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Step 1 Subjects > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

Conducting zone

A

Do not participate in gas exchange: warm, humidify, filter air; “anatomic dead space”

Large airways:

  • Nose
  • Pharynx
  • Trachea
  • Bronchi (cartilage, goblet cells to end)

Small airways:

  • Bronchioles
  • Terminal bronchioles (pseudostratified ciliated columnar cells and smooth muscle to end)
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2
Q

Respiratory zone

A

Gas exchange; NO cilia
Parenchyma:
- Respiratory bronchioles: cuboidal cells
- Alveolar ducts: simple squamous cells up to alveoli
- Alveoli: Type I, Type II pneumocytes, Clara cells, alveolar macrophages

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3
Q

Type II pneumocytes

A
  1. Pulmonary surfactant production
    Surfactant= dipalmitoylphophatidylcholine
    - Begins at week 26
    - Mature at week 35: indicated by lecithin-to-sphingomyelin ratio > 2.0 in amniotic fluid
    - Glucocorticoids enhance surfactant production in premature babies
    - Clara cells= secrete component of surfactant (also degrade toxins, act as reserve cells)
  2. Precursors to Type I pneumocytes (Type I= 97% of alveolar cells)
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4
Q

Inspiratory muscles

A

Quiet breathing= diaphragm

Exercise inspiration= External intercostals, scalene, sternocleidomastoids

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5
Q

Expiratory muscles

A

Quiet breathing= passive

Exercise expiration= Abdominals, Obliques, Internal intercostals

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6
Q

Determination of physiologic dead space

A

Vd/ Vt = (PaCO2-PeCO2)/PaCO2

dead space/tidal volume = (arterial PCO2- expired PCO2)/arterial PCO2

Tidal volume= 500 mL
Total lung capacity ~ 6 L, residual volume= ~1.2 L
* Dead space= conducting airways (think increased in snorkel breathing)

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7
Q

Lung compliance

A

Change in lung volume for given change in pressure:

  • Decreased in pulmonary fibrosis, pneumonia, pulmonary edema
  • Increased in Emphysema, normal aging, alpha-1-antitrypsin deficiency
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8
Q

Hemoglobin forms

A

4 polypeptide subunits (2 alpha, 2 beta):

Taut form= low affinity for O2

  • increases in Cl-, H+, CO2, 2,3-BPG, temperature–> taut form (dump O2 in tissue)
  • Shifts O2-hemoglobin curve to Right

Relaxed form= high affinity for O2 (300x higher)
- Seen in a decrease in any factor (temp, [H+])

Fetal hemoglobin= 2 alpha, 2 gamma subunits:

  • Lower affinity for 2,3-BPG–> higher O2 affinity (doesn’t unload as easily)
  • Left-shifted Oxygen-hemoglobin dissociation curve
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9
Q

Methemoglobin

A

Oxidized hemoglobin (Fe+3) vs normal Fe+2

  • Nitrites oxidize iron
  • Has increased affinity for cyanide
  • Treat methemoglobinemia with methylene blue

Cyanide poisoning:

  1. Nitrites administered (form methemoglobin)—> bind cyanide; allow cytochrome oxidase to function
  2. Use thiosyulfate to bind cyanide in methemoglobin–> thiocyanate–> renal excretion
  3. Convert Methemoglobin back to hemoglobin using methylene blue

Symptoms of Cyanide poisoning: mitochondrial ETC inhibitor

  • tachypnea, tachycardia, H/A, cutaneous flushing
  • N/V, confusion, weakness
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10
Q

Carboxyhemoglobin

A 
Carbon Monoxide (CO) binds hemoglobin with 200 x affinity as O2
- Decreases O2 binding capacity--> shifts curve to Left--> decreases O2 unloading in tissue

PO2= normal
- Decreased % saturation, blood O2 content

Tx: 100% O2

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11
Q

Pulmonary circulation: Perfusion and Diffusion

A

Normal:

  • Lungs are perfusion limited
  • Gas equilibrates early along length of capillary
  • Diffusion only increases if blood flow increases

Disease:

  • Lungs are diffusion limited: emphysema (decreased area for diffusion), fibrosis (increased thickness of alveolar walls
  • Gas does not equilibrate by the time it reaches the end of the capillary
  • In exercise, blood moves faster through capillaries (can’t get as much O2)–> therefore rate of respiration increased

** Blood flow (ml/min) ALWAYS= blood flow through systemic circulation

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12
Q

Pulmonary HTN

A

Normal pulmonary artery pressure= 10-14 mmHg
- Pulmonary HTN= 25+ mmHg or >35 mmHG during exercise

** Endothelial cell dysfunction

Pulmonary HTN–> arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries–> respiratory distress–> cyanosis (deoxygenated Hb > 5g/dL), R ventricular hypertrophy–> death (decompensated cor pulmonale)

Primary= inactivating mutation in BMPR2 gene (normally inhibits vascular smooth m. proliferation)

Severe respiratory distress–> cyanosis, RVH–> death from decompensated cor pulmonale

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13
Q

Causes of Secondary pulmonary HTN

A
  • COPD: hypoxic vasoconstriction–> medial hypertrophy
  • Mitral stenosis (increased resistance–> increased pressure)
  • Recurrent thromboemboli (decreased cross-sectional area of pulmonary vascular bed)
  • Autoimmune disease (inflammation (Sclerosis= T-cells–> TGF-beta)–> intimal fibrosis (collagen, ECM proteins)–> medial hypertrophy)
  • Left-Right shunt (increased shear stress–> endothelial injury)
  • Sleep apnea/high altitude (hypoxic vasoconstriction–> medial hypertrophy)
  • Drugs: diet drugs (fenfluramine, dexfenfluramine, phentamine)

Severe respiratory distress–> cyanosis, RVH–> death from decompensated cor pulmonale

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14
Q

Pulmonary vascular resistance

A

PVR= P(pulm artery)- P(left atrium= wedge pressure)/ CO

Resistance= (P(pulm artery)- P (wedge pressure))/ Q (flow)

Resistance= [8 x (viscosity of blood=n) x length]/ (pi x r^4)

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15
Q

Alveolar gas equation

A

PAO2= PIO2 - PaCO2/R

PAO2= alveolar PO2
PIO2= PO2 of inspired air (generally 150mmHg)
PaCO2= arterial PCO2
R= respiratory quotient (CO2 produced/O2 consumed) ~ 0.8

A-a gradient= PAO2-PaO2= 10-15 mmHg
- Increased in hypoxemia due to shunting, V/Q mismatch, fibrosis (ventilating fine, but blood can’t get to oxygen!)

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16
Q

V/Q mismatch

A

Apex: V/Q=3 (wasted ventilation)
- TB thrives here

Base: V/Q= 0.6 (wasted perfusion
- V and Q are greater at base

Exercise: Vasodilation–> V/Q approaches 1

V/Q= 0: airway obstruction (O2 won’t help)

V/Q= infinity: blood flow obstruction (pulmonary embolism)–> improves with 100% O2 administration

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17
Q

CO2 transport

A

Three forms:

  1. Bicarb= 90%
  2. Carbaminohemoglobin (HbCO2)= 5%
    - CO2 bound to N-terminus, binding favors taut form of hemoglobin
  3. Dissolved CO2= 5%

Haldane effect: de-oxygenated blood has increased ability to carry CO2 (vice-versa)

RBC contents:

  1. Carbonic anhydrase (converts CO2 to bicarb)
  2. Cl-/HCO3- pump:
    - RBC is impermeable to H+, but can exchange bicarb (containing H+) for Cl-
    - Venous blood therefore has lower Cl- as the increased CO2 in tissue is converted into bicarb (CO2 + H+)–> exchanged out of RBC for Cl- influx
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18
Q

Types of restrictive lung disease

A

Restricted lung expansion–> decreased lung volumes (decreased FVC and TLC)
- Pulmonary function tests: FEV1/FVC ratio > 80%

  1. Poor breaching mechanism: extrapulmonary, peripheral hypoventilation, normal A-a gradient:
    - Muscular: polio, myasthenia gravis
    - Structural: scoliosis, morbid obesity
  2. Interstitial lung disease: pulmonary, lowered diffusion capacity, increased A-a gradient:
    - ARDS
    - Neonatal RDS (hyaline membrane disease)
    - Pneumoconioses (anthracosis, silicosis, asbestosis)
    - Sarcoidosis (bilateral hilar adenopathy, noncaseating granulomas; increased ACE and calcium)
    - Idiopathic (collagen deposition)
    - Goodpasture’s
    - Granulomatosis with polyangiitis (Wegener’s)
    - Langerhans cell histiocytosis (eosinophilic granuloma)
    - Hypersensitivity pneumonitis
    - Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)
19
Q

Neonatal Respiratory distress syndrome (RDS)

A

Surfactant deficiency–> increased surface tension–> alveolar collapse

  • lecithin:sphingomyelin ratio < 1.5 (should be > 2) in amniotic fluid (administer maternal steroids to improve ratio before birth)
  • Low O2 tension–> risk of PDA
  • Supplemental O2–> retinopathy of prematurity, bronchopulmonary dysplasia (therefore administer artificial surfactant)

Risk factors:

  • Prematurity
  • maternal diabetes (elevated fetal insulin)
  • c-section (decreased fetal glucocorticoid release)
20
Q

Acute respiratory distress syndrome

A

ARDS

Caused by:

  • Trauma
  • Sepsis, shock
  • Gastric aspiration
  • Uremia
  • Acute pancreatitis
  • Amniotic fluid embolism

Path:

  • Diffuse alveolar damage–> alveolar capillary permeability increases–> protein-rich leakage into alveoli
  • Formation of intra-alveolar hyaline membrane (T2 proliferation–> fibrosis)
  • Damage due to neutrophilic substances toxic to alveolar wall, coagulation cascade, O2-derived free radicals

Findings:

  • Decreased lung compliance
  • Increased work of breaching
  • Enhanced V/Q mismatch with no change in PCWP
  • PaO2/FIO2 < 200
21
Q

Sleep apnea

A

Cessation of breathing > 10 seconds during sleep–> disrupted sleep–> daytime somnolence

Central sleep apnea= absent respiratory effeort

Obstructive= no effort against airway obstruction
- Obesity, snoring, systemic/pulmonary HTN, arrhythmias, possible sudden death

Tx: CPAP, weight loss, surgery
** Hypoxia==> increased EPO–> erythropoiesis

22
Q

Lung cancer complications

A

SPHERE:

  • Superior vena cava syndrome
  • Pancoast tumor
  • Horner’s syndrome
  • Endocrine (paraneoplastic)
  • Recurrent laryngeal sx (hoarseness)
  • Effusions (pleural/pericardial)
  • Leading cause of cancer death
  • Most common cause= mets from breast, colon, prostate, bladder
  • Metastasizes to: adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly)
23
Q

Pancoast tumor

A

Carcinoma that occurs in apex of lung (superior sulcus):

  • Affect cervical sympathetic plexus–> Horner’s syndrome (ipsilateral ptosis, miosis, anhidrosis)
  • Can invade brachial plexus–> weakness and paresthesias of arm
  • Recurrent laryngeal nerve involvement–> hoarseness
24
Q

Superior Vena Cava (SVC) syndrome

A

Obstruction of SVC–> impaired drainage from head (“facial plethora”), neck obstruction (Jugular venous distention= JVD), upper extremity edema

  • Caused by malignancy and thrombosis of indwelling catheters
  • Medical emergency
  • Can raise ICP if severe–> H/A, dizziness, increased risk of aneurysm/rupture of cranial aa
25
Q

Bronchopneumonia

A

Inflammatory infiltrates from bronchioles to adjacent alveoli
- Patchy distribution (1+ lobes involved)

26
Q

Air-fluid level on CXR

A

Lung abscess caused by:
- Bronchial obstruction (cancer)
- Aspiration (alcohlics, epileptics)
See air-fluid level due to S. aureus, anaerobes (Bacteroides, fusobacterium, peptostreptococcus) forming abscess–> gas

27
Q

Chylothorax

A

Thoracic duct injury from trauma or malignancy

  • Milk appearing fluid (pleural effusion)
  • contains increased TGs
28
Q

Albuterol

A

Beta-2 agonist
MOA:
- Upregulates adenylyl cyclase–> increased cAMP–> bronchodilation

Workhorse drug for asthma (short-acting)

  • First choice quick relief for asthma
  • As needed ~every 4 hours
  • Higher doses used in acute attack
29
Q

Salmeterol, formoterol

A

Beta-2 agonist
MOA:
- Upregulates adenylyl cyclase–> increased cAMP–> bronchodilation

Long-acting asthma drug- beta-2 agonist

  • Every 12 hours
  • Theoretical concerns of tachyphylaxis; NOT for immediate relief
  • Should not be administered without inhaled steroids

AEs: Tremor, arrhythmia
- hypokalemia: CV disease with diuretic use= highest risk–> potential arrhythmia (COPD population)

30
Q

Theophylline

A

MOA:
Methylxanthine
- Inhibits cyclic nucleotide phosphodiesterase enzymes
–> increased cAMP and cGMP,
–> bronchodilation
* Competitive inhibitor of adenosine receptor, which may mediate bronchospasm

*Efficacy probably due more to antiinflammatory and bronchoprotective effects than bronchodilatory effects

Side effects: Caffeine derivative:

  • within therapeutic index: nervousness, insomnia, dyspepsia
  • Dose-dependent toxicity: nausea, emesis, tachyarrhythmias, seizures
    • P450 metabolism
Notes:
Third line agent in asthma
Minor role in management of COPD
Requires therapeutic monitoring
BUT…Inexpensive and oral (3rd world use)
31
Q

Ipratropium

A

Anticholinergic (competitive block of muscarinic receptors)

  • Prevents bronchoconstriction
  • Effect depends on vagal tone

Use:

  • Asthma
  • COPD (tiotropium= long acting, M1 and M3 selective)
32
Q

Beclomethasone, fluticasone

A

MOA: inhaled steroids

  • Inhibit synthesis of all cytokines
  • Inactivate NF-kappaB (TF that induces TNF-alpha production)

First line for chronic asthma

  • Use in ALL except mildest disease
  • No immediate bronchorelaxation

Side effects mild and dose related:

  • HPA suppression–minimal
  • Cataracts–posterior subcapsular
  • Growth velocity in children: Titrate dose to control of disease
  • Bone mineral density: significant decrease only at higher doses
  • Fractures: no increased risk, but poor data
  • Pneumonia—mild risk in COPD patients

Local side effects:

  • Dysphonia, thrush: independent of type of steroid
  • Strategies to avoid: rinse mouth, spacer device

Treatment side effects typically better than severe disease in children

33
Q

Montelukast, Zafirlukast

A

Leukotriene receptor antagonist (modifiers): reduces inflammation in chronic asthma, bronchitis

  • Very safe
  • Good for aspirin-induced asthma
  • Add-on controller agent in asthma
  • Pediatrics: oral, steroid sparing
  • Treats allergic rhinitis
  • Heterogenous response
  • NO ROLE in COPD

Side effects:
- Churg-Strauss vasculitis (associated with severe asthma, responds to corticosteroids)

34
Q

Zileuton

A

Leukotriene synthesis inhibitor: 5-lipoxygenase pathway inhibitor (arachidonic acid–> leukotriene blocked)

  • BID sustained release
  • LFT monitoring needed
  • Also blocks LTB4
  • Limited use
35
Q

Omalizumab

A

Recombinant humanized anti-IgE antibody
MOA: Binds circulating IgE, but does not activate cell bound IgE
- Allergic asthma resistant to inhaled steroids, long-acting beta-2 agonists

36
Q

N-acetylcysteine

A

Mucolytic
MOA: reduces intramolecular disulfide bridges in mucus glycoproteins–> loosen sputum

  • Loosen mucous plugs in CF patients
  • Antidote for acetaminophen overdose
37
Q

Bosentan

A

Treatment for pulmonary HTN

MOA: Antagonism of endothelin-1 receptors (A and B)
- Causes Vasodilatation, Antiproliferative

Stabilizes smooth muscle proliferation
Teratogenic, alters metabolism of contraceptives

38
Q

Dextromethorphan

A

Antitussive (antagonizes NMDA glutamate receptors)

  • Synthetic codeine analog
  • Mild opioid effects when used in excess (abuse potential)- overdose tx= Naloxone
39
Q

Pseudoephedrine, phenylephrine

A

MOA:

  • Sympathomimetic alpha-agonist
  • Nasal decongestant
  • Constricts blood vessels in sinus passages

Use:

  • Reduce hyperemia, edema, nasal congestion
  • Open obstructed eustachian tubes
  • Stimulant

Tox:

  • Hypertension
  • CNS stimulation/anxiety
  • BPH: issues with voiding
40
Q

Methacholine

A

Muscarinic receptor agonist

- Used in asthma challenge testing

41
Q

Non-small cell lung cancer marker

A

Fusion gene between EML4 (echinoderm microtubule associated-like protein 4) and ALK (anaplastic lymphoma kinase)
–> constitutive tyrosine kinase activity

Mutation seen in young non-smokers with lung adenocarcinoma
- No accompanying EGFR or k-ras mutations

42
Q

Diaphragm structures

A

“I ate 10 eggs at 12”
IVC= T8
Esophagus (vagus trunks)= T10
Aorta, azygous, thoracic duct= T12

43
Q

Oxygen content of blood

A

O2 binding capacity= 20.1 mL O2/dL

1g hemoglobin binds 1.34 ml O2

  • Normal Hb= 15
  • Cyanosis= deoxygenated Hb > 5g/dL

** remember, O2 saturation and PO2 are normal in anemia while the O2 CONTENT is low

Step 1 Subjects (26 decks)

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