, CT, V/Q scan
73
Q

Tx of PE

A
  • heparin / warfarin
  • consider thrombolysis if massive PE
74
Q

Causes of emboli

A
  • fat, amniotic fluid, tumour, bacterial, air, thrombus
75
Q

FEV1/FVC in normal vs obstructive vs restrictive lung disease

A
  • normal: ~0.8
  • obstructive: < 0.8
  • restrictive: normal/increased
76
Q

Curshmann’s spirals

A

spiral-shaped mucus plugs & desquamated epithelium, found in asthma

77
Q

Charcot-Leyden crystals

A

assoc w eosinophilic inflamm, found in asthma

78
Q

Asthma: 2 histological findings

A

Curschmann’s spirals, Charcot-Leyden crystals

79
Q

DDx for eosinophilia

A
  • “DNAAACP”
  • Drugs
  • Neoplasm
  • Atopic diseases: allergy, asthma, Churg-Strauss
  • Addison disease
  • Acute interstitial nephritis
  • Collagen vascular disease
  • Parasites
80
Q

Reid Index

A
  • thickness of glands making up lung wall
  • >0.5 in chronic bronchitis
81
Q

Chronic bronchitis: definition and Dx

A
  • hyperplasia of goblet cells and submuscosal glands
  • Dx: daily productive cough for >3 mths, for at least 2 consecutive years
82
Q

“Blue bloaters”: which disease and why?

A
  • Chronic bronchitis
  • cyanosis and periph edema, from poor oxygenation and pulm HTN
83
Q

Emphysema: CXR findings

A

barrel-chest, flattening of diaphragm, blunting of costophrenic angles

84
Q

Types of emphysema, locations, and causes (2)

A
  • Centriacinar: smoking, upper lobes & superior segments of lower lobes
  • Panacinar: alpha 1-antitrypsin deficiency, lower lobes
85
Q

“Pink puffers”: which disease?

A

Emphysema; due to dyspnea and hyperventilation

86
Q

Name 2 causes of bronchiectasis

A

CF, Kartagener syndrome

87
Q

Function of alpha 1-antitrypsin

A

Protects against elastase

88
Q

Most common cause of pulmonary HTN

A

COPD

89
Q

N-acetylcysteine: uses (3)

A
  • acetaminophen OD
  • mucolytic
  • prevents contrast-induced nephropathy
90
Q

Inhaled Tx of choice for chronic asthma

A

inhaled steroid

91
Q

Inhaled Tx of choice for acute exacerbations of asthma

A

b2 agonist (albuterol, levalbuterol)

92
Q

Asthma drug: narrow therapeutic index, drug of last resort

A

Theophylline (methylxanthine)

93
Q

Asthma drug: blocks conversion of arachidonic acid to leukotriene

A

Zileuton

94
Q

Asthma med: inhibits mast cell release of mediators, used for prophylaxis only

A

Cromolyn

95
Q

Asthma med: inhaled Tx that blocks muscarinic receptors

A

Muscarinic antagonists (eg ipotropium, tiotropium)

96
Q

Asthma: inhaled long-acting b2 agonist

A

Salmeterol

97
Q

Asthma med: blocks leukotriene receptors

A

Zafirlukast, montelukast

98
Q

What meds if taken long term can result in rebound nasal congestion?

A

alpha agonists (nasal decongestants), eg psuedoephedrine & phenylephrine

99
Q
A

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