CM Pulm

Question 1

what are the three broad types of pneumonia source categories? which one is most common? which are most difficult to treat?

Answer 1

1. community acquired pnuemonia (CAP)

**most common**

2. healthcare/hospital acquired pneumonia (HCAP)
   - most difficult to treat
3. ventilatror associated pneumonia (VAP)

Question 2

what are the 3 components of tobacco?

Answer 2

1. nicotine (absorbed through oral mucosa and lung)
2. carcinogens
3. 4000 other substances

Question 3

what is “tar”?

Answer 3

particulate matter minus the moisture and nicotine

Question 4

how much does smoking 2 cigars a day increase your risk for oral and esophageal cancer?

Answer 4

2x

Question 5

How much does 3-4 cigarettes per day increase your risk for both oral and esophageal cancer (sepereate)?

Answer 5

8x oral cancer

4x esophageal cancer

Question 6

what are four risks of smokeless tobacco?

aka chewing tobacco

Answer 6

1. dental caries
2. gingivitis
3. oral leukoplakia (white lace on inside of the mouth, precancerous)
4. oral cancer

Question 7

what is nicotine?

Answer 7

the addictive part of cigarettes that causes dependence

Question 8

what is the most reducible risk factor for cardiovascular disease and cancer?

Answer 8

smoking

Question 9

what percent of premature deaths are from smoking? how much does it shorten the life expectancy by?

Answer 9

20% deaths

shortens life expectancy by 10 years

Question 10

how much does the life expectancy increase if a person stops smoking by 35?

Answer 10

3-5 years!

Question 11

what are the seven mechnanism by which smoking effects the cardiovascular system?

Answer 11

1. increases thrombus formation
2. plaque instability
3. increases MI
4. increase in death rates
5. angina
6. stroke
7. PVD

Question 12

what percent of PVD cases are caused or attributed to smoking?

Answer 12

90%

Question 13

how does smoking effect the lung?

Answer 13

1. COPD/emphysema

2. chronic cough

3. spontaneous pneumothorax

4. bronchiolitis

5. interstitial lung disease
6. eosinophilic granuloma
7. pulmonary hemmorage
8. desquamative interstitial pneumonia (DIP)

Question 14

what is the risk of cancer in smokers compared to non smokers?

Answer 14

13x greater in smokers

thank god I don’t smoke!

Question 15

****what is a interesting and random type of cancer you can correlate to smoking?****

Answer 15

bladder cancer!!! HUH?!

2-4x increased risk

50% of men, 40% of women

higher risk of bladder cancer with smoking so watch if they have hematuria and smoke…need to take a look inside

Question 16

what are 5 examples of cancer types that are linked with smoking?

Answer 16

1. BLADDER (don’t forget this!)
2. esophageal (squamous, synergistic with alcohol)
3. head and neck (synergistic with alcohol)
4. lung cancer (90% of cases)
5. pancreatic (2-4x increase)

Question 17

what is one of the few cancers that prevalence is DECREASED in smoking?

Answer 17

uterian cancer…..bizarre!!

Question 18

smoking accounts for what percent of the total lung cancer cases?

Answer 18

90%

remind me never to smoke

Question 19

what is the most common lung cancer seen in non smokers?

Answer 19

adenovirus

Question 20

what are three conditions that are linked with smoking that aren’t cancer?

Answer 20

1. polycythemia (primary and secondary)

2. Peptic ulcer disease

• higher rates
• decreased healing/therapy response
• increased h. pylori

3. osteoporosis

-causes: decrease in exercise, nuitrition, increased steroid use

Question 21

what does smoking during pregnancy do?

Answer 21

pretty much everything bad

pre, during, and post pregancy!! Don’t smoke!

Premature Rupture

Placenta Previa

Abruptio Placentae

Preterm Delivery

SIDS

↓ Fertility

↓ Birth Weight

↓ Natal Pulm Function

Question 22

patients who smoke and undergo surgery are at?

Answer 22

INCREASED RISK FOR COMPLICATIONS

1.5-4x greater risk!

Question 23

of the two inflammatory bowel diseases:

ulcerative collitis

crohns

….how does smoking effect each?

Answer 23

ulcerative collitis: actually makes it better! woah…40% decrease compared to non smokers, but the risks are dangerous, not advised

crohns: 2x greater risk of crohns

**stange, it effects inflammatory bowel disorders differently**

Question 24

does a lower dose of nicotine reduce risk?

Answer 24

NOPE its a myth!!

these patients inhale harder and more frequently so it negates the decreased dose

Question 25

does cutting down smoking help?

Answer 25

NOPE its a myth

patients who go cold turkey are more likely to be successful at quitting smoking!

Question 26

is second hand smoke dangerous?

Answer 26

YES

1.5x greater risk of developing lung cancer from just being around those who smoke

take them down

Question 27

does quitting help decrease risk of cancer and CV disease?

Answer 27

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

Question 28

what does “pack years” mean?

aka how do you calculate it

Answer 28

number of years smoking X number of packs per day

Question 29

what is the percentage of smokers who try to quit each year?

what percent of smokers would like to quit?

what percent of people quit each year?

Answer 29

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%

Question 30

what are the 5 phases of quitting smoking?

Answer 30

pre-contemplation

contemplation

determination

action

maitenance

Question 31

what are the two advantages and two disadvantages of going cold turkey while trying to quit smoking?

Answer 31

Advantages:

• success rates higher
• cost

disadvantages:

• nicotein withdrawal
• weight gain–big deal!

Question 32

what are the 5 A’s of smoking consults with patients?

Answer 32

Ask about tobacco everytime

advise smokers to quit

assess readiness to quit

assist smokers in quitting

arrange follow up

Question 33

what are the three categories of pharmaceuticals that can be used to help someone stop smoking?

Answer 33

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

Question 34

what are the 5 types of nicotine replacement? list important qualities of each

Answer 34

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

Question 35

what is the antidepressant drug that is used to help in smokers? what is the success rate? What patients should you not use this in? what are two side effects you need to be concious of?

Answer 35

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

Question 36

explain how new smoking drugs like Varenicline [chantix] works? what do you need to caution patients about taking it?

Answer 36

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

Question 37

what are the 6 problems or negative side effects of quitting smoking that a patient can experience?

Answer 37

1. cough

2. weight gain

3. nicotine withdrawal

• worse mood
• anxiety
• insomnia

Question 38

what is historically the best way to quit smoking?!

Answer 38

cold turkey!

Question 39

of the lymphocytes what percent are T cells?

Answer 39

70-80% of those circulating

Question 40

what is the role of basophil in allergies?

Answer 40

amplify inflammation

cross links IgE resulting in histamine release and anaphylatic factors

Question 41

what codes antigens?

Answer 41

major histocompatability complex (MHC)

Question 42

type 1 allergic reaction

Answer 42

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

Question 43

type II allergic reaction

Answer 43

cytoxic reaction to antibody

antibody binds to antigen with complement which results in cellular lysis/tissue injury

ex: transfusion reaction resulting in RBC lysis

Question 44

type III allergic reaction

Answer 44

immune complexes not cleared by reticuloendothelial system

these deposit in blood vessles and tissues

ex: serum sickness (flu like symptoms)

Question 45

what is serum sickness?

what are the 3 main symptoms?

Answer 45

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!!

Question 46

type IV allergic reaction

Answer 46

delayed type hypersensitivity

inflammatory response from leukocytes cell mediated

cellular immune response to antigen takes 48-72 hours

ex: PPD skin test thats positive

Question 47

type V allergic reaction

Answer 47

idiopathic reaction under unclear mechanism

ex: steven johnson syndrome, soughing skin

Question 48

what is samter’s triad you see in allergies?

Answer 48

classic allergy triad: asprin allergy, asthma, nasal polyps

Question 49

what is anaphylaxis? what three this cause this? what might be elevated in this patient on a lab test even though DX made clincially?

Answer 49

life-threatening immediate reaction

occurs in seconds to minutes

caused by histamine, leukotrienes, and prostaglandin D2

may have elevated beta tryptase

Question 50

what are the 3 signs/symptoms of anaphylaxis? what are the four important treatments?

Answer 50

respiratory distress

• laryngeal edema
• bronchospasm
• intubation possible

vascular collapse/shock

pruritis

TX: epinephrine, O2, antihistamines/glucocorticoids

Question 51

explain what epi does in anaphylaxis?

Answer 51

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

Question 52

explain how allergy shots work? what do you need to make sure these patients aren’t taking for a medication?

Answer 52

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

Question 53

what is urticaria and angiodema? what is the difference? what are three things that can stimulate them other than allergies? where do they commonly appeare? what are two treatment options?

Answer 53

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

Question 54

what can cause hereditary angioedema?

Answer 54

deficiency of C1 esterase inhibitor (C1INH)

Question 55

can you be skin testing for a penicillin allergy?

Answer 55

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)

Question 56

systemic mastocytosis

what causes this? what are the symptoms? what are two tests you can do? what do you need to rule out? what do you treat with?

Answer 56

mast cell hyperplasia

repeated pruritis/urticaria, abdominal pain, headache

elevated 24 hour urine histamine level or elevated serum tryptase

rule out carcinoid

Tx: antihistamine

Question 57

what are the three genreal categories for treatment for allergic rhinitis? give common example drugs under each one.

Answer 57

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

Question 58

stevens johnson syndrome is a ….

Answer 58

exfoliative dermatitis, skin sloughs off

Question 59

what are four bacteria that are drug resistant that you worry about in pneumonia?

Answer 59

MRSA

pseudomonas aeruginosa

acinetobacter

enterobacteriaceae

Question 60

how is pneumonia spread?

Answer 60

DROPLET

good job.

aspiration from oropharynx

Question 61

name 2 inflammatory mediators and 2 chemokines that are involved in the immune response for pneumonia?

Answer 61

inflammatory mediators:

TNF and interleukins

chemokines:

IL-8 and granulocyte colony stimulating factor (GCSF)

Question 62

what are four important ways to reduce ventalator associated pneumonia (VAP)?

Answer 62

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

Question 63

what is important to do once you have finished treating pneumonia?

Answer 63

post treatment xray

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

Question 64

what is the most common organism seen in pneumoniae overall?

Answer 64

s. pneumoniae

Question 65

what four patient populations make you at an increased risk for pneumonia?

Answer 65

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

Question 66

what are four conditions you need to differentiate pneumonia from in your differential diagnosis?

Answer 66

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

Question 67

Typical pneumonia

what are four common organisms associated with this and their characterist sputum color? how long do symptoms increase? what are some of the things on the long list of symptoms

Answer 67

“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

Question 68

atypical pneumonia

Answer 68

“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

Question 69

what are the three most common organisms that cause community acquired pneumonia (CAP)?

Answer 69

#1: streptococcus pneumoniae

#2: haemophilis influenzae (esp in COPD)

#3 mycoplasma pneumoniae (atypical)

Question 70

what are the three common organisms that cause hospital acquired pneumonia?

Answer 70

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

Question 71

what is the mortality rate in hospital acquired pneumonia?

Answer 71

50-70%

Question 72

what are the five tests you use to diagnose pneumonia?

Answer 72

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

Question 73

streptococcus pneumoniae=

Answer 73

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**

Question 74

if a patient has pneumonia with MRSA, what should you use to treat?

Answer 74

vancomycin

Question 75

streptococcus pneumoniae in pneumonia

(what color is the sputum? what is it sensitive to? what can happen if this is systemic? is there a immunization for this?)

Answer 75

• rusty blood colored sputum
• beta lactam sensitivity
• if systemic can cause confusion

**immunizable** this is what the vaccine is for!

Question 76

what is the treatment for patients with pneumonia? how long is the treatment regimen?

Answer 76

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**

Question 77

Explain the new vaccine regimen that is reccomeded?

Answer 77

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

Question 78

explain which pneumonia organism these populations are at the most risk to get:

ETOH-

COPD-

CF-

Air-conditioning-

children <2-

Children <1-

Answer 78

ETOH- klebsiella

COPD- haemophilis influenzae

CF-pseudomonas

Air-conditioning-legionella

children <2-parainfluenza

Children <1-RSV

Question 79

How many people are infected with TB? how many of those go on to develope the disease?

Answer 79

2 billion people are infected

9 million people develop the disease

Infected does not mean you will develop the disease!! Two completely different things!!!

Question 80

what bacteria cause the most TB in the US? what are 4 other bacteria that can cause it?

Answer 80

mycobacterium tuberculosis

mycobacterium bovis

mycobacterium africanum

mycobacterium microti

mycobacterium canetti

Question 81

what are the two populations of people that TB can be divided by?

Answer 81

hight risk for becoming INFECTED with TB

high risk for DEVELOPING TB DISEASE

Question 82

what are 7 things that can put someone at high risk for TB INFECTION (not disease)

Answer 82

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

Question 83

name five areas of the world where TB is common?

Answer 83

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

Question 84

what groups of people are at risk for developing TB disease!? (7)

Answer 84

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

Question 85

what is the greatest risk factor for devloping TB?

Answer 85

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

Question 86

are people with LTBI infectious? what percent of these people will go on to develope the disease?

Answer 86

no they aren’t infectious!!

10% will go on to develope disease!

Question 87

Explain the pathogenisis steps for TB (5 steps)

Answer 87

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*

Question 88

In TB, explain the differences between LTBI and TB disease in these characteristic:

1. active/inactive bacilli
2. chest xray findings
3. sputum smears
4. symptoms
5. infectivity
6. a case of TB or not

Answer 88

Question 89

Is LTBI treated with medication?

Answer 89

YES IT IS

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

Question 90

who is high priority treatment for LTBI with a TST >5 mm or postitive IGRA? (5 things)

Answer 90

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

Question 91

who is high priority for LTBI treatment >10 mm or positive IGRA test? (5 things)

Answer 91

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

Question 92

what are the two ways HIV can influence the path of TB?

Answer 92

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

Question 93

what is primary resistance?

Answer 93

cause by person to person transmission of drug resistant organisms

Question 94

secondary resistance

Answer 94

develops during TB treatment

1. patients were not given appropriate treatment regimen
2. patients didn’t follow the medication as it was prescribed

Question 95

multi-drug resistant TB is resistant to which drugs?

Answer 95

isoniazid and rifampin (2 first line drugs avaliable)

Question 96

extensively drug resistant (XDR-TB), what drugs are they resistant to?

Answer 96

isoniazid and rifampin, PLUS fluoroquinolones and at least 1 of the 3 second line drugs

**this is a major issue around the world**

Question 97

how long should a patient be treated for TB?

what if this person has pos sputum after 2 months of treatment?

Answer 97

at least 6 months

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

Question 98

what are the three phases of TB infection treatment?

Answer 98

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

Question 99

in order to prevent drug resistance, TB disease must be treated with at least how many drugs?

Answer 99

2 ones the organism is suseptible to

Question 100

Tuberculosis

what are the classic symptoms assosicated with TB (clinical and xray)?

Answer 100

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)

Question 101

what tests do you use to diagnose TB?

Answer 101

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

Question 102

explain the tuberculin skin test? what can’t this test do? what are positive test results for the three groups of people?

Answer 102

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

Question 103

explain the difference on chest xray between primary and reactivated TB?

Answer 103

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**

Question 104

what does milliary TB look like?

Answer 104

millet seed like nodule lesions (2-4 mm)

Question 105

what should you connect Ghon complexes and Ranke complexes? what are they?

Answer 105

TB

ghon complexes: calcified primary focus

ranke complexes: calcified primary focus and hilar lymph nodes

**these represent healed primary infection**

Question 106

what is the gold standard for TB testing?

Answer 106

acid fast bacilli tests

3 negative tests are considered negative!!

Question 107

how long should a person be isolated and on treatment before being allowed in public when they have TB?

Answer 107

need to be isolated for a minimum of 2 weeks

Question 108

what are the four drugs you use during the initial treatment phase for TB? what are their side effects? how do you treat someone if they have been exposed to someone with active TB? what is the treatment regiment for LBTI?

Answer 108

“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**

Question 109

what is the structure of influenza? what family? what types?

Answer 109

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

Question 110

what is the composition of influenza A? of these two, how many are there in humans?

Answer 110

hemagglutinin (HA)

neuramidase (NA)

3 HA types in humans

2 NA types in humans

Question 111

what does drift and shift mean in terms of influenza?

Answer 111

shift: pandemics, have NEW HA or NA

drift: epidemics, development of new strains, but not whole new component

Question 112

what are 3 challenges of containment of influenza?

Answer 112

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)

Question 113

Avian flu (H5N1)

who does this infect? how was this introduced into N. america? why are we so scared of this?

Answer 113

• 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***

Question 114

influenza

what are the three types and which one is most pathogenic? what is the season for this disease, how is it spread and how long can it survive on a surface? how long does it incubate? how long do symptoms last? when is a person contagious? when is peak shedding and what does it correlate with? what is the definition? what is the best choice for diagnosis?

Answer 114

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

Question 115

what is the best way to prevent influenza?

what are the two mechanisms of this? which age groups should be considereded for these two methods? what form is the virus in? which patients should you NOT use this in???

Answer 115

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***

Question 116

what are the treatment options for influenza?

how are they used?

when do they need to be started?

who don’t you use these in?

Answer 116

neuriamidase inhibitors

• oseltamivir
• zanamirvir

used for treatment and prophylaxis

need to be started within 48 hours

don’t use in <12 year olds

Question 117

what do you worry about when a child has influenza and are given asprin? what is the fatality rate?

Answer 117

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

Question 118

what do you worry about as a complication in elderly and chronically ill who have influenza? (2 things)

Answer 118

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

Question 119

what are the two major buffer systems in the body?

Answer 119

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

Question 120

explain how the endocrine system plays an important role in the respiratory system?

Answer 120

lungs play an important part in renin/angiotensin/aldosterone

this controls BP and ultimately profusion, make sure oxygen can get to the tissus

Question 121

what are the 7 maine functions of the respiratory system?

Answer 121

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

Question 122

explain the structure of hemoglobin A? explain what happens to the molecule as it binds oxygen

Answer 122

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

Question 123

myoglobin, where is it, what does it do?

explain what happens when the tissues are starved of oxygen?

Answer 123

monomeric heme protein in muscle tissue, intracellular storage site for oxygen

during times of oxygen deprevation it oxymyoglobin releases the oxygen for metabolic purposes

Question 124

explain what the PO2 and P50 value means and how it is related to the affinity of oxygen for molecules?

(explain myoglobin and hemoglobin and hemoglobin F)

Answer 124

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***

Question 125

explain the Bohr effect

Answer 125

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!

Question 126

explain the haldane effect?

Answer 126

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

Question 127

explain the role of 2,3 Diphosphoglyerate in hemeoglobin affinity?

Answer 127

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

Question 128

explain the effect tempreature has on the Hb affinity for oxygen?

Answer 128

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!!

Question 129

explain what four things increase P50, therefore decreasing affinity (remember by increases P50, you the heme wants to get rid of o2)

Answer 129

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)

Question 130

explain what four things decrease the P50, therefore increasing heme affinity for O2

Answer 130

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)

Question 131

what is carboxyhaemoglobin (COHb)?

Answer 131

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

**think of carbon monoxide poisoning**

Question 132

what percent of CO is lethal? why is this small amount so deadly?

Answer 132

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.

Question 133

what is the equation to measure the A-a gradient? what does this value tell you?

Answer 133

reflection of the difficulty oxygen has crossing the alveolar capillary membrane

Question 134

what is the alveloar gas exchange equation? what does this mean?

Answer 134

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

Question 135

explain what the respiratory quotient means? how much CO2 is produced for how much O2 is consumed? what does this mean in terms of molecules?

Answer 135

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

Question 136

what is the equation to calculate the A-a gradient? so if this value is NORMAL, what are the other two causes of hypoxemia (2)? If the A-a gradient is ABNORMAL, what are the 3 causes of this?

A-a gradient is alveolar membrane diffiusion

Answer 136

(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

Question 137

Explain Ficks law of diffusion?

Answer 137

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

Question 138

what are five qualities you need for effective diffusion?

Answer 138

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

Question 139

what is surfactant?

Answer 139

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

Question 140

what is CO2 a potent stimulus of? what two things does it stimulate and where? what does it keep in equilibrium? how does it effect dilation and blood flow?

Answer 140

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

Question 141

what do the periphreal chemoreceptors in the carotid and aorta respond to to regulate breathing (3 things) ? what percent of ventilation are they responsible for?

Answer 141

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

Question 142

what are the five 6 parts of the body that can send signals to the respiratory center in the medulla oblongata and pons to modify respiration? what effect do they have?

Answer 142

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 = +

Question 143

what is the tidal volume?

Answer 143

the normal volume displaced between inhale and exhale without effort or quiet breathing

normal: 500-750 mL per inspiration

Question 144

what is inspiratory reserve volume (IRV)?

Answer 144

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

Question 145

what is expiratory reserve volume (ERV)?

Answer 145

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

Question 146

what is the residual volume?

Answer 146

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

Question 147

what is the forced vital capactiy (FVC) and FEV1?

Answer 147

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!

Question 148

what is the inspiratory capactiy?

Answer 148

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

Question 149

what is the functional residual capcity?

Answer 149

the volume in the lungs after qiuet expiration

AKA, the expiratort reserve volume +residual volume

Question 150

what is the total lung compactiy?

Answer 150

the total volume in the lungs at maximal inflation

Question 151

explain what the pleura is made of? what do each line? what are the 2 function of the pleura?

Answer 151

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

Question 152

explain what a transudate fluid is?

what is the most common case of this in pleural effusion? cause number 2?

Answer 152

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)

Question 153

explain what an exudate fluid is?

what should be done about these types of exudative pleural effusions:

1. inflammation
2. bacterial pneumonia
3. abscess

Answer 153

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

Question 154

what percent of patients with a pulmonary embolism present with exudative pleural effusion?

Answer 154

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

Question 155

what are two other types of pleural effusions besides exudative and transudative?

Answer 155

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

Question 156

what can pleural effusions often lead to or commonly post surgery?

Answer 156

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

Question 157

what are 5 general causes of hypoxemia?

Answer 157

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

Question 158

alpha 1 antitrypsin deficiency

what does this protein to? what happens if there is a deficiency here?

Answer 158

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

Question 159

what are five lung sounds you may hear on examination and what conditions do they correlate with?

Answer 159

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

Question 160

what are three PE tests you can do to confirm consolidation?

Answer 160

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”

Question 161

what is Beta natruretic peptide (BNP) used to test for and rule out?

Answer 161

rule out cardiac disease

Question 162

what does D-dimer test access form?

Answer 162

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

Question 163

what are the 3 main parts of a pulmonary function test? what happens if the ration is increased or decreased; what types of pulmonary issues would you suspect?

Answer 163

1. flow rates/spirometry

• 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)

Question 164

what is body plethysmography?

Answer 164

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

Question 165

what is the DLCO test? what are three things that can cause this value to decrease?

Answer 165

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

Question 166

when is a decubitus chest xray improtant?

Answer 166

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

Question 167

explain what a VQ scan is used for?

Answer 167

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

Question 168

what is a thoroscopy?

Answer 168

the scope is inserted into the trocar and into the pleura

this is used for video-assisted thorascopic surgery (VATS)

Question 169

what is a mediastinoscopy?

Answer 169

suprasternal approach to look anterior to the trachea

Question 170

what is the best way to prevent trauma when using a ventilator in patient with ARDS? what is a tool you can use to prevent a patients alveoli from collapsing after expiration?

Answer 170

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!

Question 171

why is it important to have judicious fluid management in ICU patients with ARDS? (two things)

Answer 171

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

Question 172

what two test do you do to determine if a fluid is transudative or exudative for a pulmonary effusion?

1. what two things must you compare?
2. what are the values that makes this exudative fluid?

Answer 172

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

Question 173

explain why patients with massive PE or a PE will have right heart failure?

Answer 173

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.

Question 174

what is the percent mortality of undiagnosed PE?

Answer 174

40-50%

Question 175

explain what V/Q mismatch is?

where are the three places this can go wrong and what can be some causes? does it lead to dead space or shunting?

Answer 175

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)

Question 176

what is the primary mechanism for hypoxemia?

Answer 176

increased alveolar dead space “still ventilated but not profused”

Question 177

what are four mechanisms you can use to prevent DVT/PE?

Answer 177

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

Question 178

what is the normal ratio of FEV1/FVC?

Answer 178

75-80%

Question 179

what is the peak expiratory flow rate PEFR? how is this helpful in determining asthma?

Answer 179

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

Question 180

what dose pulse oximetry do?

Answer 180

measures the percent of oxygenation of hemoglobin

measures O2 saturation in aterial blood

normal=97%

Question 181

what information do you get from an arterial blood gas? what do they measure or indicate? what are the normal values for these?

(4 things)

Answer 181

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

Question 182

what is cor pulmonale?

what is an acute cause?

what are two chronic causes?

what are the two treatments

Answer 182

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**

Question 183

in a patient with COPD when in O2 indicated? what is the goal PO2 for someone on oxygent? what does it do?

Answer 183

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!

Question 184

pleuritis

what are the two most common causes of this? what are three less common causes? what makes this worse?

Answer 184

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

Question 185

pleural effusion

what is an effusion? what are two causes? what are the four different types? what are four symptoms? what are the two radiology views you wanna do and what do they show?

Answer 185

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

lat 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

Question 186

what percent of pleural effusions are related to malignancy?

Answer 186

25%

HOLY MOLY

Question 187

transudative pleural effusion

how does a transudative pleural effusion occur? what type of fluid would you find? what is the most common cause of this? what percent of people are effected with this and what test do you do to confirm this? and second most common cause of this?

Answer 187

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

Question 188

exudative pleural effusion

what is this caused from? what is another name for this? what does the fluid contain and what can form that needs surgical removal? what are the 4 lab characteristics for this? what are the four most common causes? what is the treatment, and the specific 3 treatments if malignancy related? what are the three common cancers that can cause this?

Answer 188

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

Question 189

what are the requirements for thoracentesis for a pleural effusion? (3)

Answer 189

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

Question 190

what are the requirements for an empyema to be drained off?

Answer 190

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

Question 191

what are 80% of malignant pleural effusions caused by?

Answer 191

asbestos exsposure

malignant mesothelioma

Question 192

pneumothorax

what is this? what are the three different types of pneumothorax and explain them?

Answer 192

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

Question 193

pneumothorax

what are the two general categories? what are four symptoms you might see? what two tests do you want to do to confirm? what might you see on each? what is the treatment for small, large and tension pneumothroax? what do you need to do to monitor the pneumothorax?

Answer 193

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

Question 194

tension pneumothorax

what is this? what are 4 symptoms the patient will have? is this an emergency? what do you need to do ASAP to relieve the pressure?

Answer 194

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

Question 195

**pleurisy**

what is this? what are two things it is commonly associated with? what causes it? how does the patient present and complain with? what is the likely source and what does it respond to?

Answer 195

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

Question 196

pneumomediastinum

what causes this and where would you likely find the perforation? where can the air displace?

Answer 196

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

Question 197

Pulmonary Embolism

explain the pathophysiology of this and what happens!

Answer 197

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

Question 198

what are 3 risk factors for DVT? what is this collectively know as?

Answer 198

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

Question 199

where is the most common site for development of a thrombus/embolus?

Answer 199

DVT is most common in

popliteal

iliofemoral

pelvic veins

90% arise here!

calf involvement alone is much less risky!

Question 200

pulmonary embolism

what are the 3 symptoms a patient with often present with ? what are 6 signs you may see on examination?

Answer 200

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)

Question 201

pulmonary embolism

what are the four test you use to diagnose and what would you see on each test? Explain the flow chart for PE diagnosis?

Answer 201

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+

Question 202

pulmonary embolism

what are the four treatment options and order for treating PE? when do you use each and explain them!

Answer 202

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

Question 203

when wouldn’t you do a mechanical/surgical intervention for PE? (5 things)

Answer 203

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

Question 204

what can you do in a patient who has an absolute contraindication for coagulation for PE prophylaxis?

Answer 204

venal caval interruption filters

Question 205

PE is the _______ cause of inpatient death?

Answer 205

3rd leading cause of inpatient death

Question 206

pulmonary hypertension

explain the sequence of event that cause this? what is the most potent stimulus of this pathway and explain why this happens?

Answer 206

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

Question 207

pulmonary hypertension

what are the two different causes of pulmonary hypertension? what are the examples under those categories that can cause them? (1/5)

Answer 207

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

Question 208

explain three causes that can contribute to pumonary hypertension? what is the most important?

Answer 208

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

Question 209

according to the clinical peals book, when looking at the heart, what are four causes of pulmonary hypertension?

Answer 209

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**

Question 210

pulmonary hypertension

what are 8 symptoms you would see with PH?

Answer 210

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

Question 211

pulmonary hypertension

what are the 3 tests you use to diagnose PH? what are 2 things you find on the first? 3 on the second? and how does the last one work? what three drugs do you test?

Answer 211

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

Question 212

pulmonary hypertension

what are the 5 treatment options for pulmonary hypertension?

Answer 212

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

Question 213

when treating a patient with heparin, what do you need to be cautious of?

Answer 213

bleeding and thrombocytopenia

Question 214

what is the test of choice for DVT?

Answer 214

venous ultrasound with doppler (non-invasive)

Question 215

asthma

what type of OBSTRUCTION is this? when does it typically develope? what are 5 things that can cause it to develope? what are the 3 main characteristics of asthma?

Answer 215

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

Question 216

what are the four mediators of asthma? what do each of them do?

Answer 216

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

Question 217

explain the pulsus paradoxus that can be seen in asthma? why can asthma patients have decreased periphreal pulses?

Answer 217

• 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

Question 218

intrinsic vs. extrinsic asthma

explain the difference between the two? what are examples that can cause them? who are they most common in? is there a genetic link?

Answer 218

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)

Question 219

asthma

what are 3 symptoms you might see with asthma?

Answer 219

• 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%

Question 220

what is the admission and discharge criteria for a patient and the hospital?

Answer 220

admission criteria: Peak expiratory flow rate (PEFR) <50% predicted

discharge criteria: Peak expiratory flow rate (PEFR) >70% predicted

Question 221

explain the four classifications of asthma severtiy and the treatment used for each step? WHAT SHOULD YOU NEVER DO???

Answer 221

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************

Question 222

explain what the test results are when a patient should be in the ICU with intubation for asthma?

Answer 222

PO2: <60 mmHG

PCO2: >42

Question 223

asthma

what are the 5 tests you can do to help diagnose asthma? what are the results you woudl expect to see?

1.

2.

3. (3)
4. (1)
5. (4)

Answer 223

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

Question 224

what is the atopic triad that you see with extrinsic (allergy induced) asthma?

Answer 224

**this is the greatest predisposing factor for asthma**

1. wheeze
2. eczema
3. rhinnitis

(TYPICALLY AT NIGHT)

Question 225

what weird condition is randomly assocaited with a persons risk for developing extrinsic (allergy) associated asthma?

Answer 225

ECZEMA

werid!!!

Question 226

how does having asthma effect the V/Q ration?

Answer 226

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

Question 227

explain the receptors in asthma to understand how the medications work?

Answer 227

you want to activate the beta receptor because this causes relaxation

you want BLOCK the muscarinic receptor because this causes constriction

Question 228

COPD

what number cause of death is this? what is this characterized? what are the two conditions that contribute to this diagnosis? what is the pathophys of this disease and how it occurs?

Answer 228

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

Question 229

what is the most contributory cause of COPD?

Answer 229

smoking in 90%

Question 230

what is the only genetic link with COPD?

Answer 230

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

Question 231

what is really important to make sure the COPD patients do?

Answer 231

VACCINATION

1. pnuemonia
2. influenza

***they can get sicker faster! prefect breading gound**

Question 232

what three bacteria are COPD patients particullarly suceptible to? what do you do for treatment?

Answer 232

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**

Question 233

COPD staging

explain the four stages of COPD and the medication classes you would use to treat or any other methods?

Answer 233

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

Question 234

explain the 3 surgical options considered if a patient has respiratory failure from COPD

Answer 234

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!

Question 235

when would you hospitalize a patient for COPD? (5 things)

Answer 235

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

Question 236

what do you need to watch for in a patient who has COPD?

Answer 236

cor pulmonale (esp with bronchitis)

multifocal atrial tachycardia, check with EKG

Question 237

what lab results can suggest COPD? (2)

Answer 237

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

Question 238

COPD TREATMENT

what is the most improtant factor? what is the goal of treatment? what are the two main classes you use and the drugs within those class? what do you need to do for COR pulmonale?!?!

Answer 238

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!!!****

Question 239

emphysema-COPD

explain the pathophys of this and the two many things that happen? what does this cause?

Answer 239

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

Question 240

What is the 2 step process in emphysema causing

1st: obstructive issues
2nd: diffusion issues

in the green book how does it explain emphysema in one sentence ?

and what is alveolar septae

Answer 240

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!)

Question 241

emphysema-COPD

Name 8 symptoms you would see on PE. what would you see for the FEV1, FEV1/FVC, DLCO, CXR (2)?

Answer 241

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

Question 242

what can you see in severe emphysema?

Answer 242

bullae or blebs

“large cystic areas in the lungs

INCREASED DEAD SPACE

Question 243

what is centrilobar emphysema? what is panlobar emphysema?

Answer 243

centrilobar: cells affected near where the smoke enters the lungs

Panlobar: effects the entire lung, seen with genetic cause alpha-1 antitrypsin deficiency

Question 244

chronic bronchitis-COPD

explain the pathophys of this and how it occurs?

Answer 244

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

Question 245

what often causes exacerbations of COPD caused from chronic bronchitis? what is the complication you really worry about?

Answer 245

minor URI, esp in winter months

complication: pulmonary hypertension leading to heart failure

Question 246

COPD-chronic bronchitis

what are the 8 symtoms you would see?

Answer 246

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%

Question 247

what is the treatment for COPD-chronic bronchitus?

Answer 247

the exact same as emphysema, so see that flashcard!

Question 248

Cystic fibrosis

what type of genetic disorder is this? what does it cause? what 6 organs are the most commonly effected? this is classified as what two main conditions? what are the 7 symptoms that you will see with this?

Answer 248

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

Question 249

cystic fibrosis

what are the three tests you use to diagnose this? what would you find as results for these three tests?

Answer 249

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

Question 250

cystic fibrosis treatment

4 things

Answer 250

1. clearance of airway secretions

2. bronchodilation

3. nuitritional support

-replace pancreatic enzymes A, D, E and K

4. lung or pancreatic transplant

Question 251

what are the five presentations that a patient could have that should point you into suspecting cystic fibrosis?

Answer 251

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

Question 252

what is the gene that is mutated in cystic fibrosis?

Answer 252

CFTR protein that is a chloride transporter

“salty kisses”

Question 253

what is the average survival rate for someone with CF? what are they at increased risk for?

Answer 253

31 is avg survival rate

increased risk for:

1. GI tract malignancies
2. osteopenia
3. arthropathies

Question 254

bronchiectasis

explain the pathophys of this aka how does this happen? what are the two ways this can happen?

Answer 254

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*

Question 255

if a patient has bronchiectasis what four infections do you worry about?

Answer 255

1: haemophilis influenzae (most common in world)

the mucous build up creates a perfect breeding ground for pathogens

#2: pseudomonas (CF, #1 cause in US)

4. aspergillis (brown sputum)

Question 256

bronchiectasis

what are the 6 symptoms you would see with a pt with bronchiectasis? what are the 3 tests you would do to test patient for this? what would you see on these?

Answer 256

1. recurrent pneumonia
2. chronic cough
3. hemoptysis (50-70%), bronchiectasis is main cause of this
4. foul smelling mucopurlulent sputum
5. clubbing (as seen with CF)
6. 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

Question 257

bronchiectasis

what are the 4 treatment options?

Answer 257

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

Question 258

what is kartagener syndrome? what is it associated with?

Answer 258

associated with bronchiectasis

classic triad:

1. sinusitis
2. situs inversus
3. infertility

Question 259

what is the single largest risk factor for developing asthma?

Answer 259

ATOPY

ALLERGIES!!!

Question 260

explain why PCO2 is important in asthma to monitor?

Answer 260

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!!

Question 261

idiopathic pulmonary fibrosis

aka idiopathic interstitial pneumonia

what type of pulmonary condition is this? what is caused by? how long does a patient typically have after diagnosis? what are the three types?

Answer 261

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

Question 262

idiopathic pulmonary fibrosis

what are 3 symptoms you would see of this? what are the 3 tests you would use diagnose this? what do you see on them?

Answer 262

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

Question 263

idiopathic pulmonary fibrosis

what is the treatment

Answer 263

none, you’re out of luck!!

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

Question 264

who wants some pics of idiopathic pulmonary fibrosis?

Answer 264

these help to show honeycombing!!

Question 265

what is the treatment for persistant asthma, according to handler?

Answer 265

inhaled corticosteroids

Question 266

what is the difference between ground glass appearance and honeycombing?

Answer 266

Question 267

asbestosis

what type of lung condition is this? how long after exspsure does the patient present? what happens over this time that causes this? what sources can a patient get this from and what are two common geographic locations for this? what does this lead to as a cancer? what 3 changes does this cause on the lungs and surround structures?

Answer 267

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

Question 268

asbestosis

what are the two testing methods you used for this? what do you see on each? what is the treatment?

Answer 268

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

Question 269

what is the most common thing that can come from abestosis?

1. how long do you need to be exsposed to be at risk?
2. what percent of these willl metastasize?
3. what often accompanies this?

Answer 269

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

Question 270

when do you a ABG on a asthma patient?

Answer 270

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**

Question 271

what can magnesium sulfate do in an asthma patient?

Answer 271

has some bronchial relaxation

Question 272

why is smoking cessation particullary important in abestosis? what type of relationship do smoking and abestosis have?

Answer 272

smoking interferes with abestos fiber clearance from the lung, smoking allows it to stay in the lung

smoking and abestosis are synergestically linked!

Question 273

abestosis increases the risk for __________.

what can abestosis causes increased risk for ________? (3)

Answer 273

asbestosis increases risk for ALL CANCERS, esp bronchogenic cancers

increase risk for TB, bronchogenic carcinoma, mesothelioma

Question 274

sarcoidosis

what is this condition? what type of cells respond to this? what percent of people have lung involvment? what is the intial lesion called? and what about when its progressed? what are the 6 common parts of the body that it effects?

Answer 274

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%)

Question 275

what are the three tests you can do to confirm sarcoidosis?

Answer 275

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

Question 276

what percent of people with sarcoidosis can be asymptomatic?

what is the treatment?

Answer 276

50% can be asymptomatic

Very responsive to high dose corticosteroids!

Question 277

Acute Respiratory Distress Syndrome

(ARDS)

what type of condition is this? what is the most common cause and 4 others? what are the three phases of this disease? decribe each phase!

Answer 277

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

Question 278

acute respiratory distress

what are the five things you will find in a patient who has this for symptoms and on exam?

Answer 278

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

Question 279

what do you use to diagnose acute respiratory distress syndrome?

(3 tests used for diagnosis, really explain what the last one is and what each one means

Answer 279

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**

Question 280

what are three things that put a person at increased risk for ARDS?

Answer 280

age

alcoholism

metabolic acidosis

10% of ICU patiends have ARDS

Question 281

what are the two types of treatment for ARDS? what are the three goals of this type of treatment?

Answer 281

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

Question 282

what are three important things to try to prevent in a ARDS patient while they are in the ICU for ventilation?

Answer 282

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

Question 283

what is the mortality data for ARDS?

2 stats

Answer 283

25-44% mortality

1/3 of deaths occur in first 3 days and the rest within 2 weeks

Question 284

obstructive sleep apnea

what are the qualitifications to have this? what physical body part fails during this? what are the daytime symptoms and what are the nighttime symtoms? what test is most important for diagnosis?

Answer 284

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

Question 285

obstructive sleep apnea

what is the most important treatment for this? what are some lifestyle adjustments you can make?

Answer 285

nasal continous positive airway pressure (CPAP)

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

Question 286

obstrucive sleep apnea

what are six RF and which is the most important one??

Answer 286

OBESITY (85%)…so loose weight

male

>40

alochol before bed

anatomic narrowing of nasopharynx

neck size, large tongue

Question 287

aspiration of foreign bodies

what are the types of materials this can include? what aspiration is closely related to ARDS? what can aspiration of a foreign body set the pt up for? what are the two tests that are useful?

Answer 287

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

Question 288

occupational lung disease

“pneumoconiosis”

what type of lung condition is this? what does the particulate matter cause? what percent of COPD patients have the influence of this? what are the 4 sources of this and where do you get them from?

Answer 288

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

Question 289

pneumoconiosis

“black lung”

what do you get from this? how does it happen? what are the two major things you would see on the CXR that would suggest this?

Answer 289

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

Question 290

what is caplan syndrome?

Answer 290

coal workers pneumoconiosis and RA

Question 291

silicosis

what exsposure caues this? where do you get it? what two things does it cause? and what specific three diseases does it make you at increases risk for?

Answer 291

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

Question 292

beryllium

Answer 292

nuclear reactor exsposure causes granulomas

DX: beryllium lymphocyte proliferation test

Question 293

what do you use a cadium urine test for?

Answer 293

exsposure at battery plants

Question 294

hyaline membrane disease

(NARD)

what is the other name for this? what does this patient lack and what does this lead to? what are the two most common things associated with this disease? what do you see on the CXR? what are the two treatment options?

Answer 294

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

Question 295

acute bronchitis

What is this condition characterized by? how long does the cough last? what other symptoms might you see? what are 90% caused by (4)? what are the 3 bacteria that cause it in CHRONIC disease? when do you do a CXR?

Answer 295

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

Question 296

acute bronchitis

what are the four OTC treatments for this? what is the DOC for bacterial and what two types of patients qualify for this treatment?

Answer 296

• 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****

Question 297

hypersensitivity pneumonitis

aka “allergic extrinsic alveolitis”

what are three things that can cause this? what should you think about this as? what type of hypersensitivity is this and what is the name of the type of allergic rxn? what type of cells drive this and what forms? what are the three classifications and how long does each one take?

Answer 297

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,

Question 298

hypersensitivity pneumonitis

“extrinsic allergic alveolitis”

what are the four symtpms you might see with htis? what are the two patterns you would see on the CXR for bird and farmers lung? what is the range of symptoms? what are the two treatment options?

Answer 298

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!

Question 299

acute epiglottitis

is this severe? what are the two age ranges this effects? what are the four bacteria that cause this in adults? why are children more protected than adults? what are the 5 systoms that a patient will present with? what are two things you will find when looking at the patient?

Answer 299

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!!

Question 300

acute epiglottitis

what is the really important thin you see on xray to suggest this? what are the other two ways you can help confirm this? what are the two treatment methods?

Answer 300

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

Question 301

Croup

“viral laryngotrachobronchitis”

what age group is this most common in? what is the most common cause? what four symptoms does the patient present with? how do you diagnose it and what must you differentiate it from? usually it doesn’t require treatment, but if severe what are 3 treatment options?

Answer 301

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

Question 302

pertussis

what bacteria causes this? who are the only reservoir? is there a vaccination? what pateints havet the highest risk; who can get it? describe the 3 stages and what happens at each one?

Answer 302

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

Question 303

pertussis

what does the physical exam show in adults? what are the two diagnosis methods? what types of cells are ususally elevated? what is the DOC?

Answer 303

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”

Question 304

acute bronchiolitis

what age group patients do you see this in? what size airways does this occur in? what is the most common cause and 3 others? what are two test you often do? what do you see on a chest xray? what drug do you want to use for treatment if RSV is present? what about if not?

Answer 304

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

Question 305

general bronchogenic carcinoma

“Lung cancer”

what is this the leading cause of? what are the two types? where are the four locations these mets are likely to spread? what is the main cause of these? what are 7 symptoms associated with lung cancer in general?

Answer 305

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

Question 306

small-cell carcinoma “oat cell”

is this fast or slow? WHERE IS IT LOCATED? what is the doubling time? what are the 6 paraneoplastic syndroms associated with it? what is the treatment? what is the difference between limited and extensive stage?

Answer 306

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

Question 307

what are the three types of non small cell carcinoma?

(NSLC)

Answer 307

1. squamous, central with cavitary lesions

2. adenocarcinoma (non smokers), periphreal

3. large cell periphreal very aggressive!

Question 308

which is more common, small cell or non small cell lung carcinoma

Answer 308

non small cell carcinoma

80-85% of LC

Question 309

squamous cell cancer

which cells does this occur in? where is it located? how can you dianose/what is major symtom? what is a random paraneoplastic syndrome associated with this? what is interesting about the metastsis of this? who is this most common in?

Answer 309

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

Question 310

adenocarcinoma

what is this the most common of? where does the cancer occur and where does it appear? what does it metastasize to? what is the treatment? what are two paraneoplastic syndromes? what can you get it from? smokers or nonsmokers?

Answer 310

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

Question 311

large cell cancer

where is this located? what is the doubling time? is there metastasis? what is the paraneoplastic syndrome? what is the treatment?

Answer 311

periphreal or centrally located

cavitation

rapid growth

early metastasis

doubling time 100 days

paraneoplastic syndrome: gynecomastic

TX: surgical

Question 312

pancoast syndrome

what is this?

Answer 312

combination of:

1. shoulder pain
2. horners syndrome
3. atrophy of the hand and arm muscles

See particullarly with squamous cell carcinoma

Question 313

bronchial carcinoid tumor

what type of tumor is this? where else is it commonly found? describe what this tumor would look like if you saw it? what does it secrete (4), what are two symptoms you can have with this? what is the treatment?

Answer 313

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

Question 314

solitary pulmonary nodules

what is the nickname for these? what makes it likely defined? what percent are benign/maligant? how do you diangnose? what are the three treatment for high, medium, and low maligancy risk?

Answer 314

“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

Question 315

explain the pathway for tumor diagnosis and determining removal?

Answer 315

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

Question 316

what are three symptoms that can help push you towards cancer?

Answer 316

1. hemoptosis
2. fever
3. weight loss

Question 317

how many Abx prescriptions does the CDC estimate are inappropriately prescribed a year?

Answer 317

10 million

holy cow

Question 318

what are 3 problems created from unneeded antibiotic use?

Answer 318

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

Question 319

what are four reasons that providers might overprescribe antibiotics?

Answer 319

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)

Question 320

what are the 3 groups of problematic pathogens we worry about?

Answer 320

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

Question 321

what percent of antibiotics that are prescribed are done so inappropraitely?

Answer 321

50% damn!

Question 322

what are 3 factors leading to development of resistance?

Answer 322

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

Question 323

what is the CDC’s get smart program?

Answer 323

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

Question 324

common cold/uri

how long does the virus last? do you give antibiotics? what should you give?

Answer 324

viral URI lasts 3-7 days

mucopurluent rhinitis is NOT an indication for abx

DO NOT GIVE ANTIBIOTICS!!

GIVE NSAIDS to help with symptoms

Question 325

acute pharyngitis

what percent of these are viral? what do you need to distinguis it from? what is the DOC if bacterial? what if allergic to this? what are the 5 symptoms you need to evalute for?

Answer 325

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

Question 326

acute bronchitis in normal host

do you treat this patient? what is the requirement for the length of time before giving them treatment? what are the two abx reccomended if they meet the criteria? what is the treatment for the different age groups?

Answer 326

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

Question 327

acute bacterial sinusitis

can you test for this? what are the three qualify presentations that make this “severe”? when do the guidelines suggest prescribing abx? what is the DOC? and if allergic?

Answer 327

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)
2. onset of severe symptoms with high fever >39* and purluent nasal discharge and facial pain lasting 3-4 days
3. 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

Question 328

what is the most common infection in children?

Answer 328

acute ottitis media

Question 329

acute ottitis media

do most of these typically resolve on their own? what two considerations would you prescribe abx? what is the DOC? and what about if they have had that in the last 30 days?

Answer 329

if you don’t treat with abx, the majority will clinically resolve in 7-14 days!

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

Question 330

what does exacerbation of COPD improve with?

Answer 330

often improves faster with abx and a short “burst” of steroids

Question 331

in the diagnosis of pharyngitis in a sexually active young adult, what do you need to consider?

Answer 331

gonococcal pharyngitis

this doens’t respond to penicillin or amoxicillin

Question 332

explain the difference between a shunt and alveolar dead space?

Answer 332

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

Question 333

is purluent sputum enough to give someone antibiotics?!

how long can the effusions last for AOM? antibiotics?

Answer 333

NO!!!!

viruses cause purlulent sputum too, consider more the length of time rather than the

AOM effusion can cause effusion for WEEKS!

Question 334

why are less antiobiotics being developed?

Answer 334

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

Question 335

the common cold is really what type of condition?

Answer 335

a RHINOSINUSITIS

Question 336

do you do a strep test for children < 3?

Answer 336

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

Question 337

if a patient has COPD or structual lung disease like CF and has acute bronchitis, do you treat them?

what about immunosuppressant patients?

Answer 337

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!

Question 338

in acute bacterial sinusitis, why is CT of sinuses not reccomended?

Answer 338

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!

Question 339

of the malignant lung tumors, what percent are from bronchogenic origin?

Answer 339

99%!

Question 340

Benign tumors

slow or fast?

what do they look like?

invasive or metastatic?

Answer 340

can be slow OR FAST

encapsulated, well demarcated/defined

not invasive or metastatic

Question 341

where do malignant tumors usually originate?

Answer 341

tracheobronchial mucosa (bronchogenic origin)

Question 342

what are 4 neoplastic random signs you can see with lung cancer and should keep in the back of your mind?

Answer 342

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

Question 343

is chest xray screening reccomended for general public?

Answer 343

NOPE!!

but can do Low dose chest CT for high risk patients

Question 344

what percent of solitary pulmonary nodules are primary lung cancer?

Answer 344

75%

Question 345

pulmonary solitary lesions

explain

always benign

likely benign

likely malignant

likely metastatic

Answer 345

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

Question 346

what is the overall survivale time for untreated small cell lung cancer?

Answer 346

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

Question 347

what two non small cell lung cancers have cavitation?

Answer 347

1. squamous
2. large cell

Question 348

TNM

**she said we don’t need to know the specific places they metastsize, just genreally what each stage means for involvemnet**

Answer 348

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!

Question 349

TNM

Answer 349

lymph nodes!

NX: not assessed

N0: no nodes

N1: mets in ipsilateral peri bronchial/hilar

N2: mets in ipsilateral mediastinal or subcarinal

N3: mets in contralateral bronchial/hilar/scalene/suprclavicular

Question 350

TNM

Answer 350

MX: not accessed

M0: no distant mets

M1: distant mets present

Question 351

where are four most common places for metastases for lung?

Answer 351

liver-common

bone-symptomatic

adrenal

brain

Question 352

On a ABG….

PaCO2 tells you….

PaO2 tells you…

together they tell you…

Answer 352

PaCO2 tells you….ventilation

PaO2 tells you…oxygenation

together they tell you…acid base relationship, PH

Question 353

mesothelioma

what cells is this in? what two places can this arise and which one is more common? what are three symptoms? what is the TX? what precent are dead after 1 year?

Answer 353

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

Question 354

*****which cancer is associated with paraneoplastic type syndromes******

what are the 6?

Answer 354

SMALL CELL CARCINOMA

associated with:

cushings (buffalo hump), cortico levels, hyponaturemia, SAIDH, periphreal neuropathy, eaton lambert, cerebral degeneration

Question 355

explain respiratory acidosis/alkalosis

and metabolic acidosis/alkalosis

Answer 355

Question 356

explain respiratory acidosis

PH

PaCO2

compensation?

Answer 356

decreased PH

Increased PaCO2

compensation: increase HCO3

Question 357

explain respiratory alkalosis

ph

Co2

HCO3

what are 7 causes

Answer 357

Over ventilation

Pain/anxiety

Hypoxemia high altitude

+/- Pulmonary embolism and pulmonary edema

Increased progesterone PREGNANCY

CNS irritation infection, tumors

Drugs theophylline, ASA, strychnine, doxapram

Question 358

Name 3 indications for ABG from respiratory cause

Name 5 indications for ABG from metabolic cause

Answer 358

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

Question 359

what are the two most common ABG sites?

Answer 359

1. radial
2. femoral

Question 360

what are 5 complications from ABG test?

Answer 360

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)

Question 361

what is a base excess/base deficiet? what is this indicative of?

Answer 361

indicative of metabolic process

amount of base or acid needed to titrate serum pH back to normal

Question 362

what two components of the equation must you consider when calculated the TOTAL CO2? what is the ration?

Answer 362

H2CO3 and HCO3

ratio: 1 : 20

a lot more HCO3

Question 363

what is the differnce of emia and osis?

Answer 363

emia is the finding

osis is the process

*consider this difference for pH*

Question 364

what is the most important concept to understand for ABG interpretation

Answer 364

Question 365

chronic broncitis=

emphysema=

Answer 365

chronic broncitis=conducting airways effected, bronchioles

emphysema=terminal alveoli effected

Question 366

explain the timing of response in ABG for:

chemical buffers

respiratory

renal

what is the significance of this?

Answer 366

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**

Question 367

in respiratory alkalosis explain:

pH

PaCo2

compensation

Answer 367

increase pH

decrease PaCO2

compensation: decrease HCO3

Question 368

metabolic acidosis:

1. anion gap
2. hyperchoremic normal anion gap

explain the concepts of both of these. what are the cations and what are the anions?

Answer 368

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

Question 369

explain four major causes of elevated anion gap for metabolic acidosis?

Answer 369

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

Question 370

what are two main causes of metabolic acidosis with NORMAL anion gap.

(this is caused with increase Cl)

2 THINGS

Answer 370

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

Question 371

metabolic acidosis with normal anion gap=

(why does it look normal)

Answer 371

hyperchloremic acidosis

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

Question 372

what are 3 major causes of metabolic alkalosis?

Answer 372

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)

Question 373

respiratory acidosis is caused by…

and leads to….

Answer 373

respiratory acidosis is caused by hypoventilation

and leads to hyperventilation

Question 373

when interpreting a ABG, how do you determine which one is compensating?

Answer 373

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