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153 Cards in this Set

  • Front
  • Back

when do lung buds develop

week 4

embryonic phase of lung development

weeks 4-7


lung bud -> tertiary bronchi




error = TE Fistula

pseudoglandular phase of lung development

weeks 5-16


terminal bronchioles




incompatable with life still

canalicular phase of lung development

16-26 weeks


terminal bronchioles -> alveolar ducts


prominent capillary netowrk




capable at 25 weeks

saccular phase of lung development

26-birth


terminal sacks develop


pneumocytes develop + surfactant



alveolar phase of lung development

32wks - 8 yrs




terminal sacs to adult alveoli



pulmonary hypoplasia

poorly developed bronchial tree with right lung most often involved




associated with


-congenital diaphragmatic hernia


-bilateral renal agenisis


- potter sequence

broncogenic cysts

abnormal budding of the foregut and dialation of terminal and large bronchi




discrete air filled densities on CXR


they drain poorly & cause chronic infections

most common pneumonia in immunocompromised

pneumocystitis jirovecii

most common cause of atypical pneumonia

mycoplasma pneumonia

most common cause of pneumonia in alcoholics

klebsiella pneumonia

cause of interstitial pneumonia in bird handlers

chlamydophilla psittaci

pneumonia in pt with history of bats/bat droppings

histoplasma

pneumonia in someone whos recently been to the SW USA

coccidiodies

pneumonia and Q fever

coxiella burnetti

pneumonia associated with air conditioners

legionella

most common cause of pneumonia in kids less than 1yo

RSV

most common cause of pneumonia in neonates


(>1 month)

GSB


E.Coli

most common case of pneumonia in kids, young adults, college kids, military recruits, prison inmates

mycoplasma pneumonia

most common cause of viral pneumonia

RSV

most common cause of wool sorters disease

bacillis anthracis

most common pneumonia in vent pt

MRSA


Pseudomonas

most common cause of pneumonia in CF pts

Pseudomonas


MRSA

name of ingredient of surfactant

lecithin


-dipalmitoylphosphatidylcholine

when does surfactant production begin & when are the lungs mature

26weeks




35 weeks

club cells

non -ciliated columnar/cubiodal


-secretory granules




actions


-secrete parts of surfactant


-degrade toxins


-reserve cells

characteristic description of a CXR of a neonate with NRDS

groundglass lungfields

L:S ratio predictive of NRDS

<1.5

complications of NRDS

1.metabolic acidosis


2.PDA


3.necrotizing enterocolitis

Risk factors for NRDS

Premature


Maternal DM (due to high fetal insulin)


C-section (decrased steroid release)

complication of O2 supplementation in NRDS

RIB


Retinopathy of prematurity


Intraventricular hemorrhage


Bronchopulmonary dysplasia

part of bronchial tree with least resistance

terminal bronchioles

how far down do goblet cells & cartilage go

end of bronchi

primary epithelium of upper airways & how far down does it go

Psuedostratified ciliated columnar


-to terminal bronchioles


-work as the mucociliary escalator

how far down does smooth muscle go in the airways

terminal bronchioles

tissue type in respiratory bronchioles

cuboidal

where do cilia end

respiratory bronchioles

if you aspirate a peanut sitting up where will it go

inferior segment of right inferior lobe

if you asiprate a peanut while laying down where will it go

superior segment of the right inferior lobe

where structures perforate the diaphragm

I ate 10 eggs at 12




T8 - IVC


T10 - esophagus & vagus


T12 - Aorta, Azygous, Thoracic duct





common bifurcations

biFOURcations




C4 - common carotid


T4 - trachea


L4 - abdominal aorta

typical tidal volume

500mL

inspiratory reserve volume

amount that can be breathed in after normal inspiration

expiratory reserve volume

air that can be breathed out after normal expiration

inspiratory capacity

tidal volume plus all the extra you can breath in

functional residual capacity

RV + ERV




volume in lungs after normal expiration

vital capacity

max volume that can be expired after max inhalation




everything but RV

equation for physiologic dead space



Vd = Vt x (PaCO2 - PeCO2 / PaCO2)




vt = tidal volume


Pa = arterial CO2

normal respiratory rate

12-20breaths/min

minute ventilation equation

Ve- minute ventilation




Ve = Vt x RR




tidal volume x respiratory rate

alveolar ventilation equation (VA)

VA = (Vt - Vd) x RR

values at FRC

Airway & alveolar pressures are 0


intrapleural pressure = (-)

taut form of Hb

T=tissues




deoxygenated


-low affinity for O2


-promotes unloading in tissues



R form of Hb

relaxed - R=Receptive to O2


wants to bind O2

things that favor the Taught form of Hb

-shifts curve to the right


-promotes O2 unloading




H+


Cl-


CO2


high Temp


2,3-BPG

Methemoglobin

Fe3+ - ferric


-does not bind O2 as well but binds CN- very well




Presents


-cyanosis


-chocolate colored blood




causes


-nitrates from diet, pollution, high altitude water


-benzocaine poisoining


-nitrates, antimalarial, dapsone, sulfonamide, lidocaine, metoclopromide




Tx


-methylene blue


-vitamin c




+ cimetidine for long term tx of drugs known to induce methemoglobin like dapsone & sulfonamides in HIV prophylaxis

Tx of CN- poisoning

induce methemoglobinemia


-Nitrites followed by thiosulfate


-higher binding affinity for CN than for O2

Carboxyhemoglobin

CO poisoning


-left shift on O2 dissociation curve = less unloading in tissues

equation for O2 content

(1.34x Hb x SaO2) + (0.003 x PaO2)




SaO2 = arterial O2 saturation


PaO2 = partial pressure of O2

normal amount of Hb in the blood

15g/dL




1g of Hb can bind 1.34mL O2

O2 binding capacity

20.1mL O2/ dL blood

equation for O2 delivery to tissues

cardiac output x O2 content of blood

Anemia affect on




1. Hb concentration


2.%O2 sat of Hb


3.PaO2 (dissolved)


4. Total O2 content

1. Hb concentration - down


2.%O2 sat of Hb - normal


3.PaO2 (dissolved) - normal


4. Total O2 content - down

polycythemia affect on




1. Hb concentration


2.%O2 sat of Hb


3.PaO2 (dissolved)


4. Total O2 content

1. Hb concentration - increased


2.%O2 sat of Hb - normal


3.PaO2 (dissolved) - normal


4. Total O2 content - increased

COPD affect on



1. Hb concentration


2.%O2 sat of Hb


3.PaO2 (dissolved)


4. Total O2 content

1. Hb concentration - normal


2.%O2 sat of Hb -


3.PaO2 (dissolved) - low


4. Total O2 content - low

Perfusion limited

normal (O2)


CO2


N2O




diffusion can be increased only with increased flow

diffusion limited

O2 in emphysema or fibrosis or CO




gas doesnt equilibrate by the end of the capillary

equation for pulmonary vascular resistance (PVR)

PVR = Pressure in pulm A - Pressure in L atrium


cardiac output

alveolar gas equation

PaO2 = 150 - (PaCO2/0.8)




needed to calculate A-a gradient to determine source of hypoxia

hypoxemia with a normal A-a gradient

high altitude


hypoventilation (opiod)

Hypoxemia with an elevated A-a gradeint

V/Q mismatch


Diffusion limitation (fibrosis)


Right to left shunt

V/Q = O

Oirway obstruction (shunt) = O




100% O2 doesnt help




example = foreign body aspiration

V/Q = infinity

blood flow obstruction = infinity




100% O2 helps

PA, Pa and Pv in different parts of lungs

Top : PA > Pa > Pv




Middle : Pa > PA > Pv




Bottom : Pa > Pv > PA




*big A moves to the right everytime

how CO2 is transported back to lungs

1. HCO3-




2. Carbaminohemoglobin or HbCO2


-Co2 binds to N-terminus of globin (not heme)


-favors taut form = releases O2




3. Dissolved Co2

Haldane effect

in the lungs O2 added to Hb dissociates the H+


-shifts towards formation of CO2

Bohr effect

increased H+ in tissues from metabolism shifts curve to right unloading O2

Response to high altitude

low PaO2 -> hyperventilation -> low CO2


= resp alkalosis




1. chronic increased ventilation


2.high EPO - increased Hct & Hb


3. high 2-3BPG


4.more mitochondria


5.more excretion of bicarb


6.vasoconstricted lungs & RV hypertrophy

physiologic changes in lungs during exercise

no change in PaO2 & PaCO2




increased


-venous CO2


-decrease venous O2 content

where do maxillary sinuses drain into

middle meatus

causes of Rhinosinusitis

1. acute viral URI


2. superimposed bacterial infection


--strep pneumo


--H. flu


--M catarrhalis

where do epistaxis occur

most common - anterior segment in Keisselbach plexus

location of life threatening nasal hemorrhage

posterior segment


-sphenopalantine artery (maxillary A branch)

most common type of head and neck cancer

squamous cell

risk factors for head and neck cancer

EtOH


Tabacco


HPV-16 (oropharyngeal)


EBV - (nasopharyngeal)

fat emboli

long bone fracture


liposuction




triad


-hypoxemia


-neurologic abnormalities


-petechial rash

imaging test of choice for PE

CT pulmonary angiography

length of time needed to diagnose chronic bronchitis

productive cough for >3 months (not consecutive) for 2 years

complications of chronic bronchitis

polycythemia


pulmonary HTN (hypoxemia)


cor pulmonale

centroacinar vs panacinar emphysema locations

centro = upperlobes


pan = lower lowbes

cause of emphysema

increased elastase activity and decreased anti-trypsin activity to stop it



findings in asthma

1. Smooth muscle hypertrophy


2. Curshmann spirals


--shed endothelium forms whorled mucus plugs


3.Carcot-Leydig crystals


--hexagonal double pointed needle like crystals fromed from breakdown of eosinophils in sputum

drugs known to cause restrictive lung disease

Bleomycin


-pneumonitis with infiltrates




Busulfan


-acute lung injury, chronic fibrosis, alveolar hemorrhage




Amiodarone


-pulmonary fibrosis




Methotrexate


-hypersensitivity like rxn



Idiopathic pulmonary fibrosis

mutation in TELOMERASE or MUC5B




risk - age, smoking, genetics


survival - 3 years post dx




presents


-honeycomb lung


-patchy intersitial fibrosis

Pulmonary langerhans cell histiocytosis

eosinophillic granuloma associated with restrictive lung disease




+birbeck granules (tennis racket)




-young smoker , goes away if they stop

hypersensitivity pneumonitis

can cause Restrictive lung disease




mixed type 3/4 HS RXN to environmental antigen




-dyspnea, cough, chest tightness, HA




-farmers


-exposed to birds

Caplan syndrome

Rheumatoid arthritis




+




Pneumoconiosis with intrapulmonary nodules


-silicosis, asbestosis, coal

asbestosis

Shipbuilding, roofing & plumbing




presents


-calcified pleural plauques & on diaphragm


-lower lobes


-ferruginous bodies (golden dumbells)


-->found in sputum on prussian blue stain




complications


-pleural effusion


-bronchogenic carcinoma


-laryngeal carcinoma


-mesothelioma

Berylliosis

Aerospace or high tech industry




presents


-noncaseating granulomas


-upper lobes




occasionally responsive to steroids

Coal workers Pneumoconiosis

1. Anthracosis - asymptomatic in urban people black lung




2. simple - fibrous nodules


3. complex - progressive fibrosis




Macrophages filled with carbon


upper lobe

Silicosis

miners, sandblasters


-macrophages release fibrogenic factors


-disrupts phagolysosome and impairs macrophages increasing RISK FOR TB & lungCA




Presents


-upper lobes


-Egg shell calcifications of hilar lymph nodes



pathophysiology of ARDS

Endothelial damage (neutrophillic substances, coag cascade, ROS) -> increased alveolar capillary permeability -> protein rich fluid into alveoli -> diffuse alveolar damage and non cardiogenic pulmonary edema (normal PCWP)




->hyaline membrane





sequelae of nocturnal hypoxia

systemic/pulmonary HTN




arrythmia (afib/aflutter)




sudden death




increased EPO

obstructive sleep apnea

obesity


snoring




adenotonsillar hypertrophy in kids


excess pharyngeal tissue adults



central sleep apnea

No respiratory effort due to CNS injury, HF, opoids




common in premature infants




tx - CPAP, Resp stimulatory drugs, acetozolamide

Obesity hypoventilation syndrome

BMI>30 -> low RR -> low PaO2 and high PaCO2 during sleep




high PaCO2 during wakeful hours due to retention

normal mean pulmonary pressure




definition of pulmonary HTN

normal = 10-14mmHg




HTN = >25mmHg

Heritable primary pulmonary HTN

inactivation of BMPR2


-normally inhibits vasc smooth muscle proliferation


-leads to increased resistance




associated with kaposi sarcoma & HIV


women under 30 usually

other causes of primary pulmonary HTN

Drugs - meth/coke


CT disease


HIV


Portal HTN


Congenital HD


Schistosomiasis

treatment for pulmonary HTN

Bosentan/Ambrisentan - competitive antagonist of entothelin 1 (decrase pulm resistance)




Prostaglandin analog




Sidenafil




Nifedipine

Physical findings with pleural effusion

-decreased breath sounds


-dull to percussion


-low fremitus


-tracheal deviation away if large enough

physical findings with atelectasis


(bronchial obstruction)

-decreased breath sounds


-dull to percussion


-low fremitus


-trachea deviates TOWARD lesion

physical findings on simple pneumothorax

-decreased breath sounds


-hyperresonant


-decreased fremitus

physical findings on tension pneumothorax

-decreased breath sounds


-hyperresonant


-decreased fremitus


-deviates away from lesion

lobar pneumonia findings on physical

late inspiratory crackles


dullness to percussion


increased fremitus

superior vena cava syndrom

obstruction of SVC that limits drainage




presents


-Jugular venous distention


-upper extremity edema




causes


-pancoast tumor


-thrombosis of indwelling catheter


-increased ICP


-increased aneurism or rupture risk

transudate

transparent = no protein


due to hydrostatic pressure increase or low oncotic presssure

exudate

high protein content - cloudy




causes


-malignancy


-pneumonia


-trauma




must be drained due to infection risk

primary spontaneous pneumothorax

young tall thin male


due to apical subpleural bleb

secondary sponteanous pneumothorax

due to diseased lung


-bullae in emphysema


-mechanical vent -> barotrauma

traumatic pneumothorax

due to a penetrating or blunt wound to the lung

most common cause of lobar pneumonia

strep pneumo


-intraalveolar exudate

most common cause of broncopneumonia

Strep pneumo


Staph aureus


H. flu


klebsiella




acute inflammaory infiltrates


patchy distribution involving less than a whole lobe

most common causes of interstital pneumonia

Mycoplasma


Chlamydia


Leigonella


Viruses




diffuse patchy inflammation located to interstital areas

treatment for aspiration pneumonia

clindamycin

presentation of aspiration pneumonia

person is at risk (epilepsy, etoh)




air fluid level on CXR




often right lung

histology of mesothelioma

Psammoma bodies


Cytokeratin & calretinin +



where does lung cancer like to met to

adrenals


brain


bone


liver

gene mutations associated with small cell lung cancer

-amplification of myc


-TP53


-RB

histology of small cell lung cancer

+ neuroendocrine cells - kulchisky cells


(small dark blue cells)




+ chromogarnin A


+neuron specific enolase



mutations associated with adenocarcinoma of the lung

EGFR


ALK


KRAS


ROS


MET


RET

histology associated with adencocarcinoma of the lung

Glandular with mucin + staining

squamous cell lung cancer histology

keratin pearls


intracellular bridges

histology of large cell lung cancer

pleomorphic giant cells


can secrete B-HcG

bronchial carcinoid tumor histology

nests of neuroendocrine cells


chromogranin +

names of first generation antihistamines & MOA

MOA - reversibly inhibition of H1




Diphenhydramine


Dimenhydrinate


Chlorpheniramine


Hydroxizine

guanfinesin

thins respiratory secretions

N-acetylcysteine

mucolytic


-liquifies mucus in COPD by disrupting sulfide bonds




-also antidote for tylenol OD


-also prevents contrast induced nephropathy

dextromethoraphan

anti-tussive


antagonizes NMDA glutamate receptor




mild opiod efects in excess


naloxone for OD




May cause seritonin syndrome

Bosentan

competitively antagonizes endothelin -1 receptors




-reduces pulmonary vascular resistance




S/E = hepatotoxic

Epoprostenol & Iloprost

PGI2 with direct vasodialatory effect on pulmonary and arterial vascular beds




inhibits platelet aggregation




S/E - flushing & jaw pain

cyproheptadine

antihistamine




used as an appetite stimulant

promethazine

antihistamine




used for n/v

hydroxyzine

antihistamine used for sedation & itchyness

meclizine

antihistamine used for vertigo

inhaled corticosteroids

fluticasone & budesonide


-inhibit synthesis of all cytokines


-inactivate nf-Kb (trascription factor that produces TNF-alpha




first line for chronic asthma

ipatropium

muscarinic antagonist - competitive


-prevents bronchoconstriction




used in COPD




Tiotropium - long acting

montelukast and zafirlukast

block leukotriene receptors CysLT1




esp good for asa induced asthma

Zileuton

5-lipooxygenase pathway inhibitor


-blocks conversion of AA to leukotrienes




s/e = hepatotoxic

omalizumab

anti-igE & blocks FceRI




used in allergic asthma with high IgE levels resistant to inhaled steroids and long acting beta 2 agonists

theophylline

methylxanthine


-inhibits phosphodiesterase increaseing cAMP


-narrow theraputic index




s/e


-cardiotoxic


-neurotoxic


-metabolized by cyto P450


-block adenosine action

long acting beta 2 agonits used in asthma

salmeterol


formoterol

short acting beta 2 agonsts used as rescue inhalers

albuerol


levalbuterol (slightly longer)