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My step 1 mnemonics > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Lung development - stages and time frames

A

Embryonic -> weeks 4-7

Pseudoglandular ->weeks 5-17

Canalicular -> weeks 16- 25

Saccular -> week 26-birth

Alveolar -> week 36- 8 years

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2
Q

Lung development - Embryonic

A 
Lung bud -> 
trachea - >
bronchial buds-> 
mainstem bronchi - >
secondary (lobar) bronchi ->
tertiary (segmental) bronchi.

Errors at this stage can lead to tracheoesophageal fistula.

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3
Q

Lung development - Pseudoglandular

A

Endodermal tubules -> terminal bronchioles.

Surrounded by modest capillary network.

PseuDOglandular - EnDOdermal tubules

Respiration impossible, incompatible with life.

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4
Q

Lung development - Canalicular

A

Terminal bronchioles -> respiratory bronchioles
-> alveolar ducts.

Surrounded by prominent capillary network.

CanaliculaR - TeRminal bronchioles -> Respiratory bronchioles -> alveolAR ducts.

Airways increase in diameter.
Respiration is capable at 25 weeks.
Pneumocytes develop starting at 20 weeks.

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5
Q

Lung development - Saccular

A

Alveolar ducts -> terminal sacs.

Terminal sacs separated by 1° septae.

ends w/ Sacs

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6
Q

Lung development - Alveolar

A

Terminal sacs -> adult alveoli (due to 2° septation).

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7
Q

Septation & capillary networks

A

PseuDoglandular - moDest capillary network.
Canalicular - prominent Capillary network.

Saccular - separated by 1° septae.
Alveolar - 2° septation

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8
Q

In utero “breathing” and development times:

A

In utero, “breathing” occurs via aspiration and expulsion of amniotic fluid - inc vascular resistance through gestation.

At birth, fluid gets replaced with air -> dec in pulmonary vascular resistance.

Respiration is capable at 25 weeks.

Pneumocytes develop starting at 20 weeks.

At birth: 20-70 million alveoli.
By 8 years: 300 - 400 million alveoli.

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9
Q

Pulmonary hypoplasia

A

Poorly developed bronchial tree with abnormal histology.

Associated with congenital diaphragmatic hernia (usually left-sided), bilateral renal agenesis (Potter sequence).

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10
Q

Bronchogenic cysts

A

Caused by abnormal budding of the foregut and dilation of terminal or large bronchi.

Discrete, round, sharply defined, fluid-filled densities on CXR (air-filled if infected).

Generally asymptomatic but can drain poorly, causing airway compression and/or recurrent respiratory infections.

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11
Q

Club cells

A

Nonciliated;

low columnar/cuboidal with secretory granules.

Located in bronchioles.

Degrade toxins;

secrete component of surfactant;

act as reserve cells.

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12
Q

Law of Laplace:

A

Alveoli have t tendency to collapse on expiration as radius dec.

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13
Q

Pulmonary surfactant

A

Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC).

Surfactant synthesis begins around week 20 of gestation, but mature levels are not achieved until around week 35.

Corticosteroids are important for fetus surfactant production and lung development.

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14
Q

Alveolar macrophages

A

Phagocytose foreign materials;

Release cytokines and alveolar proteases.

Hemosiderin-laden macrophages may be found in the setting of pulmonary edema or alveolar hemorrhage.

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15
Q

Screening tests for fetal lung maturity:

A

lecithin-sphingomyelin (L/S) ratio in amniotic fluid (> 2 is healthy; < 1.5 predictive of NRDS)

foam stability index

surfactant-albumin ratio

Persistently low O2 tension -> risk of PDA.

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16
Q

Therapeutic supplemental O2 can result in:

A

R - Retinopathy of prematurity,

I - Intraventricular hemorrhage,

B - Bronchopulmonary dysplasia

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17
Q

Neonatal respiratory distress syndrome

A

Surfactant deficiency -> inc surface tension -> alveolar collapse (“ground-glass” appearance of lung fields)

Risk factors:
C - C-section delivery (dec release of fetal glucocorticoids; less stressful than vaginal delivery).
u
P - prematurity
i
D - diabetes (maternal, due to inc fetal insulin)

Treatment: maternal steroids before birth; exogenous surfactant for the infant.

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18
Q

Cartilage and goblet cells extend to_______

A

Cartilage and goblet cells extend to the end of bronchi.

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19
Q

Pseudostratified ciliated columnar cells primarily makeup epithelium of__________then transition to_________.

A

bronchus and extend to beginning of terminal bronchioles, then transition to cuboidal cells.

Clear mucus and debris from the lungs (mucociliary escalator).

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20
Q

Airway smooth muscle cells extend to________.

A

end of terminal bronchioles (sparse beyond this point).

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21
Q

Respiratory zone cells:

A

Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli.

Cilia terminate in respiratory bronchioles.

Alveolar macrophages clear debris and participate in the immune response.

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22
Q

Relation of the pulmonary artery to the bronchus at each lung hilum is described by:

A

RALS- Right Anterior; Left Superior.

Carina is posterior to ascending aorta and anteromedial to descending aorta.

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23
Q

The common sites for inhaled foreign bodies

A
  • While supine -> usually enters the superior segment of the right lower lobe.
  • While lying on the right side -> usually enters the right upper lobe.
  • While upright -> usually enters the right lower lobe.
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24
Q

Structures perforating diaphragm: At T8

A

IVC

right phrenic nerve

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25
Q

Structures perforating diaphragm: At T10

A

esophagus

CN 10 - vagus

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26
Q

Structures perforating diaphragm: At T12

A

Aorta (red)

Thoracic duct (white),

Azygos vein (blue)

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27
Q

Pain from diaphragm irritation can be referred to:

A

Pain from diaphragm irritation (eg, air, blood, or pus in the peritoneal cavity) can be referred to shoulder (C5) and trapezius ridge (C3, 4).

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28
Q

Bifurcations:

A
  • The common carotid bifourcates at C4.
  • The trachea bifourcates at T4.
  • The abdominal aorta bifourcates at L4.
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29
Q

lnspiratory reserve volume

A

Air that can still be breathed in after normal inspiration

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30
Q

Tidal volume

A

Air that moves into the lung with each quiet inspiration, typically 500 mL

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31
Q

Expiratory reserve volume

A

Air that can still be breathed out after normal expiration

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32
Q

Residual volume

A

The air in the lung after maximal expiration;

RV and any lung capacity that includes RV cannot be measured by spirometry

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33
Q

lnspiratory capacity

A

IRV +TV

Air that can be breathed in after normal exhalation

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34
Q

Functional residual capacity

A

RV+ ERV

The volume of gas in the lungs after normal expiration

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35
Q

Vital capacity

A

TV + IRV + ERV

Maximum volume of gas that can be expired after a maximal inspiration

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36
Q

Total lung capacity

A

IRV +TV+ ERV+ RV

The volume of gas present in the lungs after a maximal inspiration

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37
Q

Dead space

A

VD = physiologic dead space = anatomic dead space of conducting airways plus alveolar dead space;

The apex of the healthy lung is the largest contributor of alveolar dead space.

The volume of inspired air that does not take part in gas exchange.

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38
Q

Inc/ Dec in dead space:

A

Dec in dead space: PeCO2 approaches PaCO2 -> more gas exchange and less CO2 retained

Inc in dead space: PeCO2 approaches 0 -> less gas exchange and more CO2 retained

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39
Q

Ventilation

A

Minute ventilation: VE = VT x RR

Alveolar ventilation: VA = (VT- VD) x RR

Normal values:
Respiratory rate (RR) = 12- 20 breaths/min
VT= 500 mL/breath
VD = 150 mL/breath
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40
Q

At FRC:

A

the inward pull of the lung is balanced by the outward pull of the chest wall, and system pressure is atmospheric.

At FRC, airway and alveolar pressures equal atmospheric pressure (called zero), and intrapleural pressure is negative (prevents atelectasis).

Pulmonary vascular resistance (PVR) is at a minimum.

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41
Q

Compliance:

A

change in lung volume for a change in pressure;

expressed as change in V/P and is inversely proportional to wall stiffness.

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42
Q

Hysteresis:

A

lung inflation curve follows a different curve than the lung deflation curve due to the need to overcome surface tension forces in inflation.

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43
Q

Compliance inc/dec change in:

A

High compliance= lung easier to fill (emphysema, normal aging)

lower compliance= lung harder to fill (pulmonary fibrosis, pneumonia, NRDS, pulmonary edema).

Surfactant increases compliance.

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44
Q

Respiratory system changes in the elderly - values that increase:

A 
C -compliance of lung (loss of elastic recoil) 
R - RV
A - A-a gradient
V - V/Q mismatch
e
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45
Q

Respiratory system changes in the elderly - values that decrease:

A

M - muscles of respiration strength (can impair cough)
R - response (ventilatory) to hypoxia/hypercapnia

o
F - FVC
F -FEV1

Complies - Chest wall compliance Decreases (chest wall stiffness INCREASE)

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46
Q

Hemoglobin

buffer for and what causes it to unload O2

A 
CI-
H+
CO2
2,3-BPG
temperature

all favor deoxygenated form over oxygenated form (shifts dissociation curve right -> inc O2 unloading).

hemoglobin acts as a buffer for H+ ions.

47
Q

Cyanide - Source/Tx/Sx

A

Source:
byproduct of synthetic product combustion,
ingestion of amygdalin (cyanogenic glucoside found in apricot seeds), or cyanide.

Tx:
T - thiosulfate (sodium thiosulfate, induced methemoglobinemia)
H - Hydroxocobalamin (forms cyanocobalamin)
i
N - nitrites (induced methemoglobinemia)

Sx: Breath has a bitter almond odor; cardiovascular collapse.

48
Q

Carbon monoxide

Source/Tx/Sx

A

Source: Odorless gas from fires, car exhaust, or gas heaters.

Tx: 100% O2, hyperbaric O2.

Sx: headache, dizziness.

Multiple individuals may be involved (eg, family with similar symptoms in winter).

Classically associated with bilateral globus pallidus lesions on MRI, although rarely seen with cyanide toxicity as well.

49
Q

EFFECT ON OXYGEN-HEMOGLOBIN
DISSOCIATION CURVE - Cyanide vs carbon
monoxide poisoning

A

Cyanide - Curve normal; oxygen saturation may appear normal initially.

Carbon monoxide - dec oxygen-binding capacity with a left shift in the curve, dec O2 unloading in tissues.
Binds competitively to Hb with a 200x greater affinity than O2 to form carboxyhemoglobin.

50
Q

Methemoglobin

A

The oxidized form of Hb (ferric, Fe3+) - Iron in Hb is normally in a reduced state (ferrous, Fe2+).

does not bind O2 as readily as Fe2+, but has Inc affinity for cyanide.

Leads to tissue hypoxia from dec. O2 saturation and dec O2 content.

Methemoglobinemia may present with cyanosis and chocolate-colored blood.

51
Q

Oxygen-hemoglobin dissociation curve

Left shift

A

ABCCC MoFo

A -  Alkaline pH 
B -  2,3 BPG (low)
C - CO2 (low)
C - Cold temp
C  - CO

M - MetHb
H - HbF

52
Q

Oxygen-hemoglobin dissociation curve

Right shift

A

ACE-BAT

A -Acid (low pH)
C - pCO2
E - Exercise

B - 2,3 BPG (inc)
A - Altitude (high)
T - Temperature (high)

53
Q

Oxygen content of blood

A

O2 content = (1.34 x Hb x SaO2) + (0.003 x PaO2)

Hb = hemoglobin concentration; 
SaO2 = arterial O2 saturation
PaO2 = partial pressure of O2 in arterial blood

Normally 1 g Hb can bind 1.34 mL O2;
normal Hb amount in blood is 15 g/dL.
O2 binding capacity = 20 mL O2/dL of blood.

54
Q

O2 delivery to tissues =

A

cardiac output x O2 content of the blood.

55
Q

With dec Hb there is

A

dec O2 content of arterial blood, but no change in O2 saturation and PaO2.

56
Q

Pulmonary circulation - Perfusion limited

A

Perfusion limited - O2 (normal health), CO2, N2O.

C - CO2
O - O2
N - N2O

Gas equilibrates early along the length of the capillary. Exchange can be inc only if blood flow inc.

57
Q

Pulmonary circulation - Diffusion limited

A

Diffusion limited - O2 (emphysema, fibrosis, exercise), CO.

C - CO
O - O2

Gas does not equilibrate by the time blood reaches the end of the capillary.

58
Q

A-a gradient:

A

PAO2 - PaO2.

Normal A-a gradient estimated as (age/4) + 4;

eg, for a person < 40 years old, gradient should be< 14.

59
Q

Respiratory quotient:

A

CO2 produced/ O2 consumed

60
Q

Hypoxia

A

dec O2 delivery to tissue - COACH.

CO - CO poisoning
A - Anemia
C - Cardiac output
H - hypoxemia

61
Q

Hypoxemia

A

Dec PaO2

Normal A-a gradient: Both PAO2 +PaO2 dec.

  • High altitude
  • Hypoventilation (eg, opioid use, obesity hypoventilation syndrome)

Inc A-a gradient: only PaO2 dec.

  • V/Q mismatch
  • Diffusion limitation (eg, fibrosis)
  • Right-to-left shunt
62
Q

lschemia

A

loss of blood flow:

Impeded arterial flow

Dec. venous drainage

63
Q

V/Q = 0 =

A

Airway “oirway” obstruction (shunt).

In shunt, 100% O2 does not improve Pao2 (eg, foreign body aspiration).

64
Q

V/Q = infinity =

A

blood flow obstruction (physiologic dead space).

Assuming< 100% dead space, 100% O2 improves Pao2 (eg, pulmonary embolus).

65
Q

PE pathophysiology:

A

Flow forced through a few remaining vessels, and the ventilation stays the same

  • > V (same)/ Q (Inc) -> dec V/Q

even though there in inc dead space, the dec O2 -> Inc RR -> dec Co2.

66
Q

CO2 transported form types:

A

CO2 is transported from tissues to lungs in 3 forms:

  1. HCO3 - 70%
  2. Carbaminohemoglobin or HbCO2 - 21-25%
    CO2 bound to Hb at N-terminus of globin (not heme). CO2 favors the deoxygenated form (O2 unloaded).
  3. Dissolved CO2 - 5-9%
67
Q

Carbon dioxide transport - Haldane effect

A

In the lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shift equilibrium toward CO2 formation;
therefore, CO2 is released from RBCs ( Haldane effect).

The majority of blood CO2 is carried as HCO3- in the plasma.

68
Q

Carbon dioxide transport - Bohr effect

A

In peripheral tissue, inc H+ from tissue metabolism shifts curve to the right, unloading O2 (Bohr effect).

The majority of blood CO2 is carried as HCO3- in the plasma.

69
Q

Response to high altitude

A

pH:

  1. Inc RR -> dec. PaCO2 -> respiratory alkalosis -> altitude sickness.
  2. Inc renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide).

Cellular:

  1. Erythropoietin -> Hct and Hb inc (due to chronic hypoxia).
  2. Inc 2,3-BPG (binds to Hb causing a rightward shift of the ODC so that Hb releases more O2).
  3. Cellular changes (inc mitochondria).

Lung and heart:
Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.

70
Q

Response to exercise

A

Tissues:

  1. Inc CO2 production.
  2. Inc O2 consumption.
  3. Dec pH during strenuous exercise (2° to lactic acidosis).

Lungs:

  1. Inc ventilation rate to meet O2 demand.
  2. V/Q ratio from apex to base -becomes more uniform.
  3. Inc pulmonary blood flow due to inc cardiac output.

Peripheral vessels:
Arteries - no change in PaO2 and PaCO2
Veins - Inc in venous CO2 content and dec in venous O2 content.

71
Q

Rhinosinusitis

A

Obstruction of sinus drainage into the nasal cavity -> inflammation and pain over affected area.

Typically affects maxillary sinuses, which drain against gravity due to ostia located superomedially

Infections in sphenoid or ethmoid sinuses may extend to the cavernous sinus and cause complications.

72
Q

Superior meatus drains:

middle meatus drains:

inferior meatus drains:

A

Superior meatus drains: sphenoid, posterior ethmoid;

middle meatus drains: frontal, maxillary, and anterior ethmoid;

inferior meatus drains: nasolacrimal duct.

73
Q

Epistaxis

A

Most commonly occurs in the anterior segment of nostril (Kiesselbach plexus).

Life-threatening hemorrhages occur in the posterior segment (sphenopalatine artery, a branch of maxillary artery).

74
Q

Kiesselbach plexus made up by:

A

Kiesselbach drives his Lexus with his LEGS:

L - Labial artery, superior
E - Ethmoidal arteries (anterior and posterior)
G - Greater palatine artery,
S - Sphenopalatine artery.

75
Q

Head and neck cancer - Field cancerization:

A

carcinogen damages a wide mucosal area - multiple tumors that develop independently after exposure.

76
Q

Pulmonary emboli types:

A

F - Fat
A - Air
T - Thrombus

B - Bacteria
A - Amniotic fluid
T - Tumor

77
Q

Lines of Zahn:

A

Interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death;

Help distinguish pre- and postmortem thrombi.

78
Q

Mediastinal masses (Anterior, Middle, Posterior)

A
  • Anterior- 4Ts: Thyroid, Thymic neoplasm, Teratoma, “Terrible” lymphoma.
  • Middle - esophageal carcinoma, metastases, hiatal hernia, bronchogenic cysts.
  • Posterior- neurogenic tumor (eg, neurofibroma), multiple myeloma.
79
Q

Mediastinitis

A

Commonly due to postoperative complications of cardiothoracic procedures (pathology < 14 days),

esophageal perforation, or contiguous spread of odontogenic/retropharyngeal infection.

Chronic mediastinitis- a lso known as fibrosing mediastinitis; due to inc formation of connective tissue in mediastinum. Histoplasma capsulatum is a common cause.

80
Q

Obstructive lung diseases have inc volume/capacity:

A

Airways close prematurely at high lung volumes - Inc FRC, RV, TLC.

81
Q

Chronic bronchitis
(“blue bloater”)

Dx and pathophysiology:

A

Hypertrophy and hyperplasia of mucus-secreting glands in bronchi -> Reid index (thickness of mucosal gland layer to thickness of wall between epithelium and cartilage) > 50% . DLCO usually normal.

Diagnostic criteria: productive cough for> 3 months in a year for > 2 consecutive years.

82
Q

Asthma pathology:

A 
Hyperresponsive bronchi - reversible bronchoconstriction.
Smooth muscle hypertrophy and hyperplasia
Curschmann spirals (shed epithelium forms whorled mucous plugs)
Charcot-Leyden crystals m(eosinophilic, hexagonal, double-pointed crystals formed from breakdown of eosinophils in sputum).

DLCO normal or inc.

83
Q

Asthma pathophysiology:

A

Type I hypersensitivity reaction.
Aspirin-induced asthma is a combination of COX inhibition (leukotriene overproduction - airway constriction), chronic sinusitis
with nasal polyps, and asthma symptoms.

84
Q

Bronchiectasis

A

Chronic necrotizing infection of bronchi or obstruction -> permanently dilated airways.

Associated with :
A -Allergic bronchopulmonary aspergillosis.
B - Bronchial obstruction
C - Cystic fibrosis/ Ciliary motility poor (eg, smoking, Kartagener syndrome)

85
Q

Restrictive lung diseases - Interstitial lung diseases (pulmonary, dec DLCO, Inc A-a gradient):

A

W - Wegener (Granulomatosis with polyangiitis)
I - Idiopathic pulmonary fibrosis
S - Sarcoidosis
H - Hypersensitivity pneumonitis - mixed type III/IV
E - eosinophilic granuloma (Pulmonary Langerhans cell histiocytosis)
D - Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)

for a

Good - Goodpasture syndrome

Pft - Pneumoconioses (eg, coal workers pneumoconiosis, silicosis, asbestosis)

86
Q

Sarcoidosis - presentation + Dx

A

immune-mediated, widespread noncaseating granulomas

Elevated serum ACE levels, and elevated CD4/CD8 ratio in bronchoalveolar lavage fluid

Treatment: steroids (if symptomatic).

87
Q

Sarcoidosis - assosiations

A

Bell palsy and hypercalcemia (due to inc 1alfa -hydroxylase -> mediated vitamin D activation in macrophages).

U - Uveitis
G - Granulomas (noncaseating epithelioid, containing microscopic Schaumann and asteroid bodies)
L - Lupus pernio (skin lesions on face resembling lupus)
I - Interstitial fibrosis (restrictive lung disease)
E - Erythema nodosum
R - Rheumatoid arthritis-like arthropathy

A facial droop is UGLIER.

88
Q

Inhalation injury and sequelae

A

Caused by heat, particulates (< I μm diameter), or irritants (eg, NH3) - chemical tracheobronchitis, edema, pneumonia, ARDS.

Bronchoscopy shows severe edema, congestion of bronchus, and soot deposition (18 hours after inhalation injury, resolution at 11 days after injury).

89
Q

Asbestosis

A

Associated with shipbuilding, roofing, plumbing.

“Ivory white,” calcified, supradiaphragmatic and pleural plaques are pathognomonic of asbestosis.

Affects lower lobes.

Asbestos (ferruginous) bodies are golden-brown fusiform rods resembling dumbbells found in alveolar sputum sample, visualized using Prussian blue stain, often obtained by bronchoalveolar lavage.

90
Q

Mesothelioma is _______ (+)

A

Calretinin

91
Q

Acute respiratory distress syndrome - PATHOPHYSIOLOGY & CONSEQUENCES

A

PATHOPHYSIOLOGY:
Alveolar insult ->

release of pro-inflammatory cytokines ->

neutrophil recruitment, activation, and release of toxic mediators->

capillary endothelial damage and vessel permeability ->

leakage of protein-rich fluid into alveoli ->

formation of intra-alveolar hyaline membranes and noncardiogenic pulmonary edema (normal PCWP).

Loss of surfactant also contributes to alveolar collapse.

CONSEQUENCES:
Leads to -> Impaired gas exchange, dec lung compliance; pulmonary hypertension.

92
Q

Acute respiratory distress syndrome - CAUSES & MANAGEMENT

A 
CAUSES
P - pneumonia
A - aspiration
S - Sepsis (most common)
T - trauma

Pancreatitis.

MANAGEMENT:
Treat the underlying cause.
Mechanical ventilation: dec tidal volumes, inc PEEP.

93
Q

Acute respiratory distress syndrome - DIAGNOSIS

A

X - X-ray (Abnormal chest X-ray - bilateral lung opacities)
T - Time (Respiratory failure within 1 week of alveolar insult)
R - Ratio (Decreased PaO2/FiO2 - ratio< 300, hypoxemia due to inc intrapulmonary shunting and diffusion abnormalities)
a
S - Symptoms of respiratory failure are not due to HF/fluid overload

94
Q

Sleep apnea

A

Repeated cessation of breathing > l0 seconds during sleep -> disrupted sleep -> daytime somnolence.

Normal Pao2 during the day.

Diagnosis confirmed by a sleep study.

Nocturnal hypoxia -> systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), sudden death.

Hypoxia -> EPO release

95
Q

Obstructive sleep apnea

A

Respiratory effort against airway obstruction.

Associated with obesity, loud snoring, daytime sleepiness.

Caused by excess para-pharyngeal tissue in adults, adenotonsillar hypertrophy in children.

Treatment: weight loss, CPAP, surgery.

96
Q

Central sleep apnea

A

Think 3 C’s:

Congestive HF
CNS toxicity/opioids
Cheyne-Stokes respirations.

Treat with positive airway pressure.

97
Q

Obesity hypoventilation syndrome

A

Obesity (BMI > 30 kg/m2) -> hypoventilation -> inc PaCO2 during waking hours (retention);

Dec PaO2 and inc PaCO2 during sleep.

Also known as Pickwickian syndrome.

98
Q

Pulmonary hypertension

A

Normal mean pulmonary artery pressure = I0- 14 mm Hg;

pulmonary hypertension > 25 mm Hg at rest.

Results in:
P - plexiform lesions
I - intimal fibrosis of pulmonary arteries
M - medial hypertrophy
A - arteriosclerosis

Course: severe respiratory distress -> cyanosis and RVH -> death from decompensated cor pulmonale.

99
Q

Pulmonary arterial hypertension

A

Pulmonary vasculature endothelial dysfunction results in inc vasoconstrictors (eg, endothelin) and dec vasodilators (eg, NO and prostacyclins).

D - drugs (eg, amphetamines, cocaine)
a
M - mutation in BMPR2 gene (inactivating mutation, inhibits vascular smooth muscle proliferation)

H - HIV infection
i
C - connective tissue disease
C - congenital heart disease
u
P - portal hypertension
S - schistosomiasis
100
Q

Pulmonary hypertension - other etiologies:

A

H - Heart (Left) disease -> systolic/diastolic dysfunction and valvular disease

A - arterial

L - Lung diseases or hypoxia - >lung parenchyma. inflammation/fibrosis, hypoxemic vasoconstriction

T - thromboembolic (Chronic) - > Recurrent microthrombi - > dec cross-sectional area of the pulmonary vascular bed.

M - Multifactorial - > hematologic, systemic, and metabolic

101
Q

Atelectasis

A

Alveolar collapse, which can be due to multiple etiologies:

C - Compressive- external compression on lung decreases lung volumes
O - Obstructive- airway obstruction prevents new air from reaching distal airways, old air is resorbed
C - Contraction (cicatrization) - scarring of lung parenchyma that distorts alveoli
A - Adhesive-due to lack of surfactant

102
Q

Lobar pneumonia vs. Bronchopneumonia

TYPICAL ORGANISMS

A

Both: S pneumoniae, Klebsiella

Lobar pneumonia: Legionella

Bronchopneumonia: S aureus, H influenzae

103
Q

Lobar pneumonia vs. Bronchopneumonia

CHARACTERISTICS

A

Lobar pneumonia: Intra-alveolar exudate - consolidation.
may involve entire lobe or the whole lung.

Bronchopneumonia: Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving > 1 lobe

104
Q

Cryptogenic organizing pneumonia

A

Etiology unknown.

Secondary organizing pneumonia caused by chronic inflammatory diseases (eg, rheumatoid arthritis) or medication side effects (eg, amiodarone).

(-) sputum and blood cultures, no response to antibiotics.

105
Q

The natural history of lobar pneumonia - Congestion

Days + findings

A

Days: 1-2

Red-purple, partial consolidation of parenchyma

Exudate: mostly bacteria

106
Q

The natural history of lobar pneumonia - Red hepatization

Days + findings

A

Days: 3-4

Red-brown consolidation

Exudate: fibrin, bacteria, RBCs, and WBCs

107
Q

The natural history of lobar pneumonia - Gray hepatization

Days + findings

A

Days: 5-7

Uniformly gray

Exudate: WBCs, lysed RBCs, and fibrin

108
Q

The natural history of lobar pneumonia - Resolution

Days + findings

A

Days: 8+

Enzymes digest components of the exudate

109
Q

Lung cancer - Metastasis to and from the lung

A 
Sites of metastases from lung cancer:
B - Brain
L - Liver (jaundice, hepatomegaly)
A - Adrenals
B - Bone (pathologic fracture)
Sites of metastases to lungs from other cancers:
P - prostate
u
B - breast
B -  bladder cancer
i
C - colon
110
Q

Lung cancer - complications:

A

S - Superior vena cava/thoracic outlet syndromes
P - Pancoast tumor
H - Horner syndrome
E - Endocrine (paraneoplastic)
R - Recurrent laryngeal nerve compression (hoarseness)
E - Effusions (pleural or pericardial)

111
Q

Small cell (oat cell) carcinoma - HISTOLOGY

A

Neoplasm of neuroendocrine Kulchitsky cells ->small dark blue cells.

Chromogranin A +
neuron-specific enolase +
synaptophysin +

Amplification of myc oncogenes common.

112
Q

Large cell carcinoma

A

Peripheral.

Highly anaplastic undifferentiated tumor -> Pleomorphic giant cells;

Poor prognosis -> Less responsive to chemotherapy; removed surgically.

Strong association with smoking.

113
Q

Pancoast tumor

A

Compress ion of locoregional structures may cause an array of findings:

S - Stellate ganglion - Horner syndrome (ipsilateral ptosis, miosis, anhidrosis)
u
B - Brachiocephalic vein - brachiocephalic syndrome (unilateral symptoms)
u
R - Recurrent laryngeal nerve - hoarseness
B - Brachial plexus - sensorimotor deficits
S - Superior vena cava - SVC syndrome

Suburbs of Pan -coast!

114
Q

Superior vena cava syndrome

A

Medical emergency - “facial plethora”

Blanching after fingertip pressure in, neck (jugular venous distention), and upper extremities (edema).

Caused by malignancy and thrombosis from indwelling catheters.

Can raise intracranial pressure (if severe) -> headaches, dizziness, inc risk of aneurysm/ rupture of intracranial arteries.

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