KEUHN [6Q]

1. Tracheoesophageal Fistula: Abn connection bw trachea & esoph, results in impr

oper division of foregut be the tracheoesophageal septum. Assoc w esophageal at
resia and polyhydramnios. Leads to excessive accum of saliva/mucus in nose & mou
th. Episodes of gagging and cyanosis after swallowing milk.
2. Pseudoglandular period (wk7-16)-non-viable; Canalicular period (wk 16-24)-sur
factant production begins ~wk20. Viability wk 24 minimum!
3. Terminal Sac Period (wk 24-birth); Alveolar Period (birth-8 yrs)-superior par
t of lungs develop functional alveoli before inferior parts.
4. PHARYNGEAL ARCH 6 (neural crest): Arytenoid and Cricoid Cartilage
5. Epiglottis & Thyroid Cartilage from PHARYNGEAL ARCH 4.
6. Structures thru Diaphragm: IVC @ T8; CNX & Esophagus @ T10; Aorta, Thoracic D
uct, Azygos V @ T12.
7. Congenital Herniation of the Diaphragm: failure of pleuroperitoneal canal clo
sure. Stomach, spleen, intestines herniate up unto Left Pleural Cavity.
8. Recurrent Laryngeal N: Enters the larynx deep to inferior pharyngeal constric
tor mm. Becomes inferior laryngeal nerve above the cricothyroid joint.
9. Sibson s Fascia (a thickened area of endothoracic fascia at the apex of the lun
g)
10. Relation of Pulmonary A to the bronchus at each lung hilus is: R-A-L-S (Righ
t-Anterior; Left-Superior)
ALTIKRITI [3Q]
1. [CLARA CELLS]
2. [GOBLET CELLS] - in bronchi only
3. [PSEUDOSTRATIFIED COLUMNAR CILIATED EPITHELIUM]
ZHONG [Mech of Breathing/Airway/Alveolar Vent]
1. SURFACTANT: reduces surface tension such that pressure is equalized in alveol
i (P=2T/r). Also promotes stability and prevents transudation of fluid into alve
oli.
2. COMPLIANCE: C=deltaV/deltaP. Distensibility of the system. Inversely related
to elasticiy. Compliance differs bw inspiration and expiration due to HYSTERESI
S.
3. End of Inspiration=lower surface tension but higher surfactant. End of Expira
tion=high surface tension but requires surfactant to break restrictive H-bonding
forces and become compliant. At LOW compliance (low slope portions of graph)--m
ore work is required to produce inflation.
4. [Graph] Compliance of lungs-chest wall system (3 lines) in terms of airway pr
essure and volume. NEGATIVE PRESSURE=volumes below FRC=Expanding force. POSITIVE
PRESSURE=volumes ABOVE FRC=Collapsing force.
5. Chief Site of Airway Resistance occurs in MEDIUM-SIZED BRONCHI. (recall: R=8n
L/pi*r^4). Most of pressure drop @ 7th division. Very small bronchioles have ver
y little resistance.
6. Airflow is driven by pressure difference bw atm (mouth/nose) and alveoli ("tr
anspulmonary pressure"), and is INVERSELY proportional to airway resistance.
7. During FORCED EXPIRATION: intrapleural pressure becomes positive, COMPRESSING
airways and making expiration more difficult ("Dynamic Compression")
8. PFT Equations: VC=IRV+TV+ERV. TLC=IRV+ERV+TV+RV. etc.
9. HELIUM DILUTION METHOD measures FRC (and residual volume): V1C1=V2C2. disadva
ntage- poor estimation in COPD pts because helium cant reach all lung spaces.
10. Body Plethymography for FRC measurement- More Accurate than Helium dilution
method.
11. DLCO=Vco/PAco. Normally 25 mg/min/mmHg. Decreased in Restrictive dz's, space
occupying tumors, lung resection, loss of lung tissue (eg emphysema)
12. Flow-Volume Loops to distinguish obstructive vs restrictive lung diseases.
13. PERFUSION LIMITED EXCHANGE (aka Flow limited): O2 (normal conditions), CO2,
N2O. Reaches equilibrium early on in pulmonary capillaries. Diffusion increases
only if flow increases (Q).
14. DIFFUSION LIMITED EXCHANGE: O2 (strenuous exercise, in Emphysema & Fibrosis)

and CO. Partial pressures never reach equilibrium.

15. ALVEOLAR GAS EQN: PAO2 = (PICO2) - (PaCO2/R); PAO2 = [150 - (PaCO2/0.8)].
GUO
1. ASTHMA: type I hypersensitivity rxn involving CD4+ Th2 cells which release IL
-4 (class-switch to IgE), IL-5 (recruits eosinophils), IL-10 (stim Th2 productio
n & represses Th1 production). IgE @ mast cells release HISTAMINE-->incr vascula
r permeability and smooth mm contractions (BRONCHOCONSTRICTION)
2. BRONCHIECTASIS: due to infection+obstruction of other dz's leading to destruc
tion & dilation of bronchioles & bronchi. Causes: CF, Karagener, Apergillosis, N
ecrotizing infxn, tumor. Complications: hemoptysis, pulm HTN, Hypoxemia/cor pul
monale, Secondary Amyloidosis (AA)
3. CHRONIC BRONCHITIS: clinical dx of productive cough for >3 mo for 2 consecuti
ve yrs. Hyperplasia of mucous glands in bronchi (Reid index >50% mucous lands in
histo), mucous plugging, "Blue Bloaters" due to cyanosis. PFTs show increased T
LC with decreased FEV1.
4. EMPHYSEMA: loss of elastic recoil--> airway collapse + air trapping. PFTs sho
w increased TLC, Increased RV and Decreased FEV1/FVC ratio. "Pink Puffer", barr
el chested, chronic resp acidosis w compensatory alkalosis, pulmonary cachexia (
wt loss)
5. Smoking causes CENTROacinar Emphysema. most common @ UPPER lobes. Nicotine at
tracts Neutrophils via NF-kB--> produces TNF and IL-8, release of proteases and
ROS.
6. a1-antitrypsin deficiency (PiZZ allele) causes PANacinar Emphysma. more commo
n LOWER lobes, distends terminal blind alveoli. assoc w LIVER cirrhosis--> misfo
lded antitrypsin proteins build up in ER of hepatocytes.
7. TUMOR MARKERS: primary lung adenoca CK7 and TTF1 positive; squamous cell ca C
K5/6 positive; small cell ca TTF1 and neuroendocrine markers positive
VISHY [9Q]
1. IL-8 cues neutrophils to leave bloodstream and migrate to lungs to mediate in
flammation. Neutrophils: short-lived, for acute infxn, myeloperoxidase.
2. PERTUSSIS: Cytotoxin (LPS and peptidoglycan) release NO that kills ciliated e
pith
3. MYCOPLASMA PENUMONIAE (ATYPICAL PNA): no cell wall, cyotadhesions with ROS, C
atalase+
4.
5.
6.
7.
8.
9.
GOYA LARGE GRP 1
1. FEV1/FVC < 70% is OBSTRUCTIVE. FEV1 for Severity: FEV1 >70%=mild; FEV1 60-69%
=moderate; FEV1 35-49%=severe. ALSO see INCREASED FRC and RV due to air trapping
.
2. MUST do LUNG VOLUME TESTS to diagnose a restrictive defect (also consider DLC
O tests). FEV1/FVC > 80% but DECREASE OF ALL LUNG VOLUMES, particularly VC and T
LC.
3. ASTHMA: Reversibility is defined as positive response to bronchodilator (SABA
): FEV1 >200mL and >12% from baseline.
4. LABA MUST be given with inhaled corticosteroids in persistent asthma pts! (LA

BA alone increases mortality risk). See Treatment chart.

5. TX Acute Asthma Exacerbation: O2, Short-Acting B-agonist (SABA, albuterol), C
orticosteroids, Ipratropium bromide
6. Classifying COPD: Mild (FEV1 >80% predicted); Moderate (FEV1 60-80% predicted
); Severe (FEV1 <60% predicted)
7. Pt w/ asthma usually have LOW pCO2 that could progress to HYPERCAPNIA, which
has a HIGH pCO2 and could be indicative of HYPOXEMIC RESPIRATORY FAILURE (Wide A
-a)
8.
9. CXR of COPD: Increased AP diam, Flat Diaphragm, Enlarged retrosternal air spa
ce, Heart appears long/narrow. Poss evidence of cor pulmonale. Normal lung paryn
chyma.
10. Macrolides (eg Azithromicin) used to reduce COPD (and CF) exacerbations via
REDUCING INFLAMMATION (NOT to treat any bacterial infection). Side effects: long
QT, tinnitus, hearing loss.
11. O2 therapy: only tx that will IMPROVE SURVIVAL in COPD. Goals: PaCO2 > 55 m
mHg, SpO2 < 88%, and PaO2 <55 mmHg. Careful not to drop pH below 7.25
12. Cystic Fibrosis: Auto rec. Chromosome 7 deletion at F508 locus. affects UPPE
R lobes. Leads to recurrent bronchitis->bronchiectasis->Chronic resp failure-> d
eath
13.
14.
15.
GOYA LARGE GRP 2
1.
2.
3.
4. HYPERSENSITIVITY PNEUMONITIS:
5. LOFGREN SYNDROME: presentation of sarcoidosis with (1) erythema nodosum (skin
rash); (2) bilateral hilar LAD; (3) arthralgias. Good prognosis, resolves in 2
yrs.
6. CXRs of Sarcoidosis: Stage 1: B/L Hilar LAD WITHOUT lung involvement. Stage 2
: B/L Hilar LAD WITH LUNG involvement (symptomatic). Stage 3: LUNG FIBROSIS with
out hilar LAD. Stage 4: Honeycombing pulm fibrosis at UPPER LOBES.
7. Sarcoidosis Laboratory Findings: elevated ACE, Hypercalcemia/Hypercaluria, El
evated LFTs/Creatinine. Biopsy: epitheliod histiocytes+giant cells in NON-CASEAT
ING Granulomas.
8.
9. If you suspect a PE and Pt has a NORMAL D-Dimer (<500pg/mL), then pt DOESNT h
ave a PE. Also, if DVT clot is in the pt's calf, it is NOT a PE.
10.
11.
12.
GOYA LARGE GRP 4
1.
2.
3.
4.
5.
6.
7.
8.
9.
GOYA LARGE GRP 5 [sepsis/ARDS/resp failure/acid-base]
1. HYPOXEMIC RESPIRATORY FAILURE: PaO2 < 60 mmHg. WIDENED A-a GRADIENT! Most oft
en due to V/Q mismatch. SUPPLEMENTAL O2 will improve this, ventilation can't.
2. HYPERCAPNIC RESPIRATORY FAILURE: NORMAL A-a GRADIENT! PaCO2 > 50 mmHg. CANNOT

VENTILATE (due to brainstem disorders, guillaine-barre). supplemental O2 doesn'

t help.
3. TREATMENT OF ARDS: LUNG PROTECTIVE VENTILATION - ventilation with LOW TIDAL V
OLUMES (~ 6 mL/kg) to decrease potential barotrauma.
4. MANAGEMNT of ARDS: Tx UNDERLYING CAUSELess fluids, early steroids (<7 d), Pro
ne positioning, ventilate w small tidal volumes, PEEP and FiO2 < 60%. Goal O2=88
%.
5. Mixed pH disorders
6. Respiratory Alkalosis
7. DELTA GAP: by calculated AGMA MINUS expected anion gap (12) PLUS measured HCO
3. [(AG-12)+ HCO3] > 26 then METABOLIC ALKALOSIS + AGMA.
8. DISTRIBUTIVE SHOCK (includes SEPTIS): loss of vasomotor control, often SHUNTI
NG, increases CO and decreases systemic vascular resistence.
9. SEPSIS MANAGEMENT: Colloid fluids, broad spectrum Abx, vasopressors (if refra
ctory low BP), steroids, blood transfusion (if Hb 7-9 and SvO2<70%), low Vt vent
ilation
10. Dobutamine given ONLY IF SvO2<70% and LOW CARDIAC OUTPUT despite trying flui
ds or NorEpinephrine..alternate choice is Epinephrine.
11. SIRS: Temp<38, HR>90, RR>20, Leukocytes<4k or >12k or >10% band neutrophils
PLUS confirmed/suspected infxn.
12. SEVERE SEPSIS=SEPSIS+Organ hypoperfusion. SEPTIC SHOCK=Severe sepsis+hypoten
ion (systolic<90mmHg, MAP<65 mmHg) and unresponsive to IV fluids.
MATA: Anti-Asthmatic Drugs
1. In Pt with HEPATIC INSUFFICIENCY: give Prednisolone not prednisone. because p
rednisone won't become effective if liver doesn't work.
2. BBWs!
3.
YASMER [6Q]
1. PLEURAL EFFUSION: Need at least 200 mL fluid to see blunted costophrenic angl
e from A-P view.
2.
3.
4.
5.
6.
BROWNELL [6Q]
1. O2 content of blood = the sum of oxygen bound to Hb + amount of dissolved O2.
Also, the destination for oxygen is mitochondria (PO2 ~ 2 mmHg).
2. FAVORED O2 UNLOADING (SHIFTS RIGHT, Taut conformation): increases in 2,3 BPG,
altitude, temperature, acidity/H+ ions (Bohr effect), CO2, Exercise.
3. Myoglobin=monomeric O2 carrier of high affinity (low P50). Cellular oxygen re
servoirs in metabolically active tissues. HYPERBOLIC saturating kinetics/curve.
4. Fetal Hb= higher affinity for O2 binding (LEFT SHIFT) that favors transfer of
O2 from maternal blood. Two alpha and two gamma subunits; insensitive to 2,3 BP
G.
5.
6.
MESA [3Q]
1.
2.
3.
PARSA [Pneumonia-6Q]
1.
2.

3.
4.
5.
6.
MATA [Pharm Resp-9Q]
1. DIPHENHYDRAMINE: H1 receptor (Gq/11) antagonist for type I hypersensitivities
. Adverse: Sedation, photosensitivity rash, prolonged QTc.
2. AMPHOTERICIN B: wide spectrum antifungal. C-AMB (SLOW IV only). SIDES: NEPHRO
TOXIC (dose-dependent renal ischemia); Cytokine Storm (inc TNFa and IL-1), Anemi
a, arrythmia (hyperkalemia/torsades). Note: use ABCD colloidal lipid preparation
for renal patients (least nephrotoxic, but most likely to cause cytokine storm)
3. AZOLE ANTIFUNGALS: inhibit ergosterol synthesis. GENERAL SIDES: epigastric pa
in, teratogenic, CYP inhibitors. FLUCANAZOLE for fungal meningitis. ITRACONAZOLE
BBW negative inotopy. POSACONAZOLE is widest spectrum, mucormycosis. VORICONAZO
LE-good CNS penet, CYP2C19 beware poor asian metabolizers.
4.
5.
6.
7.
8.
9.
FELTON [3Q]
1. COCCIDIOIDOMYCOSIS: SW American regions. Infectious Arthroconidia become airb
orn and inhaled --> turns into SPHERULE, reproduces w ENDOSPORES in tissues. Dis
ease ranges from Valley Fever (lower resp tract infxn), acute progressive PNA to
disseminated infxn (rare) at bones, nervous system and skin.
2. CHLAMYDIA TRACHOMATIS TYPES D-K can cause pulmonary infection in neonate, acq
uired at birth from infected mother. Recall chlamydia is obligate intracellular
parasite with elementary body and reticulate bodies, seen on Giesma stain.
3. HISTOPLASMOSIS- mostly mississippi river valley. hides in macrophages. infect
ed macrophages migrate to spleen and liver. causes PNA.
SAVIOLA [3Q]
1.
2.
3.
STEINAUER [3Q]
1.
2.
3.
FAHIM [9Q]
1. CROUP/LARYNGOTRACHEITIS - Parainfluenza virus. Steeple sign (narrowed subglot
tic area). Tx: Mist, racemic epinephrine, steroids
2. LARYNGOTRACHEOBRONCHITIS/PNEUMONITIS - subglottic narrowing, S. aureus or S.
pyogenes
3. LARYNGOMALACIA - Omega Sign, INSPIRATORY STRIDOR, collapse of arytenoid carti
lage/epiglottis. vs TRACHEOMALACIA which is expiratory wheeze; hx of being venti
lated
4. EPIGLOTTITIS - cherry red epiglottis, thumb sign, drooling/toxic appearance,
Haemophilus influenzae (unimmunized). High fever, won't swallow, inspir stridor.
5. STRUCTURAL ABNORMALITIES OF AORTIC ARCH - Vascular Rings on BARIUM SWALLOW TE
ST. Sx: Stridor/dysphagia.
6. CHOANAL ATRESIA/STENOSIS - suspect when can't pass an NG tube. Sx: cyanosis w
/ feeding or resting, inspiratory stridor.
7. BRONCHIOLITIS - RSV. <2 yr old @ fall/winter. Risk: premature/chronic dz. CXR
: hyperinflation/atelectasis/infiltrate. Dx: rapid Ag test. Prevent w PALIVIZUMA

B.
8. WHOOPING COUGH - B. pertussis. >21 d cough. Catarrhal/Paroxysmal/Convaselscen
t stages. Tx: AZITHROMYCIN asap.
9. SUDDEN INFANT DEATH SYNDROME (SIDS) - may occur when baby falls asleep prone
or on side.
LARGE GRP 3 PATEL [9Q]
1. Klebsiella pneumonia-fat Gram Neg encapsulated rods (alcoholic, DM, COPD) tx
of choice: 3rd gen cephalosporin (beta lactam)ceftazidime, ceftriaxone, cefotax
ime
2.
3.
4.
5.
6.
7.
8.
9.
GUO [tumors 6Q]
1.
2.
3.
4.
5.
6.
RAJURKAR [1.5 Hr]
1.
2.
3.
4.
5.
ROSS: