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325 Cards in this Set

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  • Back
Neural Crest Cells
what does enterochromafin cell give out?
"MOTEL PASS"
Melanocytes
Odontocytes
Tracheal cartilage
Enterochromaffin cells=> 5-HT
Laryngeal cartilage
Parafollicular cells/Pseudounipolar cells
Adrenal medulla/ All ganglion cells
Schwann cells
Spiral membrane
when does the notochord, brain and lung develop?
what is what is the complication if 90% of the lung
does not develop?
Notochord develops by 4 weeks, Brain by 8 wks, Lung by 12 wks
• If 90% lung doesn't develop ⇨ pulmonary aplasia ⇨ die
when is surfractant made?
how is it tested?
how to indicate the maturity of the lung
Surfactant is made by 33 wks = alveoli lubricant (decreases surface tension to prevent atelectasis)
• Phophatidyl glycerol = surfactant precursor, can test for this
Lecithin:Sphingomyelin ratio is 2:1 to indicate maturity (brain sphingomyelin is done)
tx for baby with out/ not enough surfractant
Tx: Beclomethasone/Betamethasone IM to Mom=> surfactant production in baby
• Tx: Blow surfactant into neonate lungs (intubation)
Premie Lung Progression management
will have to leave baby on O2 for for 18-24 mo
complication of lung premies: (4)
Atelectasis
RDS
Hyaline membrane dz
BPD "bronchopulmonary dysplasia"
RDS "respiratory distress
syndrome (tx)
(Tx: 02 ⇨ free radicals)
Hyaline membrane dz
pathogenesis
restrictive/obstructive
what is increased?
⇨ thicken membrane ⇨ decrease diffusion (restrictive) ⇨ ⇧goblet cells
BPD "bronchopulmonary dysplasia"
⇨ mucus, narrow lumen (obstructive)
Atelectasis
collapsed alveoli
ARDS "Adult Respiratory Distress Syndrome": presentation
tachypnea, hypoxemia, diffuse infiltrate
ARDS: pathogenesis, most common cause of what?
PMNs cause alveocapillary damage -> increase permeability of alveolar capillaries
• Most common cause = sepsis
ARDS:
how does NO cause ARDS?
PO2/FiO2 =
NO dilates aa = > washes of surfactant, leaks proteins into interstitium
pO2/FiO2 < 150
ARDS:
what would you see on CXR?
Tx
CXR: "fluffy" infiltrates although lungs sound clear
• Tx: Glucocorticoids, Ventilator (⇧Fi02, ⇧pressure, ⇧RR, ⇧I:E ratio, ⇩TV)
Predicting 02 Saturation:
p02 dissolved / 02 bound = 100 mmHg/?
02 sat = ?
100%
Predicting 02 Saturation:
p02 or dissolved 02 = 90mmHg
02 sat or bound 02 =
98%
Predicting 02 Saturation:
p02: 02 sat:
dissolved 02/ bound 02
60mmHg
90%
Predicting 02 Saturation:
p02: 02 sat:
dissolved 02/ bound 02
40mmHg
75%
Predicting 02 Saturation:
p02: 02 sat:
dissolved 02/ bound 02
80mmHg
96%
Predicting 02 Saturation:
p02: 02 sat:
dissolved 02/ bound 02
25mmHg
50%
p02 Predictors: If p02=50
02 Sat:
Action:
02 Sat: 85%
Action: Intubate
p02 Predictors: p02=80
02 Sat:
Action:
02 Sat: 96%
Action: Normal
p02 Predictors: p02=55
02 Sat:
Action:
88%
Home 02
Pneumothorax: describe and tx
decreased breath sounds on one side,
do tx if it covers > 25% of chest
3 type of pneumothorax
Spontaneous
Tension
Asymptomatic
Spontaneous Pneumothorax: risk factors
oral contraceptives, thin male smokers, collagen vascular dz
Tension Pneumothorax: describe and tx
(can't breathe out): air in pleural space pressures lungs => tracheal shift
Tx: needle in 2nd intercostal mid-clavicle above rib on exhalation; vaseline gauze
Asymptomatic Pneumothorax:
observe if air occupies <25%
how to predict ABG, likely to die from
decide whether or not the disease is a restrictive or obstructive process, you can predict their blood gas, chest x-ray, and what they are most likely to die from.
ask yourself if they have trouble breathing in or out, and whether they have small stiff, lungs or. big mucus-filled lungs, then tell me everything you know
Restrictive: describe lungs, presentation, what capcity is decreased, FEV/FVC
interstitial problem (non-bacterial)
• Small stiff lungs a decrease VC
• Trouble breathing in=> FEV/FVC: > 0.8
Restrictive:
ABG:
CXR: (3)
They cannot breath in and therfore the pO2 is decreased =>ABG: ⇩p02 => ⇩pC02, ⇧RR, ⇧pH
• CXR: reticula-nodular pattern, ground-glass apperance or interstitial infiltrate
Restrictive:
what do they usually die of and give an cause (3)
Die of cor pulmonale (hypoxia leads to low energy state; heart failure due to lung disease is called cor pulmonale)
• Ex: NM diseases (breathing out is passive), drugs, autoimmnne dz
Restrictive: disease tx
Tx: Give pressure support on ventilator, ⇧O2, ⇧RR, ⇧inspiratory time
Obstructive:
pathogenesis
what is increased?
FEV/FVC ratio
airway problem (bacterial)
• Big mucus-filled lungs (⇧RV, ⇧Reid index = ⇧airway thickness/ airway lumen)
• Trouble breathing out=> FEV/FVC: < 0.8
Obstructive:
ABG
MCC of death
They cannot breath out and therfore the pCO2 is accumulating => ABG: ⇧pC02 => ⇧RR, ⇩pH
Die of bronchiectasis
Obstructive:
example and tx
Ex: COPD
• Tx: Manipulate rate on ventilator, ⇧RR, ⇧expiratory time, ⇧02 only if needed
Cough: name some dieseases that causes this
each cough moves mucus 1 inch
• Postnasal drip: cold, allergies
• Pertussis: whooping cough
• COPD
• Asthma
• GERD
Neck Films: Steeple sign
=> Croup
Neck Films: Thumb sign
=> Epiglottitis
Amniotic fluid: function and who makes it ?
keeps pressure off the baby
80% is mom's plasma
20% made by baby (must be able to swallow, absorb, filter, urinate)
Polyhydramnios: pathogenesis
baby can't swallow
Polyhydramnios: tx
Tx: Indomethicin <34wk: stops baby's pee
Polyhydramnios:
• NM problem:
• G I problem:
• NM problem: Werdnig-Hoffman
• G I problem: Duodenal atresia
Oligohyramnios:
baby can't pee
Oligohyramnios:
• Abdominal muscle problem: tx and its complications
• Renal agenesis:
• Abdominal muscle problem: Prune Belly => can't pee (Tx: catheter ~> UTI)
• Renal agenesis: Potter's syndrome: ⇧ atmospheric pressure => flat face
Oligohyramnios: Abdominal muscle problem: Prune Belly tx
=> can't pee (Tx: catheter ~> UTI)
Diaphragmatic hernia:
define
what are the two types?
which one is more common?
intestines are in thoracic cavity=> hypoplasia of one lung
• Bokdalek (90%): hole in back of diaphragm
• Morgagni (10%): hole in the middle of diaphragm
Bokdalek Diaphragmatic hernia
(90%): hole in back of diaphragm
Morgagni Diaphragmatic hernia
(10%): hole in the middle of diaphragm
Diaphragmatic hernia: Dx and tx
Dx: CXR with air-fluid levels
Tx: Orogastric tube with suction (to prevent bowel distension)
Lung Anatomy: describe the type of muscle and epithelium
top and bottom
Top: skeletal muscle (squamous cell epithelium)-
Bottom: smooth muscle (tall columnar ciliated epithelium)
Lung Anatomy: which zone top or bottom is increased by smoking
Top zone: smoking increases this zone
Lung Anatomy:
Extrathoracic: location, protection and what happens during inpiration
lips to glottis (not protected by rib cage)- narrows on insp
which part of the lung anatomy causes stridor
extrathoracic
Intrathoracic: location, protection
what happens during inspiration and what sound does it make pathologically?
glottis to alveoli (protected by rib cage) - expands on inspiration⇦wheeze ·
which part of the lung anatomy causes wheeze?
intrathoracic
C-shape cartilage rings
compresses airway w/ swallowing to prevent aspiration
Fully encircling cartilage
where mainstem bronchus dives into lung parenchyma
where does the Trachea divide
divides into main stem bronchi "carina" at T4
which bronchus goes straight down?
what is the other name?
Right main stem bronchus ⇨ goes straight down (bronchus intermedius)
where do aspiration go to? if on the side
Aspirations ⇨ Right Lower Lobe (or upper lobe if on the side)
where does the aspiration go if ie child is playing around (upright)?
Posterior segment
where does the aspiration go if patient is supine
Superior segment
aspiration of foreign objects:
presentation, management
Recurrent R upper lobe pneumonia=> foreign objects (do insp/exp film)
Most common aspirations:
in order
#1 peanut, #2 popcorn, #3 hot dog
if the foreign body reaches the stomach, management?
leave it alone
if a patient apirated a foreign body, and can't talk, Dx
Where stuff likes to get stuck: can't talk
if the foreign body is stuck on the glottis? tx
Tx: Heimlich maneuver (adults) or back blows (kids)
what sits on midway between glottis and carina?
LA sits on it
Main-stem bronchus: resistance and function
branches in parallel => ⇩resistance, humidify and warm air
Medium size bronchioles
most dilation/ constriction
Terminal broncioles
most dependant (small particles settle, primary lung cancer starts)
where are the most SM and β2 receptors
Medium size bronchioles
where does 1° lung cancer starts?
Terminal broncioles
what happens to the velocity from the Trachea to the alveoli?
velocity decreases
Respiratory unit function
the ONLY oxygen exchange system
what is the Respiratory unit made up of?
resp bronchiole + alveolar duct + alveolus (1 layer of epithelium)
Ventilation: Dead space (VD ):
lip to terminal bronchiole (everything except your respiratory unit)
Ventilation: Alveolar ventilation (Va): location
(Va) respiratory bronchiole to alveoli. the respiratory unit
Ventilation: Total ventilation =
VD + VA
Minute Ventilation (Vm): define and formula
TV x RR =how much you breathe in during 1 min
normal Vm minute ventilation
10-15 cc/kg (have a Vm for V0 , Va, VT, etc.)
Histology: Goblet cells:
secrete mucus to trap dirt (most abundant cell type)
Histology: Cilia
histology
movement
9+2 actin configuration: orade movement "toward mouth" (not back and forth)
Histology: Dyenin arm
what paralyses the cillia and what is its complications?
flexibility for cilia (viruses and smoke paralyzes cilia ⇨ green sputum)
Histology: Type I pneumocytes
(5%) =macrophage (in terminal bronchiole)
Type II pneumocytes
(95%) = surfactant producers (in alveolar bronchioles)
after an injury, what can type II cells do?
Type II cells can demote themselves to type I cells after injury.. .
what are Clara cells
where do they live
"dust cells": MP that eat dust (live in the terminal bronchiole)
Kartagener's
pathogenesis
3 clues
(broken dyenin arm): situs inversus, bronchiectasis, male infertility
Stridor: describe and management
extrathoracic narrowing=> narrows when breathe in => neck x-ray
Wheeze: describe and management
intrathoracic narrowing=> narrows when breathe out=> chest x-ray
Rhonchi: describe and common in what disease?
mucus in airway=> obstructive lung disease
Grunt: describe and what type of disease
blows collapsed alveoli open=> restrictive lung disease
Dull percussion
something b/w alveoli and chest wall absorbing sound (fluid, air, solid)
Hyperresonance
air
Tracheal deviation
away from pneumothorax OR toward atelectasis "air-phobic"
Fremitus, egophony, bronchophony:
consolidation=> pathognomonic for pneumonia
Crackles "rales": describe and causes
alveoli are collapsed
No surfactant
Alveolar fibrosis
causes of No surfactant in an adult
washed out due to pulmonary edema or CHF
Alveolar fibrosis: drugs and disease
Pneumoconioses, Bleomycin, Busulfan, Amiodarone, Tocainide
Barking cough (viral pathogen, x-ray)
Dx and tx
Dx: Croup, steeple sign on xray, (Parainfluenza)
Tx: 02, Dexamethasone, racemic Epi,
Stacatto cough
Dx and tx
Pneumonia (Chlamydia)
Fluoroquinolone
Whooping cough
Dx and tx
Dx: Pertussis (Bordatella)
tx: Erythromycin
Muffled voice/ drool (thumb x-ray)
Dx and tx (2)
Dx: Epiglottitis (H. influenza B)
tx:OR Intubation, Ceftriaxone
Expiratory wheeze- kid
Dx and tx
Dx: Bronchiolitis (RSV)
tx: Ribaviran, Albuterol
Inspiratory stridor - kid
Dx and tx
Dx: Laryngomalacia
tx: Observe
Inspiratory stridor - adult
Dx and tx
Dx: Subglottic stenosis
tx: Dilation
what is Asthma?
define and 2 types
wheeze on expiration
intrinsic and extrinsic asthma
Intrinsic Asthma
define and factors that can trigger it?
Genetic (cold air, exercise, NSAIDs make it worse)
Extrinisic asthma: causes and what part of the immune system reacts?
Environment-induced (dust mites, roach droppings), IgE/ Eosinophils
Benign Pulmonary Nodule
Popcorn calcifications
Radiolucent (black) X-rays
=> air
Radiopaque (white) X-rays
=> fluid/ solid
Bronchiectasis: presentation
digestion of airways ⇨ hemoptysis
Honeycomb lung = bronchiole dilation, halitosis
Bronchiectasis
Dx
Tx
Dx: high resolution CT
Tx: Antibiotics, 02
Acute bronchitis
increased mucus production
Chronic bronchitis
3 consecutive months over 2 yrs
Bugs that can cause bronchitis
color of sputum of most common cause of brochitis
Strep pneum (rusty colored sputum), H influenza, Neisseria cattaralis
Bronchitis: pathogenesis
Inflammation ⇨ dilate airways ⇨ secretion buildup ⇨ bronchial destruction
Bronchiolitis: definition
asthma symptoms< 2y/o
Bronchiolitis: presentation and caused by what bug
⇧AP diameter, flat diaphragm, usually due to RSV
Bronchiolitis: more succeptible to what?
⇧Risk of future asthma/ ear infections
Bronchiolitis: tx
Tx: Isolation/ Albuterol, Ribavirin (if resp failure)
Blue Bloater
Bronchitis
Pink Puffer
Emphysema
give 3 examples of COPD diseases?
how is prognosis determined?
Bronchitis, Emphysema, Asthma
Prognosis is determined by FEV1
COPD Tx:
1) 02
2) Albuterol (bronchodilator)
3) Me-Prednisolone (glucocorticoid)
4) Levofloxacin
which of the treatments for COPD can alter the natural history of dz
oxygen
Asthma:Early Phase: cause and tx
IgE (Tx: Antihistamines)
asthma Late Phase: cause and tx
Cytokines (Tx: Steroids)
how do you get a steeple sign in Croup?
swelling around the glottis => steeple sign on x-ray
Croup: pt. presentation
Barking cough, stridor on inspiration
• Fluctuating course (improves/worsens within 1 hr)
what are the 4 viral pathogens that causes croup?
Viruses:
• Parainfluenza
• RSV
• Adenovirus
• Influenza virus
treatment of RSV
(Tx: Ribavirin)
the most severe croup is caused by what virus?
RSV
Croup tx
Tx: Dexamethasone, racemic Epi, 02
Pulmonary Eosinophilia:
drugs, parasites and fungus
Aspergillosis
Parasites: Strongyloides
Drugs: Nitrofurantoin, Sulfonamide
Cystic Fibrosis:
mode of inheritance and chromosome, etiology and test
>>(AR): Chr #7 CFTR: Cl channel broken=> more Cl in secretions
>>Test: Pilocarpine sweat test (Cl >60mEq/L => have CF)
Cystic Fibrosis:
Tx
vaccination
>>Tx: N-acetylcysteine (breaks mucus disulfides), chest percussions, future lung transplant
>>Vaccinations: Influenza
CF: bug and tx
Bugs: Staph/Pseudo like to attack them
Tx: Tobramycin + Piperacillin
CF: Newborn with CF are succeptible to what? and tx
= > meconium ileus
(Tx: gastrografin enema)
lung and nose of a CF patient:
restrictive or obstructive
Lung => obstructive pulmonary disease
Nose => obstruction
what Pancreatic problem do CF succeptible to?
=> malabsorption=> Vit. A,D,E,K. def
what Epididymis problem do patients with CF are succeptible to?
= >infertility
what urinary problem do patients with CF are succeptible to?
oxylate stones (malabsorption)
what GI problem do patients with CF are succeptible to?
Stool => steatorrhea
Emphysema:
restrictive or obstructive
predict its ABG
how do they breath?
name the all 4 types of emphysema.
obstructive (⇧pC02,⇧RR, ⇩pH)
pursed lip breathing
4 types:
Pan-acinar
Centro-acinar
Distal acinar
Bullous "pneumatocele"
Pan-acinar
mode of inheritance
pathogenesis
test
(AR)
α1-AT def can't inhibit elastase
PAS(+)
restrictive
Centro-acinar: etiology
smoking
"comes in through the center"
Distal acinar
what is it due to
complication
aging (least blood supply) ⇨ spontaneous pneumothorax
Bullous "pneumatocele"
elastase positive bacteria = Pseudo/Staph aureus
pathogenesis of Epiglottitis?
xray?
inflammation above glottis => thumb sign on x-ray
Epiglottitis: presentation
pathogen
>>Drooling, stridor, muffled voice, high fever
>>Bug: HI-B "stick out thumb to Say HI"
Epiglottitis: tx
Tx: Intubate immediately in the OR, Ceftriaxone
Flash Pulmonary Edema:
describe
treatment
X-ray white out
Tx: 02, Morphine, Furosemide, Nitroglycerin (⇩BP)
Laryngomalacia
management
epiglottis roll in from side-to-side => feed in upright position
Pneumoconioses
associated cancer
name all 5
promote adenocarcinoma
Asbestosis
Silicosis
Beryliosis
Byssinosis
Anthracosis
4 examples of patients with increase risk of Asbestosis?
shipyard workers, pipe fitters, brake mechanics, insulation installers
Asbestosis; what is seen (2)
complication
what is the pathogenisis of this complication
o Crocodilite fibers
o Fe coating: ''ferruginous body" ⇨ MP take to pleural cavity ⇨ mesothelioma
Silicosis:
who is at risk (3)?
complication
sandblasters, glassblowers, monument engravers ⇨ pulmonary TB
Beryliosis: describe and tx
radio TV welders, dental ceramics
"Berry' the newscaster"
(Tx: steroids)
Byssinosis:
presentation
increased risk
cotton workers
"Cotton blankets in bassonettes"
chest tightness
Anthracosis:
who is at risk
lung cancer?
complication
coal workers=> Not promote lung cancer, may get massive fibrosis
Pneumonia:
define and PE
the 3 types of pneumonia
consolidation of airway (dull percussion, rales, tactile fremitus, egophony)
typical, atypical, fungal pneumonia.
Hemoptysis DDx: (5)
• Bronchiectasis
• Bronchitis
• Pneumonia
• TB
• LungCA
Typical PNA: name all types
Streptococcus pneumoniae
Haemophilus influenza
Neisseria cattarhalis
Staphylococcus aureus
Pseudomonas
Klebsiella
Anaerobes
most common typical pneumonia?
Streptococcus pneumoniae:
Haemophilus influenza: clue
2nd most common pneumonia, Gram(-) coccobacilli, kids
Neisseria cattarhalis
3rd most common pneumonia
Staphylococcus aureus
secondary infection after influenza virus
Pseudomonas
found in cystic fibrosis
Klebsiella
sputum
where is it found in the lung
increased risk
currant jelly sputum, bulging fissures, found in alcoholics, DM
Anaerobes pneumonias presentation?
who is at risk? (2)
gas, foul sputum, aspiration in dementia pt, alcoholics
name the 4 Atypical PNA? common presentation and tx
dry cough
(Tx: Erythromycin)
Mycoplasma
Chlamydia
Legionella
Actinomyces
most common atypical pneumonia in 0-2 mo?
presentation
Chlamydia
stacatto cough, eosinophils
most common atypical pneumonia in college:
presentation
ears
xray
test
Mycoplasma
reticulonodular, bullous myringitis, cold agglutinins
Legionella:
define
acquired
test
patient presentation
most common atypical pneumonia in >40y/o patients.
A/C ducts
CYAE and silver stain
low Na, CNS changes
Actinomyces
sulfur granules
Fungal PNA: name all
Histoplasma
Blastomyces
Coccidioides
Paracoccidioides
Aspergillus
Coccidioides
location
disease
describe how they look like (2)
(San Joaquin Valley), desert bump fever
budding yeast, thin walled cavity
Blastomyces
how is it acquired (2)
how does it look like
location
pigeon droppings (NY), broad-based hyphen, rotting wood in beaver dams
Histoplasma
location
how is it acquired
how does it look like
signs
bat droppings (Mississippi river),
no true capsule, MP
oral ulcers
Aspergillus
where can one aquire it (2)
complication
treatment
fungal ball, moldy hay
pulmonary bleed
(Tx: Prednisone)
Paracoccidioides
looks like a ship's wheel
(S. America)
Pulmonary Embolus
describe and presentation
blockage of blood flow in lungs=> tachypnea
PE:
what would be seen in EKG?
test for diagnosis.
name all 3
which one is the most reliable?
EKG: S1Q3T3
• ⇧V /Q scan: perfusion defects, most reliable
• Venous US
• Spiral CT
PE gold standard test?
what would you see on CXR?
Pulmonary angiogram- gold standard
CXR: Hampton's hump: wedge opacification
Only reason for: Radiation
small cell CA
Only reason for: Surgery:
V-Q mismatch (palliative)
PE: x-ray
Hampton's hump: wedge opacification
5 PE Tx:
• Anticoagulation: Heparin, Coumadin, IVC fllter
• Intervention angiography, Surgery
1° Pulmononary HTN:
pregnancy and pathogenesis
• ⇧PA pressure (enlarged right heart leads to cor pulmonale)
• ⇧Mortality rate with pregnancy
1° Pulmonary HTN: what happens in pre and post capillary
Pre-capillary: ⇧resistance to flow in pulmonary arteries (Ex: ASD/VSD/PDA/L⇨R shunts)
• Post-capillary: ⇧resistance to flow in pulmonary veins (Ex: LV dysfxn/constrictive pericarditis)
1° Pulmonary HTN + ⇧PCWP+ =Dx
⇧PCWP (LA pressure): cardiac problem
1° Pulmonary HTN + ⇩PCWP = Dx
⇩PCWP: lung problem (1⁰ Pulm HTN, ARDS, cor pulmonale)
1° Pulmonary HTN tx
Tx: Coumadin + Amlodipine
Sarcoidosis: what would be seen on x-ray, legs, lympnode
Hilar lymphadenopathy
Erythema nodosum
Non-caseating granulomas
Lymph node "eggshell califications"
sarcodisis presentation
"Potatoe nodes" ⇨ face weakness
Uveitis
sarcodisis:labs, test and tx
⇧ACE, ⇧Ca,⇩T cells
• Test: Parotid gland biopsy
• Tx: Prednisone (if eye/ heart involved)
Sinusitis: presentation, pathogenesis and tx
bacterial infection obstructing maxillary sinus
• Pain worse when bend forward
• Tx: Amoxicillin
Tonsillitis: presentation and tx
sore throat, pooling of saliva, muffled voice
• Tx: needle drainage, Abx
Tracheitis:
presentation
labs
=Diphtheria: vascularized grey pseudomembrane (don't scrape it)
Look toxic, stridor w/ cyanosis, leukocytosis
Tracheitis: bugs
Bugs: Staph, Strep
Tracheitis: pathogenesis and tx
Toxin ADP-ribosylates EF-2 => cells die
Tx:Ceftriaxone,cricothyroidotomy if suffocating
Tracheomalacia
soft cartilage, stridor since birth, outgrow by 1 y/o
what are the Physiologic Parts of Lung?
• Intrathoracic space: chest wall, pleural space
• Pulmonary vasculature
• Pulmonary airway
Compliance:
Δ V/ΔP
Elastisticity:
provides recoil
what are the lung volumes?
which on the volume are not on PFT?
Lung Volumes: "LITER"
1) IRV
2) TV
3) ERV
4) RV (not on PFT)
IRV "Inspiratory Reserve Volume":
air you can force in after a normal breath
TV "Tidal Volume"
normal breath
what is ERV "Expiratory Reserve Volume"?
what part of the lung does it fill
can force out after normal exp
fills dead space
RV "Residual Volume"
air in lungs after forced exp, keeps alveoli open (not on PFTs)
what are the Lung Capacities:
IC
VC
TLC
FRC
IC "Inspiratory Capacity":
total amount of air you can breathe in = 1 +2
VC "Vital Capacity"
all the air you can breathe in after forced expiration = 1 +2+ 3
TLC "Total Lung Capacity":
air in lungs after deep breath = 1 +2+ 3+4
FRC "Functional Residual Capacity"
what does TLC equal to?
baseline (where you stop/ start breathing) = 3+4
"FIT": FRC + IC = TLC
above/ below the FRC what is the pressure?
Above FRC = > positive pressure
Below FRC =>negative pressure
FEV/FVC normal ratio?
FEV and FVC
= 0.8
• FEV,: forced expiratory volume in 1 sec
• FVC: forced vital capacity
Obstructive Lung Dz:
what volume changes first?
what volume changes last?
what capacity changes first?
⇧RV (or FRC) first; last to change is TV
Restrictive Lung Dz:
what capacity changes first?
volume to change last
⇩VC (or TLC) first; last to change is TV
what happens during normal inspiration:
what volume is measured?
=> Tidal volume
Diaphragm - goes down
External intercostals - used during exercise "externals breathe in"
Innermost intercostals - right muscles (along sternum) move left chest wall
what muscles are used for Forced inspiration?
what volume is measured?
=> IRV
Pectoralis major and minor
Head and neck muscles:
• Scalenes
• Sternocleidomastoid
• Trapezius
Normal expiration
Recoil only (know this!)
what muscles are used for Forced expiration:
what volume is measured?
=> ERV
Internal intercostals "internals breathe out"
Abdominal muscles:
• Obliques
• Rectus abdominis
• Transversus abdominis
• Quadratus lurnborum
Intrathoracic Pressure:
function
positive/negative
>necessary to pull blood into thorax
>Pleural space is always negative
A-a Gradient (A = Alveoli; a = arteriole) : increased
Extracts 02 (restrictive)
A-a Gradient (A = Alveoli; a = arteriole) : decreased
Lose 02 (polycythemia)
High Altitude:Chronic:
Kidneys pee off bicarbonate
Acute: Mountain Sickness: tx
Tx: Acetazolamide to pee off bicarbonate)
Intrathorasic pressure for the ff.
Resting:
Normal breath:
Deep breath:
Resting: -3 to -5
Normal breath: -10 to -12
Deep breath: -20 to -24
+ intrathorasic pressure: Dx
Risk factors
Pneumothorax:
RF: oral contraceptives, thin male smokers, Staph/Pseudo
intrathorasic pressure of -40 to -60>
Dx
complication
Restrictive lung disease (negative pressure sucks in=> GERD, hiatal hernia)
Breathing: describe the pressures is the following areas: intrathorasic, pulmonary alveolar and air way pressure
Pulmonary alveolar (PA) =airway pressure= opposite sign of intrathoracic pressure)
where is the highest compliance? what does this mean for the alveoli?
Highest compliance (mid-inspiration or mid expiration) => max airflow into alveoli
during Inspiration, how does the blood move?
moves air into lungs and blood into heart
describe inspiration
start: chest wall vs lung expansile force, PA vs Patm
mid inspiration:
end of inspiration
when is compliance increased?
what is the pressure in the alveoli at end of inspiration?
>Start: chest wall > lung expansile force, PA = PATM
>Mid-inspiration (50-99%): lung > chest wall expansile force, ⇧compliance, PA<< PATM
>End-inspiration: recoil of chest wall= expansile force of lung (alveoli negative pressure)
describe expiration:
start: chest wall vs lung recoil, PA vs Patm
mid-expiration:
end expiration:
which one is effort dependant/independent
when is compliance increased
when is airway positive pressure?
Start: chest wall> lung recoil, PA >> PATM, effort dependant=> can force out
Mid-expiration (50-99%): lung > chest wall recoil, ⇧compliance, effort indep, collapse airway
End of expiration: lung recoil = chest wall expansion, PA = PATM (airway positive pressure)
Flow and Ventilation: Top of lung
when does more air flows at the bottom of the lung?
more air (more air flows into bottom during inspiration only)
Flow and Ventilation: Bottom of lung:
more blood flow (gravity, dilated capillaries, dilated arterioles)
how does a pt. with V/Q mismatch present? (restrictive or obstructive)
what does it lead to?
Every V / Q mismatch presents with a restricive pattern, leads to hypoxia
Dead space:
example and
describe V/Q and why?
High V /Q =>no blood flow
• Ex: PE, shock
Shunt:
describe V/Q and why
example
Low V /Q => no ventilation
• Ex: atelectasis, pneumonia
At FRC: PA vs Patm
Inspiration:
Expiration:
End of deep breath:
At FRC: PA=Pamt
Inspiration: PA<< Pamt
Expiration: PA >> Pamt
End of deep breath: PA=Pamt
Breathing Receptors:
J receptors:
in interstitium = > tachypnea, restrictive dz
Breathing Receptors: Slow-adapting receptors
location
what does it sense
disease
b/ w ribs and muscle fibers; sense stretch, obstructive dz
Carotid Body:
another name
measures what?
how does it work?
carotid chemoreceptor (measures everything: pO2, pC02, H+)
CN9 ⇨ carotid body ⇨ CN10/ phrenic nerve
Aortic Body:
what is it?
what does it measure
how does it work?
aortic arch chemoreceptor (measures pC02, H+)
CN10 ⇨ aortic body ⇨ CN10/ phrenic nerve
how is O2 controlled?
02: controlled by diffusion and perfusion
how is CO2 controlled?
⇩C02: controlled by ⇧ventilation (i.e. airway being open)
why not give O2 to COPD patients?
Don't give >1L 02 to COPD pts b/c hypoxia is the drive for ventilation
1) fills airways => C02 can't leave
2) knocks out apneustic center (pneumotactic center desensitized) =>coma
management for COPD?
Tx: Bronchodilators (create more space so C02 can leave)
what is the normal oxygen level in COPD?
COPD normal O2: 55-60
Forms of pCO2
90%:
7%:
3%:
90%: Bicarbonate
7%: Attached to Hb (can't measure this stuff) "carboxyhemoglobin"
3%: Dissolved (this goes to pneumotactic center) = .03 x pC02
what affect CNS more
CNS is affected more by high pC02
what is PNS affected more
PNS is affected more by low p02 (you're almost dead if have low p02 and high pCO2
how does the oxygen diffuse
Oxygen diffusion: alveolar endothelium ⇨ interstitium -⇨ capillary endothelium
most potent vasodilator of the lungs
Oxygen is the most potent vasodilator in the lung
Pneumotactic center (top):
function
sensitivity
Breathing Control Center:
prevents pneumothorax=> breath out
(C02 sensitive)
Apneustic center (bottom):
function
sensitivity
Breathing Control Center
prevents apnea=> makes you breathe in (02 sensitive)
Pons:
Breathing Control Centers:
reaction center
who sets the repiratory rate and what is the normal?
Medulla: sets respiratory rate (RR=8-10)
why do brain dead people can still breathe?
Brain death (everything above medulla is gone, can still breath)
Central apnea of neonates: pathogenesis and tx
no inspiratory effort for 20 sec
• Tx: Theophylline or Caffeine to stimulate the brain
Obstructive apnea "Pickwickian"
=>chronic hypoxia (opposite of COPD)
treatment for Obstructive apnea "Pickwickian?
CPAP:
Weight loss
Uvulopalatophatyngoplasty (cut out soft palate)
contraindicated drugs for Obstructive apnea "Pickwickian"
No BZ! (respiratory depression)
why do pregnant women breath faster?
Progesterone to stimulate respiration (pregnant women breath faster)
Carotid Body:
chemoreceptor
Carotid Sinus:
Baroreceptor
normal Breathing Patterns:
breathe in ⇨ hold 1 sec ⇨ breathe out ⇨ hold 1 sec
Restrictive breathing pattern
=>more time in inspiration (I)
Obstructive breathing pattern
=>more time in expiration (E)
Apneustic breathing:
describe and example
breathe in⇨hold for a long time⇨breathe out
Ex: Pontine hemorrhage
Cheyne-Stokes breathing:
describe and what are some of the causes (2)
deep breathing followed by apnea (sigh)
• Lesion medulla (or low blood glucose)
• Blow to back of head cuts off blood supply to medulla via the vertebral aa.
Thoracic outlet syndrome:
extra rib compress subclavian, turn neck=> paresthesia
Subclavian steel syndrome:
raised arm compress subclavian=> cyanosis
Reversal of flow in vertebral aa how does this affect the brain?
steals blood from brain
Kussmaul breathing:
describe
pathogenesis
rapid deep breathing (must stop talking to breathe)
• Metabolic acidosis produces GABA, which fight each other to breathe fast or slow
Anencephaly how do they breathe?
Medullary breathing:RR=8-10
(only have medulla)
Paroxysmal Nocturnal Dyspnea:
wake up from sleep with air hunger
Ex: CHF
Foul Sputum: give 3 DDx?
Bropchiectasis
Lung abscess
Aspiration pneumonia
Steroid Side Effects: Low Dose:
thrush, dysphonia
Steroid Side Effects: High Dose:
osteoporosis; cataracts, purpura, adrenal suppression
Managing Ventilators:
02 amount:
Restrictive needs more, Obstructive needs less
Managing Ventilators:
Rate:
12-16 (all lung diseases have tachypnea)
Managing Ventilators:
Tidal Volume:
how does this lead to low energy state
10-15cc/kg, peripheral hypoventilation (high pCO2 =>low E state)
Managing Ventilators:
I:E ratio
by how much incriment
Restrictive needs more I, Obstructive needs more E (increment by 0.1)
Managing Ventilators:
CMV:
Controlled Mandatory Ventilation- total
machine control (not used anymore)
Managing Ventilators:
Assist Control:
when is it used
machine breathes, pt helps the least. (use during sepsis)
Managing Ventilators:
SIMV / IMV (Synchronized Intermittent
Mandatory Vent.):
how is it used and what is it used for?
4 types:
pt adds extra breaths
- used to wean patient off ventilation
Pressure Support:
PEEP
ZEEP
AutoPEEP
CPAP
Managing Ventilators:
Pressure Support:
who has control
when is it used?
SIMV / IMV
pt has control, machine just helps (use w/ restrictives)
PEEP:
what does it do?
when is it used?
SIMV / IMV
Positive End Expiratory Pressure: increase FRC (use while intubated)
ZEEP:
SIMV / IMV
Zero PEEP
AutoPEEP:
breath stacking
CPAP:
define
when is it used?
Continuous Positive Airway Pressure (use in sleep apnea, CHF)
Arachadonic Acid Pathways:
Cyclooxygenase "COX" :
what do they form and what are made?
forms Prostaglandins
PGA2, PGE1, PGE2, PGF1, PGF2, PGI2
PGA1:
name
function
"Thromboxane": vasoconstriction, thrombosis
PGE1
function
example
SE
vasodilation
Ex:(keeps PDA open)
Misoprostyl for GI ulcers =>induces labor
PGE2
vasodilation, SM relaxation, used to keep PDA open
PGF1
vasoconstriction
PGF2
vasoconstriction, menstrual cramps,abortions, found in semen
PGI2
name
where is it made
function
"Prostacyclin": vasodilation, anti-thrombosis, made by endothelium
easier way to remember the prostaglandin functions
PG Summary:
A/F: vasoconstrict/ thrombose
E/I: vasodilate/ anti-thrombosis
asa vs NSAIDs
asa:irreversible inhibition
NSAIDs: reversible inhibition
Lipooxygenase "LOX" (forms Leukotrienes)
produced by what cell
pathogenesis of asa sensitive asthma
• Produced by mast cells
• asa-sensitive asthma results from closing of the COX pathway leading to LOX
what form of leukotriene is the most potent bronchoconstrictor?
LT-C4D4E4 "SRSA" = the most potent bronchoconstrictor
pathogenesis of aspirin induced asthma
asa-sensitive asthma results from closing of the COX pathway leading to LOX
Steroid Anti-inflammatory Actions:
• Stabilizes: mast cells/ endothelium
• Inhibits: MP migration/ PLA
• Kills: T cells/ eosinophils
what are the asthma treatments?
B2 Agonists
"RATS"
• Ritodine
• Albuterol
• Terbutaline
• Salmeterol
B2 Agonists:
MOA
used for
effects on the lungs
acute tx
bronchodilation
low K.+ levels (pushes K± into cells)
Ritodrine
#1 stop preterm labor
Albuterol
q4h inhalers
Tetbutaline
#2 stop preterm labor, q4h bronchodilator inhaler pm
Salmeterol
8-10 hr inhalers
what needs to be adminstered with steroids?
need adjuvant calcium /vit D/insulin
name all the Steroids and which one is inhaled
Triamcinalone - inhaled
• Prednisone
• Beclamethasone
Anti-Cholinergics:
example
MOA
effects on the lung
ie Ipratropium
decreases cGMP
bronchodilate
PDE Inhibitors:
example and what is it used for?
acute tx
• Theophylline (IV)
LT receptor blockers: when are they used?
use if steroids fail
• Zileuton
• Zafirlukas
• Montelukast
Zileuton
inhibits LOX
Zafirlukast
inhibits LTD4 * "Leukotriene inhibitor"
name the 2 Prophylactic agents: which one is used before excercising?
• Cromolyn sodium- use before exercising (eye or nasal drops)
• Nedocromil