Pulmonology Flashcards

(43 cards)

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
Bronchopneumonia
Inflammatory infiltrates from bronchioles to adjacent alveoli - Patchy distribution (1+ lobes involved)
26
Air-fluid level on CXR
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
Chylothorax
Thoracic duct injury from trauma or malignancy - Milk appearing fluid (pleural effusion) - contains increased TGs
28
Albuterol
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
Salmeterol, formoterol
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
Theophylline
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
Ipratropium
Anticholinergic (competitive block of muscarinic receptors) - Prevents bronchoconstriction - Effect depends on vagal tone Use: - Asthma - COPD (tiotropium= long acting, M1 and M3 selective)
32
Beclomethasone, fluticasone
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
Montelukast, Zafirlukast
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
Zileuton
Leukotriene synthesis inhibitor: 5-lipoxygenase pathway inhibitor (arachidonic acid--> leukotriene blocked) - BID sustained release - LFT monitoring needed - Also blocks LTB4 - Limited use
35
Omalizumab
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
N-acetylcysteine
Mucolytic MOA: reduces intramolecular disulfide bridges in mucus glycoproteins--> loosen sputum - Loosen mucous plugs in CF patients - Antidote for acetaminophen overdose
37
Bosentan
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
Dextromethorphan
Antitussive (antagonizes NMDA glutamate receptors) - Synthetic codeine analog - Mild opioid effects when used in excess (abuse potential)- overdose tx= Naloxone
39
Pseudoephedrine, phenylephrine
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
Methacholine
Muscarinic receptor agonist | - Used in asthma challenge testing
41
Non-small cell lung cancer marker
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
Diaphragm structures
"I ate 10 eggs at 12" IVC= T8 Esophagus (vagus trunks)= T10 Aorta, azygous, thoracic duct= T12
43
Oxygen content of blood
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