CM Pulm Flashcards

Question

does cutting down smoking help?

Answer 1

NOPE its a myth patients who go cold turkey are more likely to be successful at quitting smoking!

Answer 2

YES 1.5x greater risk of developing lung cancer from just being around those who smoke take them down

Answer 3

Yes risk of cancer does decrease but never to that compared to non-smoker CV disease does decrease with cessation, **after 15 years similar to a non smoker**

Answer 4

number of years smoking X number of packs per day

Answer 5

what is the percentage of smokers who try to quit each year? **1/3** what percent of smokers would like to quit? **70-80%** what percent of people quit each year? **20-25%**

Answer 6

pre-contemplation contemplation determination action maitenance

Answer 7

Advantages: - success rates higher - cost disadvantages: - nicotein withdrawal - weight gain--big deal!

Answer 8

**Ask** about tobacco everytime **advise** smokers to quit **assess** readiness to quit **assist** smokers in quitting **arrange** follow up

Answer 9

1. nicotine replacement 2. anti-depressants 3. nicotine receptor blockers

Answer 10

**deliver 25-40% levels of smoking** **GUM:** 2/4 mg, *must chew and park!! 3-6 months* **lozenge**: nicorette **patch**: 21, 14, 7 mg, *rotate location of patch since can irritate skin!* ***spray*** ***inhaler***

Answer 11

**Bupropion** marketed as zyban, same thing as welbutrin **40% success,** even higher if combined with nicotine replacement **do not use if seizure history** **DRY MOUTH AND INSOMNIA**

Answer 12

agonizes and blocks alpha-4-beta-2 nicotinic acetylcholine receptors decreases pleasure of nicotine-decreases craving **very heightened dreams!** first med that for tobacco cessation that has been coverered by insurances, because studies show it works better than bupropion

Answer 13

**1. cough** **2. weight gain** **3. nicotine withdrawal** - worse mood - anxiety - insomnia

Answer 14

cold turkey!

Answer 15

70-80% of those circulating

Answer 16

amplify inflammation cross links IgE resulting in histamine release and anaphylatic factors

Answer 17

major histocompatability complex (MHC)

Answer 18

**immediate type hypersensitivity** IgE binds to antigen, activates mast cells and basophils 1. increase in vascular permeability 2. smooth muscle contraction 3. chemotactic activation of inflammatory cells _ex: anaphylaxis_

Answer 19

**cytoxic reaction to antibody** antibody binds to antigen with complement which results in **cellular lysis/tissue injury** _ex: transfusion reaction resulting in RBC lysis_

Answer 20

**immune complexes not cleared by reticuloendothelial system** these deposit in blood vessles and tissues _ex: serum sickness (flu like symptoms)_

Answer 21

injection of a foreign substance (protein, like vaccine, antitoxin, antibiotic, or bee sting) where complexes form this reaction causes **fever, malaise, puritis** feels like the flu!!

Answer 22

**delayed type hypersensitivity** inflammatory response from leukocytes **cell mediated** cellular immune response to antigen takes **48-72 hours** _ex: PPD skin test thats positive_

Answer 23

idiopathic reaction under unclear mechanism _ex: steven johnson syndrome, soughing skin_

Answer 24

classic allergy triad: asprin allergy, asthma, nasal polyps

Answer 25

life-threatening immediate reaction occurs in seconds to minutes **caused by histamine, leukotrienes, and prostaglandin D2** **may have elevated beta tryptase**

Answer 26

**respiratory distress** - laryngeal edema - bronchospasm - intubation possible **vascular collapse/shock** **pruritis** **TX: epinephrine, O2, antihistamines/glucocorticoids**

Answer 27

alpha and beta adrenergic stimulation results in **vasoconstriction and smooth muscle relation** negative side effects are **tachycardia and hypertension** this is why you need to get them to the hospital

Answer 28

desensitization graded injection, effects last **5 years** after stopping shots _need to make sure these patients aren't on a beta blocker because it would prevent epi from working if anaphylaxis reaciton_

Answer 29

**urticaria=hives** -wheels that colase, superficial skin layers, itchy, vascula origin **angiodema** similar but deeper skin structures involved, larger wheels \*\*\*both can be acutre or chronic, stimulated by cold heat or stress and are commonly on extremities and face\*\*\* TX: antihistamines, stystemic steroids

Answer 30

deficiency of C1 esterase inhibitor (C1INH)

Answer 31

yes, but watch out if the patient is anaphylaxsis - can desensitize patient - don't desensitize if SJS - other drugs don't have a test for allergy (20% cross reaction in cephalosporins)

Answer 32

**mast cell hyperplasia** repeated pruritis/urticaria, abdominal pain, headache *elevated 24 hour urine histamine level or elevated serum tryptase* rule out carcinoid Tx: antihistamine

Answer 33

1. antihistamines Histamines1: bendryl, hydroxyzine, clemastine \*sedating\* Histamines 2: newer "nonsedating" antihistamines: loratidine, fexofendine, zyrtec ect) 2. nasal corticosteroids - ipratropium (may increase risk for cataracts) 3. leukotriene receptor antagonists modify inflammation cascade -monteleukast

Answer 34

exfoliative dermatitis, skin sloughs off

Answer 35

MRSA pseudomonas aeruginosa acinetobacter enterobacteriaceae

Answer 36

DROPLET good job. aspiration from oropharynx

Answer 37

inflammatory mediators: TNF and interleukins chemokines: IL-8 and granulocyte colony stimulating factor (GCSF)

Answer 38

1. avoid ET tube 2. keep head of bed elevated 3. reduce sedation 4. hand washing

Answer 39

post treatment xray want to make sure everything is cleared up and that the treatment has worked!

Answer 40

s. pneumoniae

Answer 41

1. ETOH 2. asthma 3. immunosupressed 4. elderly

Answer 42

1. bronchitis 2. COPD exacerbation 3. congestive heart failure 4. pulmonary embolism

Answer 43

"common symptoms", usually responsive to B-lactams **#1 most common: streptococcus pneumoniae** (rusty red color) **#2: haemophilis influenzae** (green sputum) **staph aureus** **klebsiella** (currant jelly) **pseudomonas** (foul smelling) SX: _1-10 day increase in cough, purlulent sputum, SOB,_ _dullness to precussion, **rigors**, tachycardia bronchial breath sounds, **tactile fremitis (say 99)**, friction rub, pleuritic chest pain,_ night sweats

Answer 44

"walking pneumonia" usually unresponsive to beta lactam, use *macrolide or fluorquinolone* **1. mycobacteria pneumoniae** (bullous myringitis..ear) **2. chlamydia pneumonia** **3. legionella** **4. viruses-\>** (RSV and parainfluenze in kids, and influenza in adults) PE: often normal physical exam, can have **extrapulmonary symptoms** DX: **use macrolides** (erythromycin, azithromycin, clarithromycin, doxycycline) or **fluoroquinolones**

Answer 45

**#1: streptococcus pneumoniae** **#2: haemophilis influenzae** (esp in COPD) **#3** **mycoplasma pneumoniae** (atypical)

Answer 46

1. gram negative **pseudomonas** 2. ancinetobacter 3. **staph aureus**

Answer 47

1. clinical syndrome, empirically 2. gram stain- GCP 3. sputum culture 4. urine tests **(only in legionella and pneumococcus)** 5. xray showing **white infiltrate**

Answer 48

pneumococcus they are the same thing, so if used in a test question, they mean the same thing, its just an abreviated name for this \*\*important since this is the most common organism to cause pneumoniae\*\*

Answer 49

vancomycin

Answer 50

- rusty blood colored sputum - beta lactam sensitivity - if systemic can cause confusion \*\*immunizable\*\* this is what the vaccine is for!

Answer 51

1. 80% can be treated as outpatient with macrolide **azithromycin/erythromycin/clarithromycin** (atypical or "walking pneumonia) 2. if ths same patient has chronic illness combine with **beta lactam** 3. if MRSA infection use **vacomycin or fluroquinolone** **\*\*5- 14 day treatment\*\***

Answer 52

PVC13: childhood vaccination PV23: used in 65 + \*\*\*\*new recommendations say **65+ recieve BOTH, adults get PCV13 first then PV23 second 8 weeks later\*\*\*** **if they have already had PV23, wait a year and give PVC13**

Answer 53

ETOH- klebsiella COPD- haemophilis influenzae CF-pseudomonas Air-conditioning-legionella children \<2-parainfluenza Children \<1-RSV

Answer 54

2 billion people are infected 9 million people develop the disease Infected does not mean you will develop the disease!! Two completely different things!!!

Answer 55

**mycobacterium tuberculosis** mycobacterium bovis mycobacterium africanum mycobacterium microti mycobacterium canetti

Answer 56

hight risk for _becoming INFECTED with TB_ high risk for _DEVELOPING TB DISEASE_

Answer 57

1. close contact 2. foreign born 3. low income and homeless 4. health care workers in high risk groups 5. racial and ethnic minorities 6. infants, children and adolescents 7. IV drug users

Answer 58

1. asia 2. africa 3. russia 4. eastern europe 5. latin america

Answer 59

1. people with **HIV** (thats why prevalence increased in the 80s) 2. infection of TB within **last two years (5% risk, and 10% lifetime)** 3. **infants and children \<4 years old** **4. prolonged therapy with corticosteroids** 5. IV drug use 6. diabetes 7. silicosis

Answer 60

**HIV!!! 7-10% risk for devloping TB _disease_ each year when infected with both TB and HIV**

Answer 61

no they aren't infectious!! 10% will go on to develope disease!

Answer 62

1. tubercle bacilli are inhaled and travel to alveoli 2. multiple in alveoli, infection begins 3. small number of tubercle bacilli enter bloodstream and spread throughout body 4. within **2-4 weeks** macrophages survive bacilli, form a barrier shell that keeps the bacilli contained and under control know as **LBTI** 5. if the immune system can't keep tubercle bacilli under control, they multiple rapidly and cause _TB DISEASE_ \*it can occur in other places in the body too\*

Answer 63

YES IT IS you want to prevent these patients from getting it in the future!!!

Answer 64

1. close contacts of those with infectious TB disease 2. HIV 3. chest xrays indicating previous TB 4. organ donor transplants 5. immunocomprimised patients

Answer 65

1. people who came to US within last 5 years where TB is common 2. IV drug users 3. live or work in high risk facilities 4. micro labatories 5. children \<4 years old

Answer 66

1. person with LTBI becomes infected with HIV and then developes TB disease as the immune system is weakened 2. a person with HIV becomes infected with TB and rapidly developes the disease

Answer 67

cause by person to person transmission of drug resistant organisms

Answer 68

develops during TB treatment 1. patients were not given appropriate treatment regimen 2. patients didn't follow the medication as it was prescribed

Answer 69

isoniazid and rifampin (2 first line drugs avaliable)

Answer 70

isoniazid and rifampin, PLUS fluoroquinolones and at least 1 of the 3 second line drugs \*\*this is a major issue around the world\*\*

Answer 71

**at least 6 months** if cavities on chest xray and postitive sputum cultures at 2 motnhs then treatment should be extended for **9 months**

Answer 72

1._initial phase_: first 8 weeks of treatment, four drugs are used **isoniazid, rifampin, pyrazinamide, ethambutol** _2. continuation phase_: after first 8 weeks of treatment, bacilli remaining after initial phase are treated with at least two drugs _3. relapse phase:_ occurs when treatment is not continued for long enough, surviving bacilli may cause TB disease at a later time

Answer 73

2 ones the organism is suseptible to

Answer 74

clinical symptoms: **coughing \>3 weeks** **pleuritic chest pain** **hemoptysis** **positive rales** **infiltrates** (collection of fluid and cells in lung tissues) **cavities** (hollow spaces within lung usually in the upper lobe) **caseating granuloms on biopsy** (necrotizing granulomas)

Answer 75

1. **tuberculin skin test (TST)** **2. interferon gamma assays (IGRAS)**-measures immune response to m. tuberculosis, less likely to be incorrect compared to TST **3. culture with AFB staining** **-**need 3 specimens, 8-24 hour collection intervals, can induce with inhaling saline mist spray **4. chest x-ray** (infiltrates and cavities) **5. nucleic acid amplification test** **6. bronchoscopy or gastric wash if having hard time getting sample**

Answer 76

in lastent infection positive **2-4 weeks after infection** -injected with inactive tubercle bacilli, read within 48-72 hours \*\*this test can't differentiate between latent and active TB, just that a person has been infected at some point\*\* Positive test results: **15 mm in normal patients** **10 mm in immigrants, children \<4, high risk populations** **5 mm in HIV, immunsuppressed, positive chest xray, primary TB exposure**

Answer 77

**primary:** homogeous infiltrates, hilar/paratracheal lymph node englargement, **middle/lower lobe consolidation** **reactivation:** fibrocavity **apical** disease, nodules, infiltrates **\*\*TB reactivation presents at the top of the lungs instead of wher eit happened originally\*\***

Answer 78

millet seed like nodule lesions (2-4 mm)

Answer 79

**TB** ghon complexes: calcified primary focus ranke complexes: calcified primary focus and hilar lymph nodes \*\*these represent healed primary infection\*\*

Answer 80

acid fast bacilli tests 3 negative tests are considered negative!!

Answer 81

need to be isolated for a minimum of 2 weeks

Answer 82

"RIPE acronym 1. rifampin (hepatitis, flu, **orange body secretions**) 2. isoniazid (hepatitis, periphreal neuropathy, **give B6 to prevent risk**) 3. Pyrazinamide 4. ethambutol (optic neuritis) \*\*for LBTI: treat with isoniazid and pyrazinamide for 9 months, or 12 months if HIV pos or granulomas present on CXR\*\* \*\*if someone is exposed to patient with active TB, then treat them emipircally for 12 weeks until negative TB can be obtained\*\*

Answer 83

- single stranded RNA - orthomyxovirdae family - A, B, C types

Answer 84

hemagglutinin (HA) neuramidase (NA) 3 HA types in humans 2 NA types in humans

Answer 85

**shift:** pandemics, have NEW HA or NA **drift:** epidemics, development of new strains, but not whole new component

Answer 86

1. short incubation time (1-7 days) 2. ability for person with asymptomatic infection to transmit virus (can be contagious 1 day before symptoms) 3. early symptoms of illness are likely to be non-specific, delaying recognition (need to get antivirals on board within 48 hours of onset)

Answer 87

- usually only infects birds - **effects younger patients** - longer duration of infection - introduced to N. america by **bird migration**, infected people migrating, transportation of infcted poultry \*\*\*hasn't transferred from person to person but if it does, we will basically all die because no one has immunity and 1918 will happen all over again, working on vaccines now but super scary, race agains time\*\*\*

Answer 88

3 types; A (most pathogenic), B, C; neuramidase and hemmaglutinin make up the subtypes **Fall/winter outbreaks (october-november)** spread through **aerosolized droplets**, can live on surfaces **2-8 hours** 1. incubates 1-7 days, avg 3 2. symptoms last 3-7 days, but up to 14 **3. contagious 1 day before symptoms, 5-7 days after** **4. peak shedding 3 days of illness, correlates with fever** **fever \>100 or 37.8C AND cough or sore throat in absence of know cause, ABRUPT onset,** can have myalgia in legs and lumbosacral area. Emergency if CNS symptoms. PCR is best choice for diagnosis, can do rapid from throat or nose, but not as good

Answer 89

IMMUNIZATION!! 1. **inactive intradermal vaccine:** innactive, trivalent, quadrivalent, recombinant, higher antigen, contains 3-4 viruses, 70-90% effective **everyone older than 6 months** **2. intranasal:** live attentuated, **2-49 year old**, caution in \>50 or pregnant \*\*\*_don't use if allergic to eggs or gelatin\*\*\*_

Answer 90

**neuriamidase inhibitors** - oseltamivir - zanamirvir used for treatment and prophylaxis **need to be started within 48 hours** **don't use in \<12 year olds**

Answer 91

REYE SYNDROME (fatty liver and encephalopathy) happens when pt has viral infection and given asprin, occurs 2-3 weeks after with a **30% fatality rate**

Answer 92

1. necrosis of the respiratory epithelium that leads to secondary bacterial infection by staph, strep, or haemoph 2. pneumonia development, significantly contributes to fatality

Answer 93

1. acid/base buffer system (bicarbonate/carbonic acid)=primary buffer system 2. hemoglobin accepts hydrogen atom and makes blood less acidic=secondary buffer system

Answer 94

lungs play an important part in renin/angiotensin/aldosterone **this controls BP and ultimately profusion, make sure oxygen can get to the tissus**

Answer 95

**1. gas exchange** **2. vocalization** **3. acid/base buffer system** **4. endocrine** (regulate BP via renin/angiotensin=profusion) **5. blood volume** (voume changes with breathing depth rate and disease state) **6. immunologic** (particullary macrophages) **7. filter particulates**

Answer 96

adult hemoglobin a2b2 each chain binds 1 molecule of oxygen, in doing so changes **allosteric confirmation** of the entire molecule as it changes shape it allows **oxygen to bind to the other binding site** **_coopertivity_** is amplified with each oxygen binding site occupied

Answer 97

monomeric heme protein in muscle tissue, **intracellular storage site for oxygen** during times of _oxygen deprevation_ it _oxymyoglobin_ releases the oxygen for metabolic purposes

Answer 98

PO2=the value where 50% of Hb is saturdated=P50 **so the lower the P50, the greater the affinity for oxygen!!** ex: Hemoglobin A **P50=27 mm Hg** Myoglobin **P50= 2.8 mm Hg** Hemoglobin F **19.7 mm Hg** \*\*in this case myoglobin has the lower P50, this means that it will grab the oxygen and hold onto it tight!! this explains why myglobin has to become saturdated first to oxymyoglobin before there is excess levels of oxygen in the blood\*\* \*\*\*the fetal P50 is less than the adult hemoglobin so the fetus steals the oxygen from the mother first, so if there was ever oxygen deprevation, the fetus would get it first\*\*\*

Answer 99

hemoglobins oxygen binding affinity decreases as the concentration of H and CO2 increase **think about this: as you work out you get increase of acid in the muscle and CO2, this promotes the freeing up of oxygen so the tissues can get the oxygen they need, it also promotes the bdining of co2 and h ions so they can be removed from the tissue** **COOL!**

Answer 100

in high concentrations of **oxygen**, the hemoglobin **decrease** affinity for CO2 and H ions **think about this at the lungs: as hemoglobin returns from the tissue carrying co2 and H ions, the increase in oxygen avaliability causes the hemoglobin to ditch the H and co2 for oxygen**

Answer 101

red blood cells get energy from **glycolysis** glucose=\>pyruvate gives off ATP as biphosphoglyercate is converted to diphosphoglycerate, you get a **buildup of 2,3 DPG** **_this binds to hemoglobin and decreases the affinity of Hb for oxygen, ensuring it is released to the tissues that need it instead of staying bound to RBC_**

Answer 102

as temp increases, the affinity for oxygen **decreases** **think about it: the lungs are lower temp than the muscles because they are exposed to the external environment during breathing which is typically colder than body temp, thereform, the affity for oxygen at the _lungs_ is _HIGH_ and** **_LOWER_ at the _TISSUES_. this helps to promote oxygens release at the tissues!!**

Answer 103

1. increase temp (think of lung temp vs muscle) 2. increase in PC02 3. increase 2,3-DPG (remember helps cause dissociate) 4. decrease in PH (becomes more acidic, think at tissues)

Answer 104

1. decrease in themp (think of lung temp vs tissue, lungs are less) 2. decrease PCO2 (tissues not as active) 3. decrease 2,3-DPG (this helps to keep the oxygen attached, so if less it will stay attached) 4. increase in PH (becomes more basic, means not as much CO2 and H so tissues don't need O2 as much)

Answer 105

formed when **CO** binds to the **ferrous iron in hemoglobin**, hemoglobins affinity for CO is 218 times greater than O2 **which means that CO will force the O2 off by fighting for binding sites!! DEADLY** ## Footnote **\*\*think of carbon monoxide poisoning\*\***

Answer 106

**0.2 % can be lethal within hours** its binding affinity is 218 times greater than O2, meaning the higher affinity means once it is bound to heme it stays there!! but....it binds slowly?! haha so just keep that in mind even though it is opposit and makes no sense.

Answer 107

reflection of the difficulty oxygen has crossing the alveolar capillary membrane

Answer 108

tells you how difficult it is for the oxygen to cross the alveolar membrane

Answer 109

RQ=CO2 produced/O2 consumed CO2 produced=200 ml/min O2 consumed= 250ml/min so normal RQ=.8 **8 molecules of CO2 are produced for every 10 molecules of oxygen**

Answer 110

(pt age/4)+4 _if this value is normal, then the hypoxemia must be from_ **1. hypoventilation** (High CO2 like COPD) **2. low atmospheric pressure** (high elevation sickness) _if the A-a gradient is abnormal, hypoxemia must be from:_ **1. V/Q mismatch** (ventilation/perfusion mismatch) **2. shunt** **3. impaired diffusion across alveolar capillary membrante**

Answer 111

ficks law: rate of diffusion is proportional to tissue area and the difference in partial pressures between the two side; and inversly proportional to tissue thickness

Answer 112

1. large surface area 2. small distance 3. permeable surface (2 cell layers thick in alveoli and capillary endothelium) 4. high concentration difference (A-a) gradient 5. moist exchange surface with surfactant

Answer 113

surface-active lipoprotine comples formed by **type II alveolar cells**, its main purpose is to reduce surface tension thereby allowing maximal area for gas exchange

Answer 114

CO2 is a potent stimulant of **pulmonary minute ventilation** acts by stimulating **chemoreceptors in _carotid bodies and respiratory control centers in the brain and brainstem_** changes in ventilation in response to CO2 production **keeps alveolar PCO2 in dynamic equilibrium with metabolically produced CO2** CO2 also stimulates cerebral vasodilation and blood flow

Answer 115

respond to: 1. decrease in PO2 2. decrease in PH (acidic) **only carotid** 3. increase in PCO2 _responsible for 20-40% of ventilatory reponse to CO2_

Answer 116

1. brain +/- 2. medullary chemoreceptors (decrease pH and increase CO2)= + effect 3. carotid and aortic body chemoreceptrs (decrease O2)= + effect 4. hering-breure reflext (stretch receptors in the lung)= - effect 5. proprioceptors in the muscles and joints= + effect 6. receptors for touch temp and pain stimuli = +

Answer 117

the normal volume displaced between inhale and exhale without effort or quiet breathing **normal: 500-750 mL per inspiration**

Answer 118

the maximal amount of air that can be inhaled AFTER normal inspiration

Answer 119

the additional amount of air that can be exhaled after normal expiration

Answer 120

the volume of air remaining in the lungs after maximal exhalation, the purpose of this is to maintain patency of the alveoli esp at the end of respiration

Answer 121

the maximum amount of air that can be exhaled after maximal inhalation, the majority of the air exhaled in the first **1 second** **if \>80% or more of predicted value then it is _normal_** **it is adjusted for sex, age, and race!**

Answer 122

the total amount of air that can be drawn into the lungs after normal expiration, doesn't include the residucal volume or the amount that you can't breath out, this is why the TLC is larger than this value

Answer 123

the volume in the lungs after qiuet expiration AKA, the expiratort reserve volume +residual volume

Answer 124

the total volume in the lungs at maximal inflation

Answer 125

**visceral pleura**: covers the lung **parietal pleura:** lines the chest cavity the pleura is the _space inbetween_ Functions: 1. decrease friction between lung and chest wall 2. helps regulate the pressure both inside and outside the lungs during breathing through **mechanical coupling**

Answer 126

**low protein serous fluid from _systemic factor_** **_either excessive production or decreased absorption_** Cause #1: **Heart failure** accounts for 90% of transudative fluid in pleural effusion, this comes from **Heart failure causes increase pressure in left ventricle and backs everything up into lungs and** **increases pressure in visceral pleural capillaries** so fluid is pushed into the lungs, this causes the mechanical coupling to fail cause #2: can be caused from conditions with **hypoalbuminemia** seen in **liver cirrosis and renal disease** (nephrotic syndrome)

Answer 127

high in protein (inflammatory mediators cytokines, interleukins etc), **local factor!!** **constant inflammation and these mediators causes leakiness of the capillaries and the parietal pleura so the fluid can leak out into the pleural space and build up** 1. inflammation: can be treated with medication alone 2. bacterial pneumonia: fluid must be drained with bacteria to resolve situation 3. abscess: development of Frank pus called empyema and required drainage and possibly chest tubes

Answer 128

30%, so keep this in mind when examining patients!

Answer 129

1. **hemothorax**: blood accumulates from trauma, tumor, or aneurysm 2. **chylothorax**: lymph accumulates due to a blockage in thoracic duct, sometimes can be seen post surigcally if there is a blockage of thoraic duct or with mediastinal tumors. the lymphatics help to drain out extra peural fluid so if this is blocked by a tumor it can cause a build up of pleural fluid in the lungs - high triglyceride count \>100

Answer 130

**atelectasis** -a complete or partial collapse of the lung or lobe of the lung when the alveoli within the lung become deflated one of the most common respiratory complications after surgery

Answer 131

1. high altitude 2. diffusion 3. hypoventilation 4. shunting 5. VQ mismatch

Answer 132

obstructive disease glycoprotein produced in the liver, serine protease inhibitor, **balance neutrophil-protease enzymes in the lung aka neutrophil elastase produced by neutrophils in the presence of inflammation, infection, or smoking** if there is a deficiency in A1AT then _elastase can break down elastin unchecked, if this happens in the lungs it leads to destruction of alveolar walls and emphymateous change_

Answer 133

1. dimished sounds (COPD, pneumothorax) 2. wheezes (inflammation aka asthma) 3. rales "fine crackles like tissue paper" (fibrosis, alveolar disease...must distinguish between that and heart failture) 4. rhonchi "course crackles" (consolidation, bronchitis) 5. stridor "honking/gasping" like in video in CA

Answer 134

1. **egophony=** say EEE get AHH 2. **whispered pectoriloquy=** with whispering, course sounds are heard, rather than softer sounds "99" **3. tactile fremitus=** vibrations felt of the chest wall when speaking "99"

Answer 135

rule out cardiac disease

Answer 136

used to asses for the presence of a clot, esp in PE

Answer 137

1. flow rates/spirometry ## Footnote - Forced vital capacity (FVC) - Forced expiratory volume (FEV1) - FEV1/FVC ratio _normal \>70% (restrictive disease)_ _decreased \<70% (obstructive disease)_ \*\*do pre and post bronchodilation test\*\* 2. lung volumed 3. diffusion lung capactiy for CO (DLCO)

Answer 138

when you put a patient in a clear plastic booth and it measures the change in **pressure** and **volume** of breathing through a mouthpiece **typically decreased in restrictive disease**

Answer 139

small amount of CO is inhaled, then they measure how much you breath out, since the affinity is so much higher for CO, all should be absorbed if there isn't an issue **normal 25-30 ml/min/mmHg** EFFECTED BY: 1. thickness of alveoli 2. destruction of the alveoli (both obstructive and restrictive) 3. **anemia** WEIRD, this happenes because there is decreased affinity for CO since less RBC, want to make sure this value isn't decreased because of anemia and giving a false value

Answer 140

when you suspect a pleural effusion the patient lays on their side for the image and it makes it easier to see the fluid settle and confirm diagnosis

Answer 141

nuclear medicine scan that is used to determine the **ventilation** to **perfusion**, should have good circulation in a health person, but if not they have a **"mismatch"** **this isn't used that much anymore, look for areas of the lung that are ventilated but not profused anymore because radiologists would all read the results differently** **SO USE HELICAL CT ANGIOGRAPHY INSTEAD!** **particullary important in PE**

Answer 142

the scope is inserted into the trocar and into the pleura this is used for **video-assisted thorascopic surgery (VATS)**

Answer 143

suprasternal approach to look anterior to the trachea

Answer 144

the best method to reduce trauma is using lower tidal volumes than in regular person **6 ml/kg body weight** Postivie end expiratory pressure (PEEP): used to keep the alveoli from collapsing at the end of expiration, keeps a little air in there!

Answer 145

1. fluid restriction is helpful to prevent fluid overload and help prevent edema 2. decreases left atrial filling pressure and therefore decreases pulmonary edema as a result

Answer 146

1. compare pleural fluid **protein** and serum level protein 2. comparie pleural fluid **LDH** and a serum level LDH if ratio of pleural fluid to serum protein **\>.5 then exudative** if ratio of pleural LDH to serum LDH **\>.6 then exudative**

Answer 147

the pressure in the left side of the heart is **100-140** pressure and **significantly higher pressure** than the right side of the heart. It has thicker walls and stronger since responsible for pumping the blood to the entire body and profusing the tissues. the right side of the hear has a pressure **15-30** with thinner walls. If a PE gets stuck in the pulmonary arteries on the way to the lungs, it blocks the pipes and causes the fluid to back up into the right ventricle and increase the pressure, if this continues it puts pressure on the right side of the heart and the thin walls cant take it. This causes right heart failure and if the clot is bad enough and blocks the pipes enough, the increase in pressure on the right side of the heart can cause the walls of the heart to burst or get arrythmia, hense, why people can drop dead from a PE.

Answer 148

a mismatch in the amount of ventilation or profusion of the blood, essentially it means the blood isn't getting oxygen, this can be caused by 1. ventilation issues **low V/Q** (air can't get in, **asthma, chronic bronchitis, pulmonary edema** etc so blood gets **shunted** to an area with air) 2. profusion issues (PE, blood can't get to the lungs **dead space**) 3. diffusion issues (pulmonary fibrosis, can't pass between the two)

Answer 149

increased alveolar dead space "still ventilated but not profused"

Answer 150

1. early ambulation after surgery 2. elastic stockings 3. mechanical compression stockings 4. anticoagulation 5. high risk patients can be anticoagulated with low dose anticoagulants (unfractioned heparin, LMWH, rivaroxaban), prophylatically treat after surgery as well

Answer 151

the first milliseconds of forced expiration males: 400-700 L/min women: 300-600 L/min dcreased PEFE often preceeds symptoms of asthma the peak flow in the morning and night shouldn't have a difference of more than 20%, this tends to drop before a patient has an asthma exacerbation so by having a patient measure this you can better predict their asthma management. this works for mod/severe astham

Answer 152

measures the percent of oxygenation of hemoglobin measures O2 saturation in aterial blood normal=97%

Answer 153

1. **pH 7.35-7.45 is normal** 2. **PO2**=partial pressure of O2, free gaseous O2 in blood _oxygenation measurement_ **95 is normal** 3. **PCO2**= partial pressure of CO2 _ventilation_ _measurement_ "how well the air moves in and out of the lungs, if low then your lungs are doing a good job, if high there is a problem and the body may be getting tired and the person may need to be put on a ventilator **35-45 normal** 4. **HCO3**= bicarbonate proportional to dissolved CO2 in blood _metabolic abnormalities_ **22-26**

Answer 154

right ventricular hypertension that leads to right sided heart failure, commonly seen with pulmonary hypertension when the increased fluid backs up acute causes: PE, *rapid increase in pulm arterial pressure, RV overload, dysfunction/fail* Chronic causes: COPD, PAH *progressive hypertrophy and forced dilation of RV over months, dysfunction/failure* *\*\*you literally get every symptom ever, treat with **diuretics to decrease volume of fluid and give continuous long term O2 which improves life expectancy\*\****

Answer 155

it prolongs life and prevents pulmonary hypertension because you don't have to breath as hard **PO2\< 55mmHG, SaO2 \<88%** **goal: PO2 60-80 mmhg** \*must measure with resting, exercise, sleep\* **on it for 15 hours a day!**

Answer 156

most common caues: 1. **infection (pneumonia)** **2. PE** Less common: rib fracture, cholecystitis (gall bladder infection), compression fraction of upper thoracic spine, **localized and abrupt that worsens with deep breathing, leaning forward, coughing, VERY LOUD friction rub**

Answer 157

abnormal accumulation of fluid in he pleural space can occur from inflammation of the structures adjacent to the pleural space or lesions within the chest cavity four types: **1. transudative** **2. exudative** **3. chylothorax** **4. hemothorax** _dyspnea, decrease breath sounds and dullness to percussion_ DX: **AP view:** blunting of costophrenic angle, loss of sharp demarcation of diaphram, **mediastinal shift to uneffected side** l**at decbutus view**: patient lays on side, allows you to see smaller effusion and differentiate between free flow vs loculated fluid and empyema **thoracentsis: GOLD STANDARD**, maximal removal 1.5 L in one session

Answer 158

25% HOLY MOLY

Answer 159

increase pressure in the capillaries causes it to push out into the lungs this is NOT INFLAMMATION, just fluid relocation **low protein serous fluid** **#1 cause: Heart failure 90% of cases** fluid backs up from right side of the heart and increases pressure and pushes it into the lungs **right sided heart failure, BNP \>1,500** **#2 cause: cirrhosis/nephrotic syndrome**

Answer 160

leaky capillaries are cause from **INFLAMMATION FROM INFECTION, the inflammatory mediators cause the capillaries to be leaky and allow fluid into the lungs** **also called "parapneumonic effusion"** **_fluid filled with cytokines, WBC, proteins, interleukins, the purlulent fluid can form an empyema that requires surgical removal "infected cyst"_** **_PH_** Cause #1: bacterial pneumonia Cause #2: malignant cause aka lung cancer, metastic breast cancer, and lymphoma Cause #3: PE cause #4: TB (confirm with AFB stain) TX: antibiotics specific for infection type, drainage and if malignant source *portable catheter, chest tube or thoracostomy, sclerotic agent like talc or doxycycline to prevent it from happening again*

Answer 161

1. pleural fluid protein to serum fluid protein ratio **\>.5** 2. pleural fluid LDH to serum LDH ratio **\>.6** 3. pleural fluid LDH greater than **2/3** the upper limit of normal serum LDH

Answer 162

1. PH \<7.2 2. glucose \<40 3. positive gram stain of pleural fluid

Answer 163

asbestos exsposure malignant mesothelioma

Answer 164

air escapes from lung and fills the pleural space and prevents the lung from fully expanding types: **1. traumatic** CPR, car accident, stabbing, rib fracture, medical procedure **2. spontaneous** most commonly seen in **tall thin young men**, or also scuba diving, high altitudes, but can just happen randomly when **blebs air blisters break open sending air into pleural space** **3. tension pneumothorax**: MEDICAL EMERGENCY, usually from trauma, "sucking chest wound" or pulmonary laceration allows air in during inspiration but not out in expiration, increased air pushes lungs, trachea into mediastinal shift to **contralateral** side, develops in any type of pneumothorax as symptoms progress, leads to lung collapse

Answer 165

primary: spontaneous, **no underlying lung disease** (included traumatic and spontaneous) secondary: **underlying lung disease**, not trauma, like **COPD, ASTHMA etc.** symptoms: dyspnea, **ipsilateral CP**, **hypersonance, unilateral/bilateral expansion, nasal flaring** _**expiratory cxr**:_ presence of pleural air with _visceral pleural line_ **ABG**: **hypoxemia** small: resolves spontaneously \<15% of diameter of hemithorax Large: chest tube tension: medical emergency, needle decompression _NEED TO DO SERIAL CXR EVERY 24 Hours till resolved_

Answer 166

when a large pneumothorax as so much pressure that it causes a mediastinal shift and liekly a collapse of lung from pressure **pt bluish color, extreme chest tightness, easy fatigue, rapid heart rate in attempt to increase tissue profusion** **_needle decompression at 2nd INTERCOSTAL SPACE, ABOVE 3RD RIB!! EMERGENCY!!_** typically requires mechanical ventilation

Answer 167

common form of chest pain, common with _respiratory infection, viral infection_ occurs when the nerve fibers along the parietal pleura become irritated, lasts a couple of days **sharp stabing quality, worse with inhalation** **often inflammatory in origin and responds to antiinflammatories**

Answer 168

air in the mediastinum, typically form ruptured alveoli or perforation of the esophagus, trachea, or main stem bronchus may have air and crepitus in the neck and subcutaneous emphysema

Answer 169

1. pulmonary vascular bed by thrombus 2. **vasoconstriction in pulmonary artery**, this mechanism isn't well understood it just happens in the body as protective function, however, it actually has worse effects and harms the body 3. **increased pulmonary vascular resistance (PuVR)** from vasoconstriction by **neurohumoral reflexes and hypoxia** 4. continues to increase pulmonary artery pressure 5. **increased right heart strain from backed up fluid** leading to **right heart failure THIS IS OFTEN CAUSE OF DEATH** 6. **increased alveolar dead space**, ventilated but not profused, leads to decreased surfactant, atlectasis, and **V/Q mismatch from impaired gas exchange** 7. V/Q mismatch leads to **_right to left shunting_** where blood is redirected to non obstructed lung for oxygenation all of this causes decreased pulmonary compliance, increased work of breathing so the patient becomes tachypnea and has to work harder to inflate the lungs

Answer 170

1. **venous stasis** (immobility, post op, post stroke) **2. increased venous central pressure** ( decreased cardiac output, CHF) **3. hypercoagubility** (meds, malignancy, **FACTOR V LEIDEN)** _collectively known as virchows triad_ - hypercoaguble - venous stasis - vascular intima inflammation or injury \*\*slight difference between two so I included both\*\* worry specifically about orthopedic, pelvic, or abdominal surgery or OCP

Answer 171

DVT is most common in **popliteal** **iliofemoral** **pelvic veins** 90% arise here! calf involvement alone is much less risky!

Answer 172

**_tachypnea, dyspnea, pleuritic chest pain (sharp stab) on inspiration_** must have high suspicion because 50% of pt lack these characteristc symtoms clinical signs: **1. crackles** **2. S4 gallop** (since right ventricle get stiff from the increase in pressure you hear right atrial contraction) **3. decreased S2 splitting** **4. friction rub** **5. positive homans sign** (calf pain with dorsiflexion) **6. plasma D-Dimer** (elvated in thrombus/degredation of fibrin)

Answer 173

**1. CXR** - **westermarks sign** (avascular markings distal to embolus) - **hamptons sign** (wedge shaped infiltrate that shows infarction) 2. **Helical CT angiography** proximal vessel thromboembolism **3. EKG- S1Q3T3 classic for cor pulmonae** **4. Pulmonary angiogram GOLD STANDARD** -the issue with this test is it is an invasive procedure that puts a catheter in the heart and injecting dye into a high pressure area, people can have a reaction to the dye or the kidney can be effected _only indicated when VQ and CT scans are indeterminant and PE is still suspected_ probability PE 4+

Answer 174

**1. LMWH or unfractioned heparin** low molecular weight heparin is usually preferred because it has a more predictive dose and is the same if not more effective that unfractioned heparin, but some people still use it **5-7 days while transitioning to warfarin** 2. **warfarin** goal PTINR 2-3, can use new oral drugs like **dabigatran, rivroxaban, apixaban** they don't need monitoring and may work better than warfarin, but more $$$ _FULL ANTICOAGULATION FOR 3-6 MONTHS, LONG IS BETTER AND MOST DO 6 MONTHS \*\*THIS PREVENTS FUTURE CLOTS\*\*_ 3. **Streptokinase, urokinase, TPA** used in urgent situations to directly lyse intravascular thrombi and accelerate the 1st 24 hours, _does not decrease mortality_ which is why it is used in URGENT cases **4. mechanical/surgical extraction** this is **LAST RESORT** when the patient is hemodynamically unstable and is bascailly going to die anyway because the surgery is a basic death sentence by opening them up and taking out the clot

Answer 175

1. if the patient is hemodynamically stable 2. active internal bleeding 3. stroke in prior two months 4. trauma in the last 6 weeks 5. uncontrolled hypertension

Answer 176

venal caval interruption filters

Answer 177

3rd leading cause of inpatient death

Answer 178

patient with hypoxemia... 1. **increase pulmonary vascular resistance** 2. **increase in pulmonary artery pressure** 3. **increase in right ventrical**, increases so much it can't handle the pressure 4. **chronic right ventricle pressure causes right ventricle hypertrophy** where it tries to thicken the walls to make it stronger so it can handle the increase in BV 5. eventually this leads to **right ventrical failure** _hypoxia is the most important and potent stimulus of pulmonary vasoconstriction_ think about this...its really counterintuitive, if a patient is hypoxic, you would think the body would vasodilate to get more blood to the lungs to be oxygenated but for some strange reason the body decides to vasoconstrict, which only exacerbates the issues because it caues pulmonary hypertension in ADDITION to hypoxemia and creates a positive feedback loop where the body downward spirals into heart failure from hypoxemia

Answer 179

**idiopathic**: unknown cause, rare, fatal within 5 years of diagnosis, **some random correlation with anorexigens** or fat burning pills *fenflouramine, women 30-50, 20% familia* **secondary:** caused by pretty much any lund disease that causes hypoxemia because it inself is enough to vasconstrict the pulmonary arteries *PE, vasculitis, SLE, emphysema* **chronically increase in venous pressure causes HF and mitral stenosis**, can be congenital like in septal defect

Answer 180

1. hypoxemia \*\*\*most important\*\* automatically stimualtes pulmonary arterial vasoconstriction 2. acidosis 3. venocclusive conditions

Answer 181

**1. left heart could have decreased forward flow** so it backs up into the pulmonary system **2. increase in flow from the right side of the heart** causing the pulmonary pressure to increase **3. issues with pulmonary vasculature** **4. hypoxic vasoconstriction** \*\*cause can be either cardiac or pulmonary\*\*

Answer 182

symtoms: 1. dyspnea exertion and rest 2. retrosternal CP that minics angina 3. increase JVP 4. increase right ventricle impulse 5. loud s2 6. S4 gallop 7. TR murmers 8. systolic ejection click

Answer 183

**1. CXR** - dilated/enlarged pulmonary arteries - pruning vessels **2. echocardiogram** - right ventricular hypertrophy - atrial hypertrophy - right ventricular strain **3. cardiac cath (right heart)** -measure the pulmonary artery pressure, then do drug testing and see if using vasodilators or calcium channel blockers work to decrease hypertension so that you can figure out which drugs can help the patient **adenosine, epoprostenol, nitric oxide**

Answer 184

1. calcium channel blockers if sensitive from cath, *lower systemic arterial pressure* 2. phosphodiesterase-5 inhibitor **sildenafil** *pulmonary vasodilation* 3. prostacyclins *potent pulmonary vasodilator* 4. endothelin receptor antagonist **bosentan** 5. heart-lung transplant usually needed

Answer 185

bleeding and thrombocytopenia

Answer 186

venous ultrasound with doppler (non-invasive)

Answer 187

**ACUTE REVERSIBLE OBSTRUCTION**, can develope anytime but typically -genetic, inflammatory infiltrates, injury to epithelium, thickening of airway, hyperresonsiveness 3 contirbutory causes: **1. airway obstruction**-smooth muscle constriction, bronchial wall edema, thick mucous obstruction **2. bronchial hypersensitivity-** stimulation from a mechanism either _intrinsic (non IgE)_ or _extrinsic (allergen stimulated)_ **3. inflammation of the airways**-leukotrienes, histamine released from mast cells

Answer 188

1. **acetylcholine**- NT released via vagus nerve leading to _bronchoconstriction_ **2. histamine**-_bronchoconstrictor_ in mast and basophils in lungs, in the present of inflammation it promots _capillary leaking_ **3. kinins**-_bronchoconstrictor_ released by mast cells **4. leukotrienes**-_smooth muscle constrictor_, increased mucous production

Answer 189

- asthma is obstructive, so patients have a hard time getting air out, the increase in lung volume leads to an increased "sucking" effect where blood is pulled into the heart, the increase pressure and volume strains the right side of the hear and can push the intraventricular septum into left ventricle, causing less outflow and periphreal circulation= decreased periphreal pulses - systolic pressure drop \>10 mmHg during inspiration in healthy: the decrease pressures in the chest during inspiration causes the blood to come back to the right side of the heart and go towards the right venticular wall, and there is only a small drop in systolic pressure In tompenade: the increase blood flow and pressure on the right ventricle during inspiration can't be distributed on the right ventricular wall, and instead is transmitted to the ventircular septum, causing a decrease in left ventricular filling and the reason you see the periphreal pulses decrease since decrease stroke volume and a lower systolic blood pressure

Answer 190

**INTRINSIC:** **1. NONallergic triggers** infections (viral, bacterial), pharmocologic, emotional, occupation, stress, asprin, weather etc. **EXTRINSIC:** 1. **ALLERGIES**- _largest risk factor for developing astma_, **ATOPY, most common in children/adolescents,** there is genetic disposition (tabacco, smoke, GERD)

Answer 191

* highly variable presentation* 1. coughing/wheezing/chest tightness/SOB 2. **note: in severe asthma, wheezing may decrease or stop because of decreased airflow** 3. decreased FEV1 and FEV1/FVC \<70%

Answer 192

**admission criteria:** Peak expiratory flow rate (PEFR) \<50% predicted **discharge criteria:** Peak expiratory flow rate (PEFR) \>70% predicted

Answer 193

**_Intermittent_**: **FEV1\>80%, symptom frequency \<2times/week** -DOC SABA, albuterol **_Mild persistent:_** **FEV1\>80%, symtom frequency \>2times/week** - SABA, albuterol + - inhaled corticosteroid, fluticasone (if already taking this, increase dose) - if unresponsive, oral corticosteroid, prednisone **_moderate persistent:_** **FEV1 60-80** - above, +most warrent hospitalization/O2 supplementation - repetitive/continous use of beta agonists in nebulizer with systemic corticosteroid IV - continous monitoring PEFR and PCO2 **_severe persistent_**: **FEV1\<60%** -SAME AS ABOVE \*\*\*\*\*\*\*\*\*\*NEVER SEDATE A PATIENT DURING ACUTE RESPIRATORY EXACERBATION BECAUSE IT CAN DECREASE THEIR RESPIRATORY DRIVE\*\*\*\*\*\*\*\*\*\*\*\*

Answer 194

**PO2: \<60 mmHG** **PCO2: \>42**

Answer 195

_1. Peak expiratory flow rate (PEFR)_ _2. pulse oximetry_ _3. **PFT GOLD STANDARD, proves reversible obstruction**_ **-decreased FEV1** **-decrease FEV1/FVC \<70%** \*\*give bronchodilator, then this improves\*\* postivie if **\>10% increase in FEV1 after bronchodilator** _4. bronchoprovocation challenge test_ give histamine/allergen OR METACHOLINE, and FEV1 decreases by 20%, this is DIAGNOSTIC _5. arterial blood gas_ Respiratory alkalosis hypoxemia PaO2\<60 mmHg PCO2\< 40 mmHG

Answer 196

\*\*this is the greatest predisposing factor for asthma\*\* 1. wheeze 2. eczema 3. rhinnitis (TYPICALLY AT NIGHT)

Answer 197

ECZEMA werid!!!

Answer 198

you get a **LOW V/Q** there is **low Ventilation** cause the person gets less air then a regular person from obstruction the profusion remains the same, so a smaller number divided by a constant number is a **smaller ratio**

Answer 199

you want to activate the **beta receptor because this causes _relaxation_** you want BLOCK the **muscarinic receptor** **because this causes _constriction_**

Answer 200

**3rd leading cause of death in US,** rates increasing **progressive air flow obstruction** chronic bronchitis (cough) and emphysema(enlarged sacs) these two contribute to this, it can be one or both, depends on the person **1. loss of elastic recoil:** smoking leads to chronic inflammation and decreased protective enzymes (alpha-trypsin) and increases damaging enzymes (elastase from neutrophils and macrophages), this causes **alveolar capillary and wall destruction= _decrease gas exchange_ surface area and _elastic recoil_** \*makes expiration active process\* **2. increased air resistance from above**

Answer 201

smoking in 90%

Answer 202

alpha-1 antitrypsin deficiency in patients younger than 40, associated with premature COPD **this enzyme protects the elastin in the lungs from being degrated by elastase released by WBC**

Answer 203

**VACCINATION** 1. pnuemonia 2. influenza \*\*\*they can get sicker faster! prefect breading gound\*\*

Answer 204

1. **s. pneumoniae** **2. hae influenzae** **3. moraxella** **catarrhalis** \*\*\*use antibiotics to treat these! don't usually prescribe COPD patients antibiotics, doesn't help underlying condtion\*\*

Answer 205

**_Stage 1_**: **mild, FEV1\>80%, FEV1/FVC \<70%** -bronchodilators, vaccination **_Stage 2:_** **moderate, FEV1 50-80** short term bronchodilators, long term bronchodilator **_Stage 3:_** **severe, FEV1 30-50%** Short and long term bronchdilators, pulmonary rehab with inhaled glucocorticoids **_stage 4:_** **very severe, FEV1 \<30 RESPIRATORY FAILURE****, cor pulmonale** -above plus O2 therapy, must consider *surgical options* or roflumilast

Answer 206

1. lung transplant 2. lung volume reduction surgery for diffuse emphysema 3. bullectomy, remove large bullae and reduce deadspace to increase V/Q mismatch (seen in pic, these are seen with emphysema, big floppy airs of the sacs that are huge from elastin destructio nand dn't function. by rmoving this you decrease dead space!

Answer 207

1. rapid severity 2. worsening hypoxemia 3. advanced age 4. arrythmias 5. poor hom support

Answer 208

cor pulmonale (esp with bronchitis) multifocal atrial tachycardia, check with EKG

Answer 209

1. PFT GOLD STANDARD - FEV1/FVC \<70% 2. ABG - normal early on - decreased PO2 with progression - PCO2, usually normal, but can decrease in progression

Answer 210

most important is **_SMOKING CESSATION!!_** goal of treatment: improve functional state and relieve symptoms **_Anticholingerics_** superior to B-agonists in achieving bronchodilation, since COPD has increase airway tone from acteylcholine, has less side effects **ipratropium (short), tiotropium (long)** **_bronchodilators_** most important agent to decrease symptoms **albuterol, salmetrol** **\*\*\*\*if cor pulmonale, USE OXYGEN!!!! this is the only therapy proven to decrease mortality!!!\*\*\*\***

Answer 211

OBSTRUCTIVE **abnormal and permanent enlargement of the air sacs, causing gradual destructon _without fibrosis,_** the membrane gets damaged and becomes bigger, stretched out and floppier 1. alveoli have decreased elastic recoil 2. bronchioles more likely to collapse **THIS LEADS TO OBSTRUCTION FROM EXPANDED ALVEOLI, AIR TRAPPING=decreased ability for RECOIL and SHUNTING OCCURS due to issue with perfusion (diffusion)!** "floppy sacs" Premature collapse of respiratory bronchioles in expiration results in air trapping; result is “obstructive picture” on PFT’s the destruction of the alveoli and vasculature leads to *V/Q mismatch with shunting and alveolar dead space*

Answer 212

Step 1: Elastase startes to break down elastin in CT tissue around alveoli causing the alveoil to get really big! this casues obstructive resp issues because the air is gettig tapped in the huge alveoli. Usually expiration is a passive process due to recoil but with degredation of elastic in CT the alveoli got huge and lost a lot of its recoil causing air trapping and obstructive resp disease. This also negativly effects ventilation but perfusion is still okay (this is a prime example of V/Q mismatch)! because ventilation is affected we see shunting Step 2: this is more rare in emphysema but still important to understand! The elastase does not stop its degradation of elastin in the CT it continues to the alveoli membrane and begins to degrade the membrane! this is very bad because this will now effect DIFFUSION because it is affecting the membrane. Since diffusion is now effected we have increase DEAD SPACE! this can lead to an area of dead space called a BULLAE and could lead to the patient needed a bullectomy ! IN the green book: it describes emphysema as a condition in which the air spaces are enlearged as a consequence of destruction of alveloar suptea Alvelolar septum (sputae) separates adjacent alveoli in lung tissue (so this is what i talked about above with the elastase destroying destroying the elastin in the CT causing enlargment!)

Answer 213

1. tachypnea, tachycardia 2. **barrel chested, increase AP diameter** 3. decrease breath sounds 4. **hypersonance/hyperinflation** 5. pursed lip breathing "pink puffers" 6. respiratory alkalosis 7. wheezing/whistling 8. **prolonged expiratory phase since obstructive** TESTS: 1. FEV1-decreased 2. **FEV1/FVC- \<70%,** FVC stays the same just takes longer to get it out 2**. increase RV (**increase in RV since air trapping and can't get air out) 3. decreased DLCO in later stages, increased dead space! 4. CXR: hyperinflation, flattened diaphram

Answer 214

bullae or blebs "large cystic areas in the lungs INCREASED DEAD SPACE

Answer 215

**centrilobar:** cells affected near where the smoke enters the lungs **Panlobar:** effects the entire lung, seen with genetic cause alpha-1 antitrypsin deficiency

Answer 216

**cough and plegm for 3 months for 2 years** **airways clog with mucous cause obstructed airflow**, **particularly obstructs expiration** 1. inflammation of conducting airways, damages the respiratory epithelium causing loss of cilia 2. columnar cells may be replaced by squamous cells (metaplasia) 3. **airway narrowing (remember chronic bronchitis is an inflammatory issue!!!)-\>increases mucous secretion, hypertrophy of glands and smooth muscle, causing bronchospasm** 4. bronchospams increases the work of breathing and decreases ventilation of distal alveoli 5. causes **V/Q mismatch** **positive feedback loop, continues**

Answer 217

minor URI, esp in winter months complication: pulmonary hypertension leading to heart failure

Answer 218

1. excessive "smokers" cough 2. excessive phlegm 3. crackles from mucous 4. **increased expiratory since obstructive** 5. **wheezing**/rhonchi **6. resipiratory alkalosis (the pt is breathing faster immediately as the CO2 rises, so...they are hyperventilating causing alkalosis...initially see patient increase CO2 that initiates the hyeprventilation, but this happens so quickly that you never actually see patient in acidosis)** 7. **periphreal edema and cyanotic "blue bloaters"** 8. decreased FEV1, FEV1/FVC ratio \<70%

Answer 219

the exact same as emphysema, so see that flashcard!

Answer 220

**autosomal rescessive** **disorder resulting in abnormal production of mucous by all exocrine glands causing obstruction** this mucous is thick and viscous and in _lungs, pancreus, liver, intestines_, _sinues, sex organs_ obstructive lung disease + exocrine gland dysfunction symptoms: 1. chronic sinusitis 2. **digital clubbing** 3. excess phlegm 4. **meconium ileus at birth** 5. **pancreatic insufficiency that causes decreased fat absorption and bulky pale foul smelling stool as baby** **6. reccurent resp infection with _pseudomonas and s. aureus_** **7. development of bronchiectasis**

Answer 221

1. **sweat chloride test, \>60 is DIAGNOSTIC, _needs to be elevated on two different occasions_** 2. PFTs - mixed obstructive and restrictive 3. ABG studies - hypoxemia causing respiratory acidosis

Answer 222

**1. clearance of airway secretions** **2. bronchodilation** **3. nuitritional support** **-**replace pancreatic enzymes A, D, E and K **4. lung or pancreatic transplant**

Answer 223

1. young with bronchiectasis 2. pancreatic insufficiency 3. growth delays 4. infertility 5. chronic lung infection

Answer 224

CFTR protein that is a chloride transporter "salty kisses"

Answer 225

31 is avg survival rate increased risk for: 1. GI tract malignancies 2. osteopenia 3. arthropathies

Answer 226

secondary disease that is caused by infection or other conditions that injure the walls of the airways or prevents the airways from clearing mucous. the mucous build up causes increased infection and each infection causes more damange and eventually the airways can't move air in and out from damage and scarring. \*can be congenital with CF or from obstruction\* \*as mucous builds up and stretches everything, the membranes become more floppy and can collapse easier, which is why this is obstructive, not just because of the mucous\*

Answer 227

the mucous build up creates a perfect breeding ground for pathogens #1: **haemophilis influenzae (most common in world)** **#2: pseudomonas (CF, #1 cause in US)** #3. mycobacterium avium complex (MAC) 4. aspergillis (brown sputum)

Answer 228

1. recurrent pneumonia 2. chronic cough 3. **hemoptysis (50-70%), bronchiectasis is main cause of this** 3. **foul smelling mucopurlulent sputum** 4. **clubbing (as seen with CF)** 5. crackles at base DX: 1. **high resolution CT;** imaging of choice, dilated tortuous airways **2. CXR;** crowded bronch markings, basal cystic spaces, _Tram Track markings (bronchial wall thickening)_, honeycombing, _signet ring sign (pulmonary artery coupled with dilated bronchus)_ **3. bronchoscopy** warrented to eval hemopytsis and remove secretions

Answer 229

1. ABX for 10-14 days for infections 2. supressive therapy 3. bronchodilators 4. lung transplant

Answer 230

**associated with bronchiectasis** classic triad: 1. sinusitis 2. situs inversus 3. infertility

Answer 231

ATOPY ALLERGIES!!!

Answer 232

don't need arterial blood gas **unless they are in ED and can't get it under control** having asthma causes the patient to breath faster tachypnea, which causes the CO2 to go down, thats ok, just means that CO2 is going out faster....happens initially ....if treatment isn't working and they loose their drive to breath, so the CO2 starts to increase, this gets scary! because the increase in this is toxic, so you need intervention quickly!!

Answer 233

RESTRICTIVE!! **remodeling of the lung to look like _honeycomb lung_**, fibroblasts come in and lay down fibrosis tissue, can be associated with **age** dismal prognosis, _3 years from diagnosis_ 3 Types: 1. usual interstitial fibrosis 2. respiratory bronchiolitis, associated with this 3. acute interstitial pneumonitis

Answer 234

SX: -inspiratory "squeaks" crackles - clubbing of digits - progressive dyspnea with dry non productive cough DX: **1. chest CT:** **-diffuse reticular opacities with HONEYCOMBING, ground glass opacities** **2. PFT shows decrease FEV1 and FVC, so FEV1/FVC appears normal** **3. lung biopsy** important for confirmation

Answer 235

none, you're out of luck!! ## Footnote can give supplement O2 if needed but nothing has been shown to increase survival or quality of life. lung transplant may be the only choice

Answer 236

these help to show honeycombing!!

Answer 237

inhaled corticosteroids

Answer 238

RESTRICTIVE appeares **10-15 years after abestos exsposure** when the metal fibers on the surface are **phagocytosed** leading to **interstial fibrosis** renovation old building, insulation, pipe fiters, ship building, thermal and electrical insulation **libby montana, sierra nevada**, **underserved** high exsposure What happens: **pleural plaque thickening, calcification, fibrosis of parietal pleura, visceral pleura, lower lung, diaphram, and cardiac borders** leads to mesothelioma

Answer 239

**1. CXR** **-pleural plaques, usually lower lungs** **-intersitial fibrosis** **-linear opacities at bases** **2.** **biopsy, linear abestos bodies** _treatment:_ SUPPORTIVE, O2 and steroids if needed

Answer 240

mesothelioma most common cancer of pleural space you only need to have exsposure for 1-2 years to be at risk 50% of these will metastasize often accompanied with pleural effusion

Answer 241

only when they aren't doing well and none of the treatment isn't working and you suspect they might be failing check the CO2 because it checks for respiratory fatigue \*\*do this to see if the patient should be vented becaues they are too tired form breathing and their PCO2 goes up which is toxic\*\*

Answer 242

has some bronchial relaxation

Answer 243

smoking interferes with abestos fiber clearance from the lung, smoking allows it to stay in the lung smoking and abestosis are **synergestically linked!**

Answer 244

asbestosis increases risk for ALL CANCERS, **esp bronchogenic cancers** increase risk for TB, bronchogenic carcinoma, mesothelioma

Answer 245

**MULTISYSTEM DISEASE MADE OF NONINFECTIOUS _NONCASEATING GRANULOMAS_** **CAUSING INFLAMMATION IN INVOLVED ORGANS** the granumlomas form in response to _exagerated T cell response_, these granulomas "masses" take up space and disrupt organ function 90% have lung involvement * initial lesion in lung called: CD4 T cell alveolitis* * progression of disease: transforms into noncaseating granuloma* ***most effected: 1. pulmonary 2. lymphadenopathy (_hilar lymph nodes_) 3. skin** (erythema nodosa) **4. lupus pernio 5. PAROTID ENLARGEMENT 6. visual defects** (20%)*

Answer 246

**1. serum blood tests** **-Leukopenia** **-eosinophilia** **-elevated ESR** **-hypercalcemia** **-hypercalciuria** **2. CXR** **billateral _hilar_ lymphadenopathy** **2. elevated angiotensin** (40-80%) **3. needle biopsy** needed to confirm _noncaseating granulomas_

Answer 247

50% can be asymptomatic Very responsive to **high dose corticosteroids!**

Answer 248

**MOST SEVERE/WORST KIND OF ACUTE LUNG INJURY** Cause #1: sepsis (75%) Multiple Trauma pulmomary contusion/rib fracture surgery aspiration of gastric contents **Phase 1: Exudative** starts 12 hrs-7 days post insult, causes edema from mediators; _neutrophils_ migrate to alveoli and interstital space leading to pulomary infiltrate and collapse/atelectasis, decreased V/Q, leading to increase work load andbreathing **Phase 2: proliferative** 7-12 days, show signs of clinical improvement and get off ventilator, then get _lymphocyte involvement_ **Phase 3: fibrotic** 3-4 weeks up to 6 months, interstitial fibrosis pattern or emphyseamatous changes with bullae formations "systic sacs" rather than healthy alveoli

Answer 249

1. tachypnea or tachycardia in first 12-24 horus (resp distress) 2. **severe hypoxemia, not responsive to 100% oxygen** 3. respiratory failure 4. billateral pulmomary infiltrates on CXR \*\***periphreal infiltrates** that spare costophrenic angles with air bronchograms in 80% of patients\*\* 5. absence of cardiogenic pulmomary edema (pulmonary wedge pressure

Answer 250

**_CARRICO INDEX_** **1. ABG PaO2/FIO2 ration (380 normal), not responsive to 100% O2** **2. diffuse billateral infiltrates "whiteout patter"** **3. cardiac cath of pulmonary artery (swan-ganz), pulmonary wedge pressure** \*\*aka, pulmonary edema with normal pulmonary wedge pressure=ARDS, and that the source of pulmomary edema is NON CARDIAC, this test rules out heart failure\*\* \*\*if Pulomonary wedge pressure was elevated, it would suggest edema was elevated from left ventricular output failure/HF\*\*

Answer 251

age alcoholism metabolic acidosis 10% of ICU patiends have ARDS

Answer 252

AGRESSIVE SUPPORTIVE CARE IN ICU WHILE TREATING UNDERLYING INFECTION/TRAUMA _VENTILATOR SUPPORT_ 1. **endotracheal intubation:** pos pressure ventilation and low levels of positive end-espiratory PEEP **2. mechanical ventilation** (PPV) _Goals of ventilation_ **1.** decrease worload of breathing: _pos pressure ventilation_ **2.** decrease hypoxemia: _use appropriate fraction of inspired air FiO2_ 3. avoid barotrauma due to stiff lung _"want enough to keep alveoli blown up but not enough to pop them", decrease alveolar atelectasis and prevent overinflation_

Answer 253

1. thromboembolytic events since immobile 2. gastrointestinal bleeding 3. skin breakdown

Answer 254

25-44% mortality 1/3 of deaths occur in first 3 days and the rest within 2 weeks

Answer 255

**repetitive cessation of airflow at the _naso or oropharynx (caused by their passive collapse)_ that occurs during sleep** **stop breathing for \>10 secs or hypopnea decrease in airflow \<50% for 10 seconds**, must have at least 5 episodes daytime symptoms: excessive sleepiness, sore throat, depressing, morning headache nighttime symptoms: loud snoring, snort or gasp to wake up, apneic episode witnessed **DX: polysomnograph (PSG) sleep study!!** can do EEG if brain is stimulated, or TSH

Answer 256

nasal continous positive airway pressure (CPAP) ## Footnote literally forces the air in so that way the airway can't collapse lifestyle changes: loose weight, avoid alcohol before bed, change sleeping positions, pharyngeal surgery

Answer 257

**OBESITY (85%)...so loose weight** male \>40 alochol before bed **anatomic narrowing of nasopharynx** **neck size,** large tongue

Answer 258

**gastric content, inert material, toxic material, chewed food** **acute gastric aspiration GERD is one of the most common causes are ARDS** aspiration can develop secondary to aspiration DX: *expiratory radiography:* regional hyperinflation *bronchoscopy:* may help determine how to best remove substance

Answer 259

**RESTRICTIVE** inhalation of particulate matter that causes fibrosis of interstitial lung disease duration of exsposure increases severity 15-20% of COPD patients have this involvement **asbestos-**thermal and electrical insulating **silicosis-**silica or quartz, stone cutting, glass factories **pneumoconiosis: "BLACK LUNG",** coal dusts **beryllium**: nuclear reactor conductor

Answer 260

inhalation of **coal dust** coal is inhaled by macrophages, release inflammatory mediators, fibroblast proliferation, and fibrosis and remodeling of intersitial lung **\*\* nodules/nodular opacities in upper lobe\*\*** **\*\*hyperinflation of lower lobes\*\*** Leads to progressive massive FIBROSIS

Answer 261

coal workers pneumoconiosis and RA

Answer 262

**silica or quartz exposure** stone cutting or glass factories, grantie quarries leads to **calcifications and fibrosis** increases risk for TB, and connective tissue diseases like RA and schleroderma

Answer 263

nuclear reactor exsposure causes **granulomas** DX: **beryllium lymphocyte proliferation test**

Answer 264

exsposure at battery plants

Answer 265

**neonatal respiratory distress syndrome (NARD)** prematurity disease, _pulmonary surfacants are deficient_ at birth, decreasing surface tension and compiance, decreased lung compliance leads to V/Q mismatch and _ATELECTASIS (partial or complete lung collapse)_ \*\*\*\*\*MOST COMMON CAUSE OF DEATH IN FIRST MONTH OF LIFE AND MOST COMMON CAUSE OF RESPIRATORY DISTRESS IN PRETERM INFANT\*\*\*\* DX: CXR-air bronchograms, diffuse billateral atelectasis causing **ground glass opaque appearance and doming of the diaphram** TX: _1. antenatal steroids to mature lungs if preterm delivery is expected_ _2. exogenous surfactant_

Answer 266

**inflammation of trachea, bronchi, and bronchioles resulting from RTI or chemical irritant characterized by _COUGH,_ often follors URI** _COUGH LASTS 10-20 DAYS!!_, SEE EXPIRATORY RALES/RHONCHI 90% caused by viruses including rhinovirus, adenovirus, coronavirus, and RSV in chronic lung disease, commonly caused by: **haemophilis influenzae, strep pneumoniae, m cartillis** CXR: ONLY DO IF TRYING TO DISTINGUIS BETWEEN THAT AND PNEUMONIA

Answer 267

- hydration - expectorants - analgesics - cough suppressants (children) for bacterial: DOC **cephalosporin** **-reccomended only for ELDERLY pt with underlying cardiopulmonary disease and a cough for \>7-10 days and ANY IMMUNOCOMPRISED PT** **\*\*\***for acute exacerbations in otherwise healthy.....NO TREATMENT NEEDED\*\*\*\*

Answer 268

allergen causes inflammation in terminal airways, THINK OF THIS LIKE AN ALLERGERY **Farmer's lung, bird fanciers lung** **_TYPE 4, GELL AND COOMS ALLERGIC RXN_** _T CELL DRIVEN WITH GRANULOMA FORMATION_ **ACUTE:** 4-6 HOURS, flu-like, typically resolve **SUBACUTE**: gradual onset within weeks, typically resolve **CHRONIC:** insidious onset and looks more like pulmonary fibrosis,

Answer 269

fine inspiratory crackles, dyspnea, oxygen dependence, resp failure, **later stages can have clubbing** **CXR:** bird exsposure: fibrosis farmers lung: emphysema pattern patterns range from **fibrosis** **with honeycombing** to **poorly defined infiltrate "reticulonodular" that isn't obvious** TX: avoid the allergen and corticosteroids!

Answer 270

severe and life threatening! viral or bacterial can occur in anyone, but **most common children 2-7 or adults 45-65** adults: streptococcus, streptococcus pneumoniae, hae influenzae, staph aureus **Haemophilis influenzae vaccine (HiB) has decreased most cases in children** but many adults haven't been vaccinated _sudden onset fever, resp distress, SEVERE dysphagia, drooling and muffled voice_ **mild stridor and paitients usually sit upright with their necks _extended_!!**

Answer 271

**1. direct visualization is diagnostic** but caution because you might obstruct the airway completely in children **2. CBC and epiglottic culutres** **3. Neck XR: swollen epiglottis with _thumb sign_** DX: _1. SECURE THE AIRWAY_ _2. broad spectrum_ antibiotic second or third gen cephalosporin like _cefotaxime or ceftriaxone for 7-10 days_

Answer 272

**children 6 months-5 years** ***cause #1:** parainfluenza virus type 1 and 2* also be from RSV, adenovirus, influenza, and rhinovirus _harsh, barking, seal-like cough_,_inspiratory stridor_ DX: PA neck film showing subglottic narrowing _STEEPLE SIGN!!!_ use the lateral view to differentiate croup from epiglottis TX: no treatment usually in mild - corticosteroids, humidified air, and nebulized epi - patient may need hospitalization if sever

Answer 273

**bordetella pertussis**, gram neg *pleomorphic bacillis* humans are the only reservoir there is a vaccination, so not as much of a problem in the US, but is a problem around the world! **highest risk in premature infants with cardiac, pulmonary, or neuromuscular disease**, children and adults tend to have milder disease **catarrhal stage:** hacking cough at night, often misdiagnosed as URI but this is **most infectious state** **paroxysmal stage:** spasms of rapid coughing with deep, high pitched inspiration (the WHOOP), infants at risk for apnea **convalescent stage:** decrease in severity and frequency, usually four weeks after onset

Answer 274

physical exam is unremarkable, adults are often misdianosed with URI DX: by culture on special media or PCR, see **lymphocytosis** TX: DOC: **_erythromycin_** aimed at stopping transmission "any of the mycins work"

Answer 275

inflammation of the bronchioles **\<2mm in diameter** typically young children and infants, **RSV IS THE MOST COMMON CAUSE**, can include rhinovirus, parainfluenza and adenovirus all symptoms seen with respiratory complications CBC: usually normal, **nasal washing RSV and antigen assay** often done **CXR: air trapping and peribronchial thickening** if RSV is present consider hospitalization and **ribavirin**, really important **nebulized albuterol, IV, antipyretics, o2**

Answer 276

**leading cause of cancer in men and women** made of two categories: 1. small cell lung carcinoma 2. non small cell lung carcinoma _mets to brain, bone, liver, lymph_ SX: \*\*\*\*ASYMPTOMATIC, mostly incidental finding on CXR\*\*\*\* 2. **_\*\*\*change in nature of cough (squamous, small cell)_** 3. hemoptosis 4. vague _nonpleuritic_ chest pain 5. reccurent pneumonia 6. WEIGHT LOSS ANOREXIA ASTHENIC (CLASSIC) 7. HYPERCALCEMIA, don't miss this **cigarette smoking is the main cause, 85% of lung cancer in smokers**

Answer 277

**bad actor!!-grows quickyl metastasizes early!! assume m micrometasizes on presentation!** _**CENTRAL bronchial epithelium** (near hilum because thats where all the vessels are so it can get a lot of nuitrients)_ doubleing time: 30 day!!! **limited stage:** tumor on the same side of chest, supraclavicular lymph nodes, or both (20% 2 year survival) **extensive stage:** anyhting beyond limited stage (5% 2 year survival) associated paraneoplastic syndromes: _cushings, hyponaturemia, SAIDH, periphreal neuropathy, eaton lambert, cerebral degeneration_ TX: since it matastasizes so quickly, **CHEMO** is the treatment

Answer 278

**1. squamous,** central with cavitary lesions **2. adenocarcinoma** (non smokers), periphreal **3. large cell** periphreal very aggressive!

Answer 279

non small cell carcinoma 80-85% of LC

Answer 280

**MOST COMMON NON-SMALL CELL IN SMOKERS!!!** **_basal cells of bronchial epithelium_** **_centrally located, frequency hemoptysis and change of cough, CAVITATION_** hemoptosis diagnosed with cytology *late metastasis--so if you catch it early in the patient the prognosis is better!* paraneoplastic synderome: **hypercalcemia** TX: surgical

Answer 281

most common bronchogenic CA common in non-smokers **peripheral, lung parenchyma** originates in the _**mucous glands of tracheobrachial tree** and appears in the periphreay of lung_ **moderate growth and metastatic rate** NON SMOKERS, can get from ASBESTOS!!! paraneoplastic syndrome: **thrombophlebitis, PTH-rp** TX: surgical

Answer 282

periphreal or centrally located cavitation **rapid** growth **early** metastasis doubling time 100 days paraneoplastic syndrome: **gynecomastic** TX: surgical

Answer 283

combination of: 1. shoulder pain 2. horners syndrome 3. atrophy of the hand and arm muscles See particullarly with squamous cell carcinoma

Answer 284

**_CENTRAL neuroendocrine tumor_**, slow growth, slow mets also commonly found in GI tract typical: SESSILE (attached to base) or pedunulated (cylander) atypical pink/purple well vascularized central tumor, pedunculated or sessile **secretes _SEROTONIN_, ACTH, ADH, MSH** often asymptomatic, but can have **_hemoptosis_ and c_arcinoid syndrome_ (diareah from increased serotonin and left sided hear fibrosis)** TX: steroids and surgery, resistant to chemo and radiation

Answer 285

"coin lesions", KEEP IN MIND THIS IS THE FIRST MANIFESTATION OF ANY TYPE OF LUNG CANCER, THIS ISN'T A CANCER TYPE BUT THE CLASSIFICATION FOR _ANY_ FIRST APPEARNCE OF CANCER Defined: **\<3cm in diameter, single nodule, distinct margins, may have calcification, "satalite" lesions, or central cavitation** **Most at asymptomatic** 60% benign, 40% malignant often infectious granulomas from old reactive TB, fungal infection, or foreign body rxn DX: - CT for nodules \<1 cm and intermediate risk - PET for \>1 cm and intermediate probability TX: if high probability....**RESECT LESION** if intermediate......**biopsy** if low... can be watched, need **CT every 3 months for a year, then decrease to every 6 months for two years** ***if \<8mm w/o growth, 8-30 mm and low risk, or stable for two years***

Answer 286

**CT scan allows:** 1. staging 2. PET for metastasis 3. PFT to determine if pt could tolerate lobectomy otherwise no surgery 4. Chemo/surgery **tumor location:** 1. orange bronchus tumor: bronchscopy 2. red periphreal: percutaneous 3. purple central VATS

Answer 287

1. hemoptosis 2. fever 3. weight loss

Answer 288

10 million holy cow

Answer 289

1. increased bacterial resistance 2. unwanted side effects; ie c.diff 3. unnessacary costs

Answer 290

1. insufficient time to explain to family why abx isn't appropriate, easier to just give it to them 2. lack of understanding about general cause of URI 3. clinical experience and family experience in relationship to expectations 4. economic pressures (time and reduction in future visits)

Answer 291

1. hospital acquired gram - 2. gram + MRSA, enterococci, and VRE 3. C. diff from antibiotic use

Answer 292

1. antimicrobial agents **#1 cause** 2. fewer antibiotics being developed 3. modern med induces immunosuppresion and device related infections 4. abx use in animal feed as growth promoters

Answer 293

educated health care providers and patients about the use of antibiotics, super important

Answer 294

viral URI lasts 3-7 days mucopurluent rhinitis is NOT an indication for abx **DO NOT GIVE ANTIBIOTICS!!** **GIVE NSAIDS to help with symptoms**

Answer 295

70% of cases are viral! need to determine if it is a GAS (group A strep) because then you do give **DOC penicillin for 10 days** **if allergic to penicillin, use erythromycin or first gen cephalo** must have two of the following: 1. no cough 2. tonsillar exudate or swelling 3. fever 4. tender anterior cervical adenopathy 5. 3-15 years

Answer 296

**THE TREATMENT WITH ABX IN NORMAL PATIENT HAS NOT BEEN CONFIRMED, use bronchodilators instead because they are more effective at getting rid of cough than abx** exception: **\>10-14 days,** then can treat since this is beyond the viral process and happens in atypical pathogen like *mycoplasma pneumoniae, chlamydophilia, pertussis* **\>55 years old= macrolide (mycins) or tetracycline** **\>8= doxycycline**

Answer 297

no good way to get a sample, so diagnose mainly by symptoms and severity 1. protracted sinonasal sxs **_\>10 days_** (most viral resolve by this time) 1. onset of **_severe symptoms_** with high fever \>39\* and purluent nasal discharge and facial pain lasting 3-4 days 2. progressive symptoms **_post URI_** **prescribe for severe or those lasting \>10 days or worsenting after 5-7 days** Empiric TX: **amoxicillin-clav (penicilin)** if allergic use doxy, quinolone

Answer 298

acute ottitis media

Answer 299

if you don't treat with abx, the majority will clinically resolve in _7-14 days!_ ## Footnote Abx consideration: 1. **severe AOM** with severe pain, otalgia lasting \>48 hours, T\>39, billateral involvment \<2 years **TREAT** 2. mild AOM are patients \> 2 who have non severe unilateral ds **WAIT if follow up can be assured** **DOC: amoxicillin** **amoxicillin-clavulate** in patients who have had amoxicillin in last 30 days _typically 5-7 days, but 10 course if less than two years old_

Answer 300

often improves faster with abx and a short "burst" of steroids

Answer 301

gonococcal pharyngitis this doens't respond to penicillin or amoxicillin

Answer 302

**shunt:** a area with no ventilation but has profusion is called a shunt....it is called this because the blood must find another place to go and is shunted to another location to get oxygen **alveolar dead space:** an area with no profusion and normal ventilation. YOU CAN THINK ABOUT THIS, IF YOU DON’T HAVE BLOOD FLOW YOUR DEAD. VAMPIRES DON’T HAVE BLOOD, THEYRE DEAD

Answer 303

NO!!!! viruses cause purlulent sputum too, consider more the length of time rather than the AOM effusion can cause effusion for WEEKS!

Answer 304

1. expensive 2. aimed at chonic conditions so they can make more money

Answer 305

a **RHINOSINUSITIS**

Answer 306

not usually, group A strep are rarely caused by pharyngitis in \< 3 year old

Answer 307

you can treat these patients empirically because they aren't "normal hosts" and are at increased risk for this same thing with immunosupressed patients, the rules don't apply and would want to treat them!

Answer 308

almost all patients have abornal CT so why would you check this if it doens't tell you anything! most likely viral unless surpasses 10 days!

Answer 309

can be slow OR FAST encapsulated, well demarcated/defined not invasive or metastatic

Answer 310

tracheobronchial mucosa (bronchogenic origin)

Answer 311

1. exudative pleural effusion 2. endocrinophathies- HYPERCALCEMIA, don't miss this 3. coagulopathies, they secrete things that cause this! 4. digital clubbing!

Answer 312

NOPE!! but can do Low dose chest CT for high risk patients

Answer 313

**always benign if:** double time \<30 or \>500 day **likely benign if:** young patient, assymptomatic, \<2 cm, smooth margins, calcified, and satelite lesions ( this is actually better) **likely maligant if:** older pt \>45, \>2 cm, indistinct margins, symptomatic, rarely calcified, hx smoking, spiculated **likely metastatic:** smooth/lobulated margins, located periphreally, lower lobe, absent satelite lesions

Answer 314

6-18 weeks! holy crap that is nothing!!!

Answer 315

1. squamous 2. large cell

Answer 316

TUMOR TX: unaccesible, not in sputum/washing T0: no evidence of 1\* tumor T1: **tis**, tumor in situ T2: **\<3cm, \>2 cm away from carina,** **doens't effect entire lung, just a part** this is good cause you can resect it still! T3: invades close parts of the chest, **\<2 cm from carina, ENTIRE LUNG** T4: goes anywhere, more than one nodule in the same lobe, or with malignant effusion!

Answer 317

lymph nodes! NX: not assessed N0: no nodes N1: mets in i**psilateral peri bronchial/hilar** N2: mets in **ipsilateral mediastinal or subcarinal** N3: mets in **contralateral** bronchial/hilar/scalene/suprclavicular

Answer 318

MX: not accessed M0: no distant mets M1: distant mets present

Answer 319

liver-common bone-symptomatic adrenal brain

Answer 320

PaCO2 tells you....**ventilation** PaO2 tells you...**oxygenation** together they tell you...**acid base relationship, PH**

Answer 321

arise from mesothelia cells in **lung pleura (80%)** **peritoneum (20)** **20-40 years later from asbestos exsposure** _non pleuritic chest pain!_, exudative effusion, weight loss Tx: symptomatic, drain effusions **75% dead by year 1**

Answer 322

SMALL CELL CARCINOMA associated with: cushings (buffalo hump), cortico levels, hyponaturemia, SAIDH, periphreal neuropathy, eaton lambert, cerebral degeneration

Answer 323

decreased PH Increased PaCO2 compensation: increase HCO3

Answer 324

Over ventilation Pain/anxiety Hypoxemia high altitude +/- Pulmonary embolism and pulmonary edema Increased progesterone PREGNANCY CNS irritation infection, tumors Drugs theophylline, ASA, strychnine, doxapram

Answer 325

**Assess because of respiratory status:** - in extremis - altered level of conciousness - ventilatory support **Assess because of metabolic status:** DKA, sepsis, shock, toxic exsposure, electrolyte abnormality

Answer 326

1. radial 2. femoral

Answer 327

1. difficulty: edema, hypotension 2. pain 3. thrombosis/emboli (esp A line) 4. infection (esp A line) 5. collection (excess heparin, gas bubble, incorrect storage)

Answer 328

**indicative of metabolic process** amount of base or acid needed to titrate serum pH back to normal

Answer 329

H2CO3 and HCO3 ratio: 1 : 20 a lot more HCO3

Answer 330

emia is the finding osis is the process \*consider this difference for pH\*

Answer 331

chronic broncitis=conducting airways effected, bronchioles emphysema=terminal alveoli effected

Answer 332

chemical buffers: seconds respiratory: 1-3 minutes renal: hours to days \*\*important because the most common symptom you will see when the body is trying to compensate is change the respiratory rate\*\*

Answer 333

increase pH decrease PaCO2 compensation: decrease HCO3

Answer 334

the body wants the total cation=anion so the sterum is neutral **1. anion gap**: **difference between "unmeasured" anions and "unmeasured" cations** cations=(Na+K)-(HCO3+Cl) \*\*if \>8-12 suggests there is a problem like lactate, alcohol, or toxins, so this isn't good!!\*\* **2. hyperchoremic normal anion gap: really large increase in Cl- falsely makes it look like the gap is normal, but its NOT! issue im hyperchloremia**

Answer 335

1. lactic acidosis 2. ketoacidosis 3. renal failure 4. toxins (methanol, ethanol, asprin, iron)

Answer 336

1. DIARREAH!! causes you to loose HCO3 which is acidosis 2. RENAL TUBULAR ACIDOSIS!!! causes you to loose HCO2 which is acidosis

Answer 337

hyperchloremic acidosis ## Footnote the decrease in HCO3 from diarreahh or renal tubular disease=the increase in Cl, 1:1 ration since these are both anions, it makes it look like the anion gap is normal

Answer 338

1. diuretics (cause excretion of HCO3 at kidneys so it shifts it to the right) 2. vomiting (cause loss of H+ so it shifts to the right to compensate) 3. NG suction ( loose H so shifts it to the right towards alkalosis)

Answer 339

respiratory acidosis is **caused** by **hypoventilation** and leads to **hyperventilation**

Answer 340

to determine which one is compensating, you play tic tack toe ex: PH: acidosis CO2: acidosis HCO3 alkaline respiratory acidosis (tick tak) with metabolic parial compensation

CM Pulm Flashcards

(374 cards)