Pulmonary Pathophysiology Test

Front 1

Tell me all about Isoniacid

Back 1

highly-effective
inexpensive
eliminated by acetylation
SE: liver, periph neuorpathy

Front 2

Tell me all about Rifampin

Back 2

highly-effective
BUT expensive
Eliminated by cytP450
SE: liver, inc. metabo of other drugs, like oral coags, contraceptives, skin rashes, and urine may go orange

Front 3

Tell me all about Pyrazinamide

Back 3

highly-effective INTRACELLULARLY
SE: Liver, hyperuricemia

Front 4

Ethambutol

Back 4

not active intracellularly
SE: RETROBULBAR NEURITIS

Front 5

Streptomycin

Back 5

parenteral admin, so rarely used
aminoglycoside, affects ribosomal protein syn

NOT active intracellularly

SE: oto- and nephrotoxicity- ALL AMINOGLYCOSIDES have this, and must check with audiograms to make sure people are not losing their hearing by taking this drug

Front 6

What percent of patients will have active TB?

Back 6

10%

Front 7

Of the active TB patients seen, how many will progress within the first 2 years? (Progress means to see caseating nectrotic airways, very sick people with cough and malaise. Defined as going from INFECTION to DISEASE because of an inability to contain the infection.)

Back 7

HALF will progress (50%)

Front 8

If you're HIV+, what's your risk of TB going infection --> disease?

Back 8

8-10% ANNUALLY

Front 9

Up to 20% of positive TST are FALSE POSITIVES, what are the possible causes?

Back 9

Ifx with mycobacteria other than TB

or

BCG vaccine

Front 10

Up to 20% of individuals with active TB may be FALSELY NEGATIVE, what are the most common causes?

Back 10

1) critically ill TB patient
2) Immunosuppressed person
3) Recent TB infection

Front 11

What kind of testing do you want to do for TB?

Back 11

targeted testing, based on the idea that the accuracy oft he test depends on the prevalence of the disease in the population you're testing

Front 12

Goal of targeted testing in TB?

Back 12

identify persons at high risk for TB who would benefit by treatment of LTBI

Front 13

What are 2 things that put people at higher risk of TB disease?

Back 13

1) recent ifx with Mycobacterium Tuberculosis

2) presence of clinical conditions that are associated with an inc. risk of progression of LTBI to active TB

Front 14

TST in positive if you're in the Risk group, and your induration is...

Back 14

>/= 5mm

-HIV+
-recent contacts of TB case
-fibrotic changes on chest radiograph consistent with old TB
-patients with organ transplanta and other immunosuppressed patients receiving equiv of >15mg/day prednisone >1 month (corticosteroid >1month treatment increases the risk).

Front 15

What populations fall in the TST >/= 10mm induration as a positive test?

Back 15

-recent arrivals- <5yrs- from high prevalence countries
-IVDUs
-residents and employees of high-risk congregate settings- i.e. prisons, jails, nursing homes, hospitals, residential facilities for AIDS patients, and homeless shelters

-mycobacterial personnel
-persons with clinical conditions increasing their risk
-children under 4 and adolescents exposed to adults that are at HIGH risk

Front 16

What populations fall in the TST >/= 15mm induration as a positive test?

Back 16

Persons with no risk factors for TB, but DO NOT TEST THIS POPULATION

Front 17

STD of care for community in LTBI patient?

Back 17

Isoniazid daily for 9 months.

Front 18

Signs/Sx's of TB DISEASE:

Back 18

fatigue
malaise
weight loss
fever
night sweats
cough
hemoptysis

"Patients say they had it for weeks/months/years"

Front 19

CXR in Dx of TB:

Back 19

-95% of cases have abnormalities in apical/posterior segments of upper lobe, OR superior segments of lower lobe

-poss. unusual appearance in HIV+ pt.

-CANNOT confirm Dx of TB

Front 20

How many HIV+ patients have normal CXR?

Back 20

30%!!!

Front 21

How do you Dx TB?

Back 21

-AFB smear
PROBLEM: not sensitive OR specific

Instead, do MTB test!

Front 22

What do you do to TREAT TB Disease patients?

Back 22

4 drugs:
INH
Rifampin
Pyrazinamide
Ethambutol

Front 23

Summary of XDR-TB Conclusions:

Back 23

1) HIGHLY lethal
2) resistance in most cases due to transmission of XDR
3) suspect nosocomial spread

Front 24

3 key enzymes to HIV

Back 24

1) integrase
2) reverse transcriptase
3) protease

Front 25

Discuss the copathogenicity of TB and HIV

Back 25

1) TB causes IFN-gamma release from T cells, TB-activated macrophages release TNF and IL-1, BOTH of which enhance viral replication (TB ACCELERATES HIV)

2) one year mortality rate for treated HIV-related TV: 20-35%, 4X higher than HIVnegative patients

Front 26

How do you treat pulmonary complications of HIV, ideally?

Back 26

via a DEFINITIVE microbio/patho diagnosis, over empiric therapy, whenever possible

Front 27

What are the 4 Influences on Risk of Developed HIV-Assoc Pul Disorders?

Back 27

1) severity of immunosuppression
-CD4 count
2) patient's demographic charac
-how you catch your HIV helps w/ prognosis of assoc disease
3) place of current/prior residence
-What bugs are THERE????
4) Wherther using prophylaxis against common HIV-associated infections and HAART
-MOST IMPORTANT

Front 28

HIV-Assoc Pul Disorders:

Back 28

Gay HIV+ men less likely to devo TB and bacterial pneumonia

-blacks, hispanics, and IVDUs more likely to get TB

-Whites more likely to get PCP, KS, CMV

Front 29

Where do you most often see histoplasmosis?

Back 29

Ohio and Mississippi River Valleys

Front 30

Where do you most often see coccidiomycosis?

Back 30

Southwest

Front 31

Prophylaxis and HAART have helped to decrease what two HIV-Pul associated diseases?

Back 31

PCP and TB

-NOTE: HAART reduces the incidence of ALL opportunistic infections

Front 32

What is one indication of doing an HIV test because it might be the first presentation?

Back 32

recurrence of bacterial pnemonias

Front 33

Despite the availability of an effective prophylaxis and HAART this DISEASE is still the most common AIDS-indicator infection and an important cause of respiratory illness and death among HIV infected individuals?

Back 33

PCP!!!

Front 34

PCP Presentation

Back 34

-insidious
-gradual progression of SOB, fever, dry cough over weeks, but could also be seen as a rapid development over days

-MOST COMMON CAUSE of ARDS in patients with HIV

Front 35

What's the test used to rule out PCP, for the most part?

Back 35

LDH test, if it's not high, it's UNlikely to be PCP

Front 36

Agent of choice for Tx of PCP?

Back 36

Bactrim

-may need to start steroids too to calm down inflammation they're seeing

Front 37

HIV+, CD4 <200, what is something you do?

Back 37

prophylaxis with Bactrim to hopefully prevent PCP

Front 38

What is the key to a CMV diagnosis?

Back 38

Owl-eye appearance of the cells

Front 39

What would you like to see to Dx as CMV?

Back 39

-it can be seen in a non-pathogenic situation, so to confirm it as the culprit, would prefer to see tissue invasion and inclusion bodies

Front 40

How do you treat CMV?

Back 40

-HAART to restore immune fucntion
-ganciclovir or foscarnet, too

Front 41

Most common site of infx for cryptococcus neoformans?

Back 41

meninges

-Dx est. by seeing organisms on lung specimens but HIGH cryptococcal Ag titer on BAL may be suggestive; thick-walled organisms on an india ink stain

Front 42

Histoplasmosis

Back 42

-endemic areas, so see people from those areas in order to consider this

-may see miliary pattern on CXR

TREAT: amphotercin B, if more localized seen, then you may use itraconazole

Front 43

Aspergillosis

Back 43

-VERY immunosupressed to see it there
-rare in AIDS, but it's dreaded

again, wanna see tissue invasion to Dx, and tissue inflammation as a result is as bad as, if not worse, than the fungus itself

Front 44

Key to aspergillosus Dx?

Back 44

45-degree branching hyphae on the slides

Front 45

Where do you see blastomycosis endemic?

Back 45

midwest US, sotuhwest US, and Canada

-Dx with organism isolation
-treat with Amphotercin B
-SAME AS coccidiomycosis

Front 46

Kaposi's

Back 46

-most ocmmon malignancy in patients with HIV

-skin most common presentation

Front 47

What usually causes an ACUTE pneumonia?

Back 47

bacterial in origin

manifests intraalveolar exudate

Front 48

What usually causes a CHRONIC pneumonia?

Back 48

-viral, "atypical", intracellular bacteria, nocardia, actinomyces

-manifests as interstitial or granulomatous

Front 49

Pneumonitis, usually not infectious. What are they?

Back 49

Usually toxins or sometimes "atypicals"

Front 50

4 stages of pneumonia, assuming all goes well:

Back 50

1) congestion
2) red hepatization
3) grey hepatization
4) resolution

Front 51

CHARAC of Congestion Stage of Pneumonia

Back 51

heavy- red and boggy, airless, with vascular congestion
-see proteinacious exudate, few neutrophils, and intraalveolar bacteria

Front 52

CHARAC of Red Hepatization Stage of Pneumonia

Back 52

-firm, red, airless
-feels like a liver

Front 53

Define Bronchiectasis:

Back 53

PERMANENT dilatation of bronchi and bronchioles due to destruction of muscular layer and supporting connective tissue resulting from CHRONIC NECROTIZING INFECTIONS

-Clinically presents as a severe persistent cough and production of copious amounts of purulent sputum

Front 54

Define an abscess:

Back 54

localized collection of supprative necrosis within pulmonary parenchyma--> 1 or more LARGE cavities

Front 55

How does necrotizing pneumonia differ from an abscess?

Back 55

-nectrotizing pneumonia is a SIMILAR PROCESS TO AN ABSCESS, with multiple small cavitations

Front 56

Abscess is usually often a result of acute bacterial pneumonia, often caused by one of what 3 organisms?

Back 56

1) K. pneumonia
2) P. aeruginosa
3) S. aureus

Front 57

Atypical or Chronic Pneumonia CHARAC:

Back 57

Bugs:
-MYCOPLASMA
-legionella
-viruses
-chlamydia
-fungi

Gross: red-blue AND congested, patchy OR lobar

Complications: Diffuse alveolar damage, which is also seen in ARDS

-see thickened/edematous interstitial infiltrates that are lymphocyte rich (VARIES from typical/acute because those are alveolar in nature)

-difficulty breathing because of very poor air exchange

Front 58

What is is Histoplasmosis similar to clinically?

Back 58

it mimics TB

-fibrotic granulomas, veyr lamellar lookings see epithelioid histiocytes to define it as a granuloma

-lamellar-ness is JUST A CLUE, need to find the bug!

Front 59

ANYTHING GRANULOMATOUS, what tests do you definitely do?

Back 59

AFB (acid-fast), GMS/PAS (fungi) stains

Front 60

Aspergillous is highly invasive, especially in...

Back 60

LUNGS

Front 61

What is CHARAC of PCP on an H&E?

Back 61

-see the fluffy, cotton-candy like intraalveolar eosinophilic exudate

-with silver stain, see TONS of organisms

Front 62

CMV CHARAC on a slide...

Back 62

-interstitial pneumonia, owl-like inclusions within the cell

Front 63

Why are the upper part of the lower lobes OR the lower part of the upper lobes the main locales for TB ifx?

Back 63

thought to be because of the oxygen tension in those areas

Front 64

Ghon focus

Back 64

area of caseating necrosis within the lung

Front 65

Ghon complex

Back 65

area of caseating necrosis PLUS hilar adenopathy

Front 66

Secondary TB affects what part of the lungs?

Back 66

usually the apices
HIGHLY-CONTAGIOUS now

Front 67

If pneumonia is acute, what's its cause and what pathology do you see?

Back 67

bacterial

AND

intraalveolar exudates

Front 68

If pneumonia is chronic, what's its cause and what pathology do you see?

Back 68

viral, "atypical", fungal, intracellular bacteria, Nocardia, Actinomyces

AND

interstitial OR granulomatous

Front 69

Pnumonitis is caused by...

Back 69

a toxin

OR

"Atypical"- interstitial findings; usually it's not infections though

Front 70

Bronchopnemonia means

Back 70

more than one lobe and it's patchy

Front 71

Lovar pneumonia involves...

Back 71

part of whole of one lobe, and that's how you see >90% of Strep. Pneumonia

Front 72

What kind of pathology do you see with Histoplasmosis?

Back 72

noncaseating/fibrotic granulomas with a lamellar arrangement

Front 73

What stain is used on aspergillosis?

Back 73

GMS or silver stain

Front 74

What kind of histological finding do you see with PCP that is somewhat unique?

Back 74

cotton-candy appearance
-using the GMS stain there to visualize the bugs

Front 75

CMV has what unique histo finding?

Back 75

owl-eye intranuclear inclusions

Front 76

Ghon focus is a...

Back 76

primary lesion caused by mycobacterium bacilli (tuberculosis) developed in the lung of a previously uninfected individual.

Front 77

What do you use to stain for Mycobacterium Avium Intracellulare

Back 77

Acid-Fast Stain

-it's uncommon if you're immunocompentent, BUT in AIDS patients it causes disseminated ifx's

Front 78

What are the 5 causes of hypoxemia?

Back 78

1) V/Q mismatch
2) low FiO2
3) diffusion barrier (almost never a cause at rest)
4) shunt
5) hypOventilation

Front 79

If you are talking about a suspected COPD patient, but they lack obstructive disease, what do you make as the diagnosis?

Back 79

chronic bronchitis SOLELY is the diagnosis.

Front 80

What are the main drugs used in obstructive lung disease?

Back 80

bronchodilators
anti-inflammatory agents, ESPECIALLY glucocorticosteroids
mucoavtive agents
and antimicrobials

Front 81

Distinguish between Asthma AND COPD:

Back 81

Obstruction:
Asthma- REVERSIBLE
COPD- Poorly reversible

Inflammation:
Asthma- CD4s and Eosinophils
COPD- CD8s, neutrophils, and macrophages

Front 82

In COPD describe the mechanism of destruction of lung tissue:

Back 82

inflammatory cells, mainly neutrophils and macrophages, act via proteases and ROS to:

1) destroy lung tissue
2) create mucus cell hyperplasia and hypersecretion

Front 83

In asthma, what's the mechanistic basis of constriction?

Back 83

ROS and eosinophils are acting on the epithelium and smooth muscle.
-vagus nerve is affected too

Front 84

What do methylxanthines do for asthmatics?

Back 84

they can help to improve diaphragmatic breathing functions

Front 85

What do you use leukotriene antagonists?

Back 85

the substances are very potent SM constrictors normally, so wanna BLOCK their action.

Front 86

Why would you give anticholinergics to an asthmatic?

Back 86

they act to decrease the mucous hypersecretion
-perhaps they may relax the smooth muscle as well

Front 87

What are the major group of drugs used in COPD?

Back 87

ANTICHOLINERGICS

Front 88

What's the most important target of drug therapy in obstructive lung diseases?

Back 88

Inflammatory cells and their products

Front 89

What's bad about using GCsteroids in a patient?

Back 89

-they are systemically active!
-lots of SEs
-want to avoid oral/systemic prolonged steroids

Front 90

Major effects of GCsteroids:

Back 90

-bronchial hyperreactivity (no direct dilation)
-increase airway caliber
-reduce freq. of asthma exacerbations

Front 91

What is the major class of drugs used for asthmatics?

Back 91

beta-agonists

Front 92

What is the major class of drugs used for COPD?

Back 92

anticholinergics!

Front 93

How do we make the diagnosis of asthma?

Back 93

it's a reversibility issue, so when you give bronchodilators, i.e. Beta-agonists, you see an increase in the %FEV, and that shows that it's an asthma patient because their exacerbation is reversible, as opposed to COPD which wouldn't respond very much to the Beta-agonists

Front 94

What's a good chronic drug of choice for asthmatics?

Back 94

salmeterol, it's a long-acting, with a slow onset and longer half-life, so don't use in acute exacerbation, but good for management of asthma

Front 95

What is most commonly used to potently dilate the bronchi in a short-term scenario of asthma attack?

Back 95

albuterol

Front 96

Leukotrien receptor antagonists act on which subtypes?

Back 96

C4
D4
E4

NOT B4, that's done by LOX inhibitors, but those drugs are much more toxic

Front 97

Which drugs might you nebulize?

Back 97

1) beta-agonists
2) anti-cholinergics
3) glucocorticosteroids

Front 98

How do you diagnose BPD?

Back 98

-positive pressure ventilation during the 1st 2 weeks of life for a minimum of 3 days
-clinical signs- abnormal resp. function
-KEY: requirements for supplemental O2 longer than 28 days of age to maintain pO2 above 50mmHg
-CXR w/ diffuse abnormal findings charac of BPD

"Chronic oxygen dependency with certain radiologic features at 28 days of age"

Front 99

What radiologic findings do you see in BPD?

Back 99

Stage I:
ground-glass appearance, similar to HMD

Stage II:
Whiteout BUT IT'S SELDOM SEEN

Stage III:
Same patient at 1 month of age shows the development of small cystic lucencies in the lungs.

Stage IV:
7 mo of age shows small cystic lucencies have coalesced into larger lucencies with interspersed fibrotic stranding. Hyperinflation.

Front 100

Oxygen facts in a BPD baby:

Back 100

-O2 sat needs to be >/=90-92%
-wean daytime b4 nighttime- need O2 at night due to underventilation
-hypoxia associated with failure to gain weight
-chronic hypoxia will lead to pul HTN

Front 101

What can you say about fluids in BPD babies?

Back 101

fluid intake and calories are related, they need 110-140 CC/KG/day necessary to get the needed calories, but you have to monitor closely so you're not giving them too much fluid and causing that now rarely-seen Stage II whiteout due to pulmonary edema

Front 102

What are 2 electrolyte imbalances you must consider in a BPD baby?

Back 102

hyponatremia

AND

hypokalemia

-also think of volume depletion with alkalosis
-lasix could cause some issues, too

Front 103

Would you use bronchodilators in a BPD baby?

Back 103

-quite possibly, YES
-Tx occurs with inhaled albuterol and atrovent, and they've shown beneficial short-term effects in lung mechanics

Front 104

What charac. an exacerbation of Chronic Lung disease?

Back 104

rales
retractions
tachypnea
desaturations
CO2 retention
increasing oxygen requirement

Front 105

How do you manage an exacerbation of CLD?

Back 105

oxygen
bronchodilators
diuretics
MAY need vent. support

Front 106

What is the most common cause of hospital admission in the 1st year of life?

Back 106

RSV-based bronchiolitis

Front 107

Define & describe bronchiolitis:

Back 107

-acute LRI w/ inflamm of small airways of infants
-in winter see SPIKE in RSV ifxs
-may also be caused by parainfluenza and influenza virus

Front 108

Risk factors of an RSV ifx

Back 108

LBW
prematurity
Low SES
crodwed living coniditions
parental smoking
day care
absence of breast feeding

Front 109

RSV infectivity CHARAC:

Back 109

-incubation of 2-5 days
-nasal viral shedding of 6-21 days
-secondary ifxs from fam members 46% of the time, 98% due to other kids in day care and 42% hospital staff

Front 110

RSV Presentation in infants/toddlers up to age 2

Back 110

fever
cough
dyspnea
wheeze
cyanosis: bronchiolitis, pneumonia

Front 111

RSV Presentation in children >2y/o

Back 111

febrile rhinitis
pharyngitis

Front 112

RSV Presentation in older children and adulta

Back 112

COMMON COLD

Front 113

With RSV, when greater than 2 years old, we don't get bronchiolitis, but...

Back 113

we have it in our nose and can easily spread it.

Front 114

RSV clinical features

Back 114

-profuse coryza (cold in the head)
-congestion
-low-grade fever
40% go to be an LRI w/in 2-5 days
cough
dyspnea
wheezing
feeding difficulties
usually fever has resolved
severe: FLARING, retractions, cyanosis

Front 115

RSV course is mild, and what do you see?

Back 115

func recovery- 5-7days
cough usually <2 weeks
CXR clear w/in 9 days
temporary immunity for THAT SUBTYPE

Front 116

What's the other virus, that's similar to RSV?

Back 116

hMPV, aka Human Metapneumovirus
-no good test for it!
-usually mild RTI, perhaps slightly milder than those caused by RSV
-sevrere RTI not uncommon in young children and IC pts.
-risk groups: children, elderly, Immunocomp people

Front 117

Babies in first 2-3 months of life with RSV are particularly at risk to develop...

Back 117

apnea

-typically premie
-<44weeks postconceptual age
-central, but not obstructive
-may be presenting symptom
-lasts for a few days, as they get over the acute ifx, it tends to resolve

Front 118

RSV Bronchiolitis has what indications for admission?

Back 118

HYPOXIA IS THE MOST IMPORTANT ONE!!!

-sustained O2 sat less than 90 or 92% in room air
-<6 months of age ESPECIALLY
-cannot maintain oral hydration
-markedly elevated resp rate
-CLD Tx'ed with O2
-CongenHD with Pul HTN

Front 119

Bronchiolitis hospitalization

Back 119

-median stay is 3-5 days
-vent for 5 days, O2 for 7, and discharge by the 9th day

Front 120

Bronchiolitis CXR

Back 120

-bilat perihilar and patchy parenchymal infiltrates
-peribronchial cuffing
-hyperinflations with flattened diaphragms
-atelectasis esp RUL or RML

Front 121

When does Bronchiolitis pt. get admitted to ICU?

Back 121

-O2 sat less than 92% when 50$ FiO2
-pCO2 >50mmHg
-extrapul Sx's
-arrythmia
-Congen HF
-Apnea

Front 122

SUPPORTIVE CARE/Tx of Bronchiolitis is treated how?

Back 122

-admin humidified O2
-nasal suctioning to clear the upper airway
-monitor for apnea, hypoxemia, and impending resp. failute
-normalize the body temp
-rehydrate orally or by IV
-monitor hydration status

Front 123

How do you treat the baby airway obstruction?

Back 123

-trial bronchodilator, and if clinical response, then use to treat

Front 124

Are steroids indicated in uncomplicated simple bronchiolitis?

Back 124

NO

Front 125

What is synagis?

Back 125

-reduced hospitaliztions by 55% in high-risk groups
-monthly admin necessary during RSV season but costs $1,000/dose for 4 months

Front 126

What are the JUSTIFIABLE RSV therapies:

Back 126

-supportive Tx
-nebulized epi
-mech vent
-trial of Beta-adrenergics

Front 127

What are the RCT-necessary RSV therapies:

Back 127

-physiotherapy
heliox
exogenous surfactant

Front 128

Apnea baby definitions

Back 128

>15 secs for full-term
>20 secs for preterm

Front 129

ALTEs CHARAC:

Back 129

-high recurrence risk
-not predictive of SIDS
-most common cause is idiopathic

-see them in ER with relative frequency

Front 130

Define SIDS:

Back 130

-sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including review of clinical history, performance of complete autopsy, and examination of the death scene
NEED ALL OF THESE!!!

Front 131

What's the big high-risk group for SIDS?

Back 131

prematurity

-peak age range 2-4 months
-males
-expossure to cigarette smoke
-hyperthermia

Front 132

Keys to Michael Light Infant Pul Death Lecture:

Back 132

-incidence of SIDS has declined dramatically int he last 15 years since the intro of Back 2 Sleep campaign
-smoking and co-sleeping remain risk factors for SIDS
-home monitors should NOT be prescribed to prevent SIDS

Front 133

Cystic Fibrosis lungs show..

Back 133

-bronchitis
-bronchiectasis
-pulmonary abscesses arising in the bronchi

Front 134

What's the incidence of CF?

Back 134

Caucasians:
1/2500 get it, 1/25 carry gene

AfrAmer:
1/15000 get it, 1/61 carry gene

AsianAmer:
1/31000 get it, 1/88 carry gene

Front 135

Major CF Sx's:

Back 135

-respiratory are HALF of all

-FTT/malnutirion
-steatorrheal/abnl stool
-meconium ileus/intestinal obstruction
THOSE 3 together make up a lot of the GI and malnutrition problems

MAIN FEATURES:
malnutrition
failure to thrive
diarrhea-like disease

Front 136

What's the basis of the CF defect?

Back 136

There's a deficient Cl' channel, and so you don't have Cl- REABSORPTION, and thus Cl- is on the outside, and keeps Na+ with it

Normal Cl- is 10-30mequiv/L

Positive Test: 60+
Intermed: 30-60

Front 137

Cl- Test is positive for CF when?

Back 137

Positive Test: 60+
Intermed: 30-60

Front 138

How many patients with CF present initially with meconium ileus?

Back 138

10-15%

-but when they present this way, MUST DO SWEAT TEST ON ALL OF THEM

Front 139

If you see rectal prolapse, what do you do next?

Back 139

SWEAT TEST!

-even if basal polyposis and they have allergies, do the sweat test there too

Front 140

What percent of infants with meconium ileus also have CF?

Back 140

NINETY (90%) PERCENT!

Front 141

If an infant has an intestinal obstruction or perforation in utero, do you do a sweat test?

Back 141

YES!

Front 142

Define Pancreatic insufficiency:

Back 142

-severe exocrine pancreatic disease with documented nutrient maldigestion
-requires pancreatic enzymes with meals
-supplement food with those enzyme, and the disease can start very early and be progressive with time

Front 143

Define Pancreatic Sufficiency:

Back 143

-mild/moderate exocrine pancreatic disease
-not severe enough to produce nutrient maldigestion
-do not require pancreatic enzymes with meals

Front 144

What's the basis of the pancreatic issues in a CF patient?

Back 144

There is a concentrated acidic protein secretion that blocks the tubular region and prevents the enzymes from ever even having the chance to get out

Front 145

DO a serum immunoreactive trypsinogen test in a patient with suspected CF, what do you look to see?

Back 145

a HIGH serum-level

Front 146

Describe height/weight of CF patients?

Back 146

they're shorter and thinner than normal folks

Front 147

If the CF patient has GI/pancreatic issues, what do you do to Tx?

Back 147

-give pancreatic enzyme supplements
-vitamin supplments
-high-calorie diet
-emphasis on good bowel regimen

Front 148

Newborn screening for CF follows what steps?

Back 148

-Measures the IRT- immunoreactive trypsinogen
-elevated levels get sent for genetics
-follow-up with a sweat test

Front 149

What disease is related to CF in 8-15% of patients?

Back 149

CFRD- CF-related diabetes

Front 150

What causes CFRD?

Back 150

-acinar atrophy
-fatty infiltration
-fibrosis
-dec. in # of pancreatic islets

NOT an autoimmune process
-diabetic ketoacidosis is an exception

Front 151

A small portion of CF patients see what other disease appear?

Back 151

-cholestasis, duct obstruction in the liver, so it's an overt liver disease

Front 152

CF liver disease accounts for how much mortality?

Back 152

1-2% of CF mortality

Front 153

Why do CF patients have airway problems?

Back 153

the airway fluids are underhydrated and that creates constant cough, along with a gelatinous, tenacious fluid there, when you really need mucociliary clearance to be functioning, and it's just TOO thick

Front 154

What is the major cause of morbidity and mortality in CF patients?

Back 154

MAJOR PATHOGENS:

staph. aureus and haemophilus influenzae often lead to the ability to be Ifx'ed with pseudomonas which is the ultimate killer


-also see:
Burkholderia cepacia- can cause rapid and severe advanced disease, also even septicemia

-atypical myco- can lead to more aggressive disease

-aspergillus- and it's not the aspergillus that is so brutal, but RATHER the allergic response to it- called ABPA that causes all the damage, and the most common patient pop for ABPA is CF patients

Front 155

Most common people to get ABPA?

Back 155

CF patients

Front 156

Do a lot of CF patients get pseudomonas disease?

Back 156

YES! Up to 80% over the course of the disease!!!

Front 157

What is the issue with CFTR in CF patients?

Back 157

it prevents the OUTFLOW of Cl- ions into the extracellular space when the channel is mutated

Front 158

How do you Tx CF:

Back 158

bronchodilators- albuteral
chest physiotherapy
rhDNase
Abx- Staph aureus and p. aeruginosa ESPECIALLY
-inhaled ABX
-macrolide Abx as a protection for anti-inflammation
influenza vaccine
corticosteroids
ibuprofen

Front 159

Classes of CFTR Mutation

Back 159

Class 1: no synthesis
Class 2: no maturation
Class 3: blocked regulation
Class 4: decreased conductance
Class 5: decreased abundance

class 3 and 4 may see various other mutations, but having the same degree of function

Front 160

Class 1,2, and 3 mutations give what grade of disease?

Back 160

SEVERE
-PI
-meconium ileus
CFRD
severe hepatobiliary disease

Front 161

Class 4 and 5 mutations give what grade of disease?

Back 161

Mild
pancreatic sufficiency
risk of:
acute pancreatitis
-recurrent pancreatitis
-chronic pancreatitis

Front 162

What Tx do you give to try and fix the truncated proteins of CF?

Back 162

Gentomycin!
-can bridge truncation and correct the protein, intervenes on the stop codons!

Front 163

What repro sys issues does CF deliver?

Back 163

-obstructive azoospermia

-can't conduct through the vas deferens!

Front 164

2 aspects of breathing volumes affected by a restrictive lung disease?

Back 164

1) decreased Vital Capacity, leading to:
2) DEC TLC

Recall Vital Capacity = IRV + ERV + TV

Front 165

What are all the extrinsic restrictive diseases?

Back 165

-pneumothorax
-pleural effusion
-pleural thickening as in asbestosis
-scoliosis
-ankylosing spondylitis
-polimyelitis
-GBS
-ALS
-Myasthenia gravis
-muscular dystrophies

Front 166

What are the disease of the lung parenchyma?

Back 166

-idiopathic pulmonary fibrosis
-sarcoidosis
-hypersensitivty penumonitis- extrinsic allergic alveolitis
-radiation-induced fibrosis
-collagen vacular-related fibrosis
-lymphangitis carcinomatosis

Front 167

Which type of collagen do you see in restrictive lung disorders?

Back 167

Collagen Type III

Front 168

An indication of restrictive lung disease is...

Back 168

preservation of the FEV1/FVC ratio!!!

Front 169

What is the test you would do with a suspected restrictive lung disease patient to show really strong indications of it being present? Think oxygen.

Back 169

6 minute walking test

-RLD patients OFTEN desaturate very early on in disease because of the disease's patchiness

Front 170

What do you see, in general, histologically with restrictive lung disease?

Back 170

cast-like blue collagen and hyaline, which is a result of the chronic injury to the epithelial cells

Front 171

Progressive fibrosis is seen in what part of the lungs?

Back 171

it progresses at the BASES of the lungs

-see O2 saturation dropping
-pul vasc resist INC, with co-existing or even primary vasc disease AND destruction of pul artieroles and capillaries

-pul HTN develops leading to cor pulmonale
-starts in the bases of the lungs and with exercise you'll really exacerbate the disease

Front 172

Where do you see honeycombing?

Back 172

in Usual Interstitial Pneumonia

Front 173

Distinguish the patterns of UIP and NSIP

Back 173

UIP:
heterogeneous, patchy

NSIP Fibrotic + Cellular:
-homogenous, all looks the same
-other samples of this would appear cellular and homogenous

Front 174

IPF Chief Complaint:

Back 174

shortness of breath and/or cough for several months

Front 175

Onset of IPF

Back 175

-variable
-usually age 50-70
-familial disease, SO ASK FAM Hx

Front 176

Clinical Presentation of IPF:

Back 176

-progressive dyspnea on exertion
-cough, usually nonproductive and dry
-Clubbing in HALF OF PATIENTS
-bibasilar end-inspiratory crackles
-bibasilar, subpleural reicular opacities on CXR and HRCT
-restrictive pul phys with reduced lung columes and DLCo and WIDENED AaPO2

Front 177

What are the MAJOR criteria of IPF?

Back 177

-no known other causes of interstitial lung disease
-abnorm pul func studies
-abnorm CXR/HRCT scan
-No histo or cytological features supporting another diagnosis- MOST COMMON: IFX!

Front 178

When you hear "velcro" sounds, and the duration of illness is >/= 3 months, think what disease?

Back 178

after having ALL the major criteria, think IPF!

Front 179

What are the 2 parts to the path of UIP?

Back 179

1) periph accentuation of disease
2) transition into uninvolved lung

Front 180

In what part of the lung do you typically see UIP?

Back 180

usually subpleural and more prominent in lower lobes

Front 181

What does general anesthesia do to FRC?

Back 181

DEC by about 16%/500ml

-also creates V/Q mismatch and hypoxemia

Front 182

Why do you see hypoxemia due to V/Q mismatch?

Back 182

2 things:
1) INC dead space ventilation: more vent to NON-dependent areas of the lung
2) INC shuntlike- INC perfusion to POORLY VENTILATED dependent areas of the lung

Front 183

What happens to lung volumes after abdominal surgery?

Back 183

DECREASES IN:
TLC
FRC
RV

Front 184

Which affects lung volumes more, Upper or Lower Abdo surgery?

Back 184

UPPER

Front 185

What's the normal closing volume and what happens to it with surgery?

Back 185

it's normally about 30% of TLC and it's the vol at which flow from the dependent parts of the lungs stops during expiration due to airway closure, so it INCREASES with surgery

Front 186

How do you predict post-op FEV1?

Back 186

FEV1ppo = Actual pre-op FEV1 x %perfusion of the lung to remain, determined by an isotope scan

Equation 2:
FEV1ppo as a % of the normal

Front 187

When trying to determine whether a patient is a candidate for a pneumonectomy, what is the required FEV1ppo?

Back 187

>80%

if 40-80 then look at symptoms, and if <40% predicted, don't do the surgery if their Blood Gases don't look good.

Front 188

How do you treat post-cardiac injury syndrome?

Back 188

NSAIDs and corticosteroids work well!

Front 189

Esophageal surgery post-op pul complications:

Back 189

25-50% incidence
BUT
40-60% of operative MORTALITY!!!

-there is recurrent laryngeal nerve injury
-pleural effusion is possible

Front 190

What do you measure with an incentive spirometer?

Back 190

IC = IRV + VT

Front 191

How does the expiatory curve get shifted in restrictive disorders?

Back 191

TO THE RIGHT

Front 192

Why does respiratory failure in chest bellows disorders show hypercapnia?

Back 192

see increased work of breathing
leading to
decreased Tidal Volume and thus INC dead space
leading to
alveolar hypOventilation
leading to
the Hypercapnia, and acidosis

Front 193

What is one of the major presenting features of Guillen-bairre Syndrome?

Back 193

-see a RAPID progressive parethesias and muscle weakness initially in the legs, and then later on the arms, followed by dyspnea and weak cough, with an inability to clear secretions

Front 194

What's the main cause of hypoxemia in chest bellows disorder patients experiencing respiratory failure?

Back 194

V/Q mismatch

Front 195

If you dip below what level of respiratory muscle strength do you see problems, and what is the problem?

Back 195

if you drop under 50% and it's an issue with hypercarbia

Front 196

Why do a sniff test, and what does it show if positive?

Back 196

have the patient "sniff" the air, and the diaphragm should go DOWN, but with a hemidiaphragmatic paralysis, see the paralyzed side GO UP!!!

Front 197

DIP shows what?

Back 197

numerous macrophages in the alveolar spaces in a diffuse and uniform manner
-see type II pneumocyte hyperplasia and desquamation into the air spaces

-mortality: <20%
-smokers: 90% OF THE PATIENTS WITH THIS DISEASE

Front 198

Respiratory Bronchiolitis-Associated Interstitial Lung Disease is strongly associated with...

Back 198

smoking cigarettes

-more affinity for airways
-not as diffuse as DIP
-see broncioles with a lymphocyte infiltrate extending into the interstitium creating the picture of an interstitial disease

PROGNOSIS is much better than DIP and UIP

Front 199

Where do you see NSIP?

Back 199

-patients suffering from connective tissue disease, hypersensitivity reactions, and even due to drug toxicity

-uniform pattern with mononuclear infiltrates and different grades of fibrosis

Front 200

lymphoid interstitial pneumonia is...

Back 200

considered a lymphoproliferative disorder associated occasionally with immunsuppression

Front 201

giant cell interstitial pneumonia is...

Back 201

a hard metal pneumoncniosis assoc with exposure to cobalt

Front 202

Reaction to the inhalation of organic dusts or biologic aerosolized particles int he environment

Back 202

hypersensitivty pneumonitis/extrinsic allergic alveolitis

APPEARS AS A RESTRICTIVE PATTERN

Front 203

Farmer's lung is caused by...

Back 203

thermophilic actinomycetes

Front 204

bird fancier's lung is due to...

Back 204

pigeon breeder's lung, Ag present in bird poop, feathers, or serum proteins

Front 205

Chronic Hypersensitivty pneumonia presents with.,..

Back 205

chronic bronchiolitis
NSIP pattern
scattered granulomas

Front 206

What are the complications of asthma?

Back 206

infection
bronchiectasis
cor pulmonale
emphysematous changes
status asthmaticus

Front 207

Wegener's Granulomatosis

Back 207

charac. by presence of nectrotizing granulomatous inflammation and vasculitis

-affects upper respiratory tract, causes:
sinusitis
otitis
nasal disease
ear pain
oral lesions

lower resp tract sees:
multiple lesions

kidneys get affected by glomerulonephritis

PATIENTS HAVE ANTRINEUTROPHIL ANTIBODIES- ANCA- in serum

Front 208

lung hemorrhage, glomerulonephritis, antibodies against basement membrane, with Ag being collagen IV

Back 208

Goodpasture's Syndrome

Front 209

Rheumatoid Arthritis

Back 209

Patient presents with pleuritis, pleural effusion, chronic interstitial pneumonia resembling UIP, bronchiolitis, vasculitis, and necrobiotic nodules

Front 210

Charcot-Leyden Crystals and Eosinophils

Back 210

Asthma!

-see basement membrane thickening, too

Front 211

pleuritis with pleural effusion, interstitial pneumonitis, DAD, hemorrhage, and vasculitis

Back 211

Sys Lupus Erythematous

Front 212

hypersensitive vasculopathy, chronic interstitial pneumonia with prominent fibrosis being the usual findings

Back 212

Systemic Sclerosis or a scleroderma

-also think PUL HTN when you see this

Front 213

Histo findings of sarcoidosis:

Back 213

presence of collections of histiocytes and multinucleated giant cells

-granulomas have a distribution along the bronchovascular bundles
-rare in ppl <15 or >65
-blacks > whites
-T-cells mediate the granulomatous inflamm and thought to be due to an inhaled Ag rxn

Front 214

Irreversible increase in size of air spaces distal to the terminal bronchioles

Back 214

emphysema

Front 215

2 types of emphysema:

Back 215

1) centrilobular- proximal portion of term bronchiole is affected
ASSOC WITH CIG SMOKING
-it's the func impairment that does, because of great damage to the alveolar-capillary wall and reduced elastic recoil

2) panacinar- ENTIRE resp bronchiole is effected
seen in elderly patients
also in A1A deficiency patients

NEITHER OF THESE IS RESPONS FOR CLINCAL COURSE THOUGH

Front 216

What is the pathogenic basis of emphysema?

Back 216

IMblanace of proteases and antiproteases like A1A

-the antiproteases are made in the liver and if there's low production that could lead to a problem, or if the oxidative effects of cig smoke affected them, the elastic arch of alveolar septae may be destroyed

-emphysema occurs in ~15% of smokers

Front 217

What are the major clinical Sx's of acute interstitial pneumonia?

Back 217

cyanosis and SEVERE hypoxemia

BUT there is no catasrophic event precipitating it, so it's called idiopathic ARDS

Front 218

What is the histologic pattern of ARDS?

Back 218

diffuse alveolar damage with:
-fibrinous exudates
-hyaline membranes
-interstitial edema
-type II pneumocyte hyperplasia

HOMOGENEOUS APPEARANC

Front 219

What kind of ifx in an immunosuppressed person could lead to acute interstitial pneumonia?

Back 219

VIRAL ifx

Front 220

How does an IPF patient present?

Back 220

insidious presentation and PROGRESSIVE course, which is fatal in 5-6years

Front 221

What does HRCT shown in IPF?

Back 221

a PERIPHERAL honeycombing pattern!

Front 222

How do you treat UIP?

Back 222

cyclophosphamide, if anything

Front 223

-numerous macrophages in the air spaces in a diffuse and uniform manner
-thickening of the alveolar septae with mild pneumonitis
-type II pneumocyte hyperplasia

WHAT IS IT?

Back 223

desquamative interstitial pneumonia

-disease of mainly cig smokers
-affects lung homogeneously

Front 224

-more affinity for airways
-less diffuse than other interstitial diseases
-macrophages in alveoli and bronchioles

Back 224

respiratory bronchiolitis, associated with interstitial lung disease

-could be the same as DIP but in different stages
-related to cig smoke, too!

Front 225

Interstitial lung disease with good prognosis and responsive to steroids

Back 225

non-specific interstitial pneumonitis/fibrosis

Front 226

Histology pattern is uniform w/ mononuclear infiltrates and different grades of fibrosis

Back 226

NSIP

-homogeneous appearance

Front 227

Interstitial disease due to the exaggerated reaction to the inhalation of organic dusts or biologic aerosolized particles in the home or work environment

Back 227

hypersensitivity pneuonitis

-may result in severe fibrosing disease with continuous chronic exposure to the antigens

Front 228

#1 treatment for hypersensitivty pneumonitis?

Back 228

REMOVE THE ALLERGEN

Front 229

What immune rxn is seen in hypersensitivty pneumonitis?

Back 229

type II, sometimes some type IV with granulomas present

Front 230

Chronic hypersensitivty pneumonitis presents how?

Back 230

-acute exacerbations less frequent
-progressive respiratory insufficiency
-dyspnea
-cyanosis
-hard to tell from other chronic interstitial pneumonitis because total pul capacity is reduced
-may see:
honeycombing, loss of volume, and ground-glass opacities

Front 231

See Charcot-leyden crystals, who makes em' and why?

Back 231

ASTHMA!
-made by eosinophils

Front 232

Multisystemic disorder charac by:
-necrotizing granulomatous inflammation
-vasculitis

Back 232

Wegener's granulomatosis

AFFECTS:
URT-sinusitis, otitis, nasal disease, oral lesions
LRT
Kidneys

Front 233

What is the key finding that will tell you "IT'S WEGENER'S!!!"?

Back 233

ANCA
antineutrophil cytoplasmic antibodies with either the cytoplasmic/classic or perinuclear presentation

Front 234

Autoimmune disorder consisting of the triad of:
1) glomeulonephritis
2) lung hemorrhage
3) anti-basement membrane antibody formation.

Back 234

Goodpasture's syndrome

Ab's are to collagen IV

Front 235

Pleuritis
pleural effusion
chronic interstitial pneumonia
resembles UIP
bronchiolitis
vasculitis
and
necrobiotic nodules

Back 235

Rheumatoid Arthritis

Front 236

Sarcoidosis demographic

Back 236

women > men
blacks > whites
granulomatous disease
world-wide dist.
T-cells mediate the inflamm, which is thought to be due to an inhaled Ag

Front 237

What's a very possible diagnosis when seeing a presentation involving bilateral hilar adenopathy?

Back 237

sarcoidosis, especially if a female and/or black ethnically.

Front 238

What tumors are centrally located?

Back 238

squamous cell

AND

small cell

Front 239

Breath Sounds, Resonance, and Fremitus of:

Pleural Effusion

Back 239

Breath Sounds: DEC
Resonance: DULLNESS
Fremitus : DEC

Front 240

Breath Sounds, Resonance, and Fremitus of:

Pneumonia- lobar

Back 240

Breath Sounds: might be bronchial
Resonance: DULLNESS
Fremitus : INC!!!

Front 241

Breath Sounds, Resonance, and Fremitus of:

Pneumothorax

Back 241

Breath Sounds: DED
Resonance: HYPERRESONANT
Fremitus : ABSENT

Front 242

How does the trachea displace when there's a collapse?

Back 242

TOWARDS the lesion

Front 243

Tension pneumothorax, which was does the trachea deviate?

Back 243

AWAY from the lesion, you've put pressure on one side, so trachea will be pushed by that pressure.

Front 244

What parts of the lung are usually involved in bronchiectasis?

Back 244

lower lobes, extending from hila to periphery

Front 245

How do you Dx bronchiectasis?

Back 245

CT! Most likely, HRCT to see honeycombing. See those signet rings, too.

Side note: Histologically, see a heterogeneous pattern.

Front 246

3 bugs that are most common causes of acute sinusitis, otitis media, and chronic bronchitis?

Back 246

S. pneumo
Morraxella Catarrhalis
H. Influenza

Front 247

What's the leading causes of death in AIDS patients?

Back 247

TB!

Front 248

What are the more likely risk groups for HIV-associated TB?

Back 248

blacks
hispanics
IVDUs

Gays are NOT more likely.

Front 249

Where in the lungs do you see reactivation TB?

Back 249

Apical areas

-like Dr. Goljan says, they're strict aerobes, so need to go to the place with the most air to grow, thus the apical regions!

Front 250

Key findings to make you think TB:

Back 250

-night sweats
-hemoptysis
-cough >3 weeks
-cough w/fever >3 days
-weight loss

Front 251

Atypical pneumonia causes:

Back 251

mycoplasma
viral
legionella
chlamydia, which presents more insidiuously

Front 252

Nosocomial pneumonia implies...

Back 252

gram negative and resistant

Front 253

The bugs of bronchopneumonia

Back 253

by definition, involving more than 1 lobe:

-staph
-strep
-H. influenza
-P. aeruginosa

Front 254

Bugs of lobar pneumonia

Back 254

>90% due to strep. pneumonia
-also can see Klebsiella

Front 255

What are the physical exam findings of pneumonia?

Back 255

INC:
fremitus
dullness
egophony
bronchial breath sounds

Front 256

What's a key radiologic finding of atypical pneumonia?

Back 256

widening of the interstitium
-interstitial infiltrate predominantly lymphocyte rich
with proteinaceous exudates in the alveolar spaces
-DON'T see many cells in the exudates

Front 257

What are the findings of mycoplasma pneumonia clinically/radiologically?

Back 257

bronchial wall inflamm w/ non-purulent patchy interstitial infiltrates

-assoc. with cold agglutinins- IgM

Front 258

What are good drugs to treat mycoplasma pneumonia?

Back 258

B-lactams DON'T work

fluroquinolones
macrolides- watch GI issues
tetracycline

Front 259

Most common cause of lobar pneumonia?

Back 259

strep pneumonia

Front 260

Where does strep pneumonia proliferate?

Back 260

in the alveoli, causing an influx of PMNs with minimal structural damage

Front 261

How do you Dx Step. Pneumonia?

Back 261

Gram+
a-hemolysis on agar
catalse negative
sensitive to optochin

Front 262

How do you treat strep pneumonia?

Back 262

B-Lactams
emergence of penicillin resistant strains is big probme, but use bigger doses, or different beta-lactams

ALSO combine with macrolides

Front 263

What are macrolides used to treat?

Back 263

mycoplasma

Front 264

What is the empiric therapy of a pneumonia diagnosis?

Back 264

B-lactam, possibly with a B-lactamase inhibirotr
OR
2nd-generation cephalosporin

AND macrolide (for mycoplasma, in case it's an atypical presentation)

Front 265

What's special about 2nd-generation cephalosporins?

Back 265

Have EXTENDED gram-NEGATIVE coverage

Front 266

How do you treat MRSA staph?

Back 266

vancomycin

Front 267

Patient presents with acute onset of fever, chills, chest pain and rusty sputum?

Back 267

strep. pneumonia!
-alveolar proliferation with purulent secretions and lobar consolidation

Front 268

H. influenza CHARAC

Back 268

-gram neg
-needs factors V and X to grow- so grows well on choco agar

Front 269

Moraxella catarrhalis is charac as a

Back 269

gram neg
diplococcus

makes oxidase, catalase, DNase

Front 270

What is the 2nd most common cause of COPD exacerbations?

Back 270

moraxella catarrhalis

Front 271

Legionella can't be treated with which drugs?

Back 271

Beta-lactams

it's a gram neg bacilli, hard to see in a gram stain, and easier to see in silver stain

DIFFICULT to grow, so especially consider it if you see lots of WBCs but no bacteria...but do also consider the other atypicals

MAY GIVE hyponatremia
-failure to respond to Beta-lactam may give the diagnosis

Front 272

Chlamydia pneumonia components and Tx

Back 272

elementary body is INFECTIOUS

Reticulate body is metabolically active, non-infectious.

Tx:
fluoroquinolones are good for it.
macrolides and tetracyclines could be used too.

Front 273

Adenovirus is a common cause of...

Back 273

pneumonia in AIDS patients.
-SMUDGE cell or ROUND-GLASS appearance histo-wise

Front 274

What are the bugs that often cause abscesses and empyema, especially in LRI...

Back 274

S. aureus
Klebsiella
Pseudomonas
anaerobes

also common in nosocomial pneumonia, as a side-note

SEE: alveolar prolif and necrosis, with lobar consolidation and CAVITATION!!

Front 275

Most common causes of bacterial pneumonia in HIV (2)?

Back 275

S. pneumonia

AND

H. Influenza

Front 276

What prophylaxis do you deliver in an HIV+ pt. when worried about bacterial pneumonia?

Back 276

trimethoprim (TMP)

Front 277

What prophylaxis do you deliver in an HIV+ pt. when worried about PCP?

Back 277

Bactrim, aka TMP-SMZ

use in HIV+ with CD4 <200

Front 278

Where do you see a cotton candy appearance?

Back 278

PCP histology, due to intraalveolar eosinophilic exudates

-lots of edema and eosin in the alveolar spaces, not much damage to the tissues

-helmet-like or cup-shaped organisms

Front 279

What's the threshold for seeing CMV?

Back 279

HIV+ with CD4 <50 typically

-IFX of alveolar macrophages, endo and epi cells
-SEE RETINITIS, along with other GI issues

-OWL-EYE INCLUSIONS are indicative of CMV

Front 280

How do you treat CMV?

Back 280

HAART with IV ganciclovir or foscarnet

Front 281

Most common fungus-based life-threatnening HIV+ illness?

Back 281

cryptoccous

-meninges are most common ifx site
-CD4<100 usually
-FOAMY CELLS with big thick capsule on india ink

Dx. by seeing via histo
TREAT WITH AMPHOTERCIN B

Front 282

Treating with amphotercin B, what do I have?

Back 282

HIV+, likely CD4<100, Cryptococcus neoformans

Front 283

Mimics TB with peripheral pulmonary lesion and hilar adenopathy, certain parts of U.S. specific, what is the bug?

Back 283

Histoplasmosis

-MILIARY infiltrates on CXR
-NON-CASEATING fibrotic granulomas

AMPHOTERCIN B treatment or Itraconazole in pts with milder disease

Front 284

CD4<30
brancing, septate organisms with 40 degree angles

Back 284

Aspergillosis!

Front 285

How does aspergillosis present?

Back 285

NECROTIZING pneumonia and propensity for blood vessels so CXR shows UL disease with CAVITATION AND HEMOPTYSIS

Tx with AMPHOTERCIN B

Front 286

What all do you treat with Amphotercin B?

Back 286

1) Cryptococcus
2) Histoplasmosis
3) Aspergillosis
4) Coccidiomycosis
5) Blastomycosis

Front 287

Where do you see blastmycosis

Back 287

patient is immunosuppressed and localized to Midwest US, Southwest US and Canada

Front 288

What's the major mutation of CF and the associated complication?

Back 288

Δf508
-associated with pancreatic insufficiency!

Front 289

Explain the CF mutation

Back 289

Cl- channel is blocked and Cl- can't leave the bronchial cells, so Na+ goes inside and creates and extra-thick mucous that gets stuck and can't be moved by the mucociliary elevator

Front 290

Do you see clubbing in CF?

Back 290

yes, true.

Front 291

Meconium ileus

Back 291

CYSTIC FIBROSIS

Front 292

What's the means of diagnosis of CF?

Back 292

Sweat test with Cl- >60, intermediate if 30-60

Front 293

Common organisms colonizing CF pt. airways?

Back 293

P. AERUGINOSA
S. aureus
H. Influenza

Front 294

BPD is characterized by...

Back 294

INC vasc perm
-lungs are leaky and inflamm cells go where they're not supposed to, creating a significant inflammatory response

Front 295

Is RSV seasonal?

Back 295

Yes, but in Florida it's not as pronounced in terms of spikes during certain months, but rather it's higher most of the time!

Front 296

Clinical Sx's of bronchiolitis?

Back 296

-profuse coryza, or runny nose
-low grade fever
-LRI w/in 2-5 days
-cough, dyspnea, wheezing, feeding issues, flaring, retractions, and cyanosis

Front 297

CXR of Bronchiolitis shows...

Back 297

-bilateral perihilar and patchy parenchymal infiltrates with peribronchial cuffing

hyperinflation with flattened diaphragm

atelectasis especially in the right upper and middle lobes

Front 298

What's the prophylaxis of Bronchiolitis?

Back 298

synagis
1X/month, but $1,000/Tx

Front 299

What are the intrinsic restrictive lung diseases?

Back 299

PARENCHYMAL RESTRICTIVE:
IPF
sarcoidosis
hypersensitivity pneumonitis
radiation-induced fibrosis
autiommune-related fibrosis
or
lymphangitic carcinomas

OR

AIR-SPACE FILLING DEFECTS:
i.e. pneumonia, could result in diffusion problems

Front 300

What are the extrinsic restrictive lung diseases?

Back 300

Pleura:
-pneumothorax
-pleural effusion
-pleural thickening- asbestosis

Chest wall:
-scoliosis
-ankylosing spondylitis

Neurmuscular disease:
-polio
-GBS
-ALS
-Myasthenia Gravis
-Muscular dystrophies

Front 301

In diseases of the lung parenchyma, where do you see the fibrosis?

Back 301

starts at the bottom of the lung and works its way up.

Front 302

Diseases that may lead to IPF:

Back 302

scleroderma
asbestosis
amiodarone (lipid containing vesicles)
methotexate drug-use

Front 303

Does IPF respond to steroids?

Back 303

NO!
only tx if any is supplemental O2

Front 304

How does IPF spread?

Back 304

usually starts at the periphery and works its way inward, there is also scattered fibroblast foci, and representative areas of active fibrosis

Front 305

How many IPF patients have clubbing?

Back 305

HALF!

Front 306

If you hear velcro crackles, think...

Back 306

IPF

Front 307

Clinical presentation of IPF shows 3 big things:

Back 307

-clubbing in half of patients
-velcro crackles
-reticular opacities, i.e. ground-glass appearance

Front 308

Clinical features of AIP?

Back 308

diffuse infiltrates on CXR
hypoxemia
cyanosis
hyaline membranes
interstitial edema
type II hyperplasia

fluid in the alveolar space
organizing DAD
DIFFUSE PROLIFERATION OF INTERSTITIAL FIBROBLASTS

Front 309

NSIP is what kind of process?

Back 309

VERY CELLULAR, LOTS of inflammation

Front 310

Does NSIP respond to steroids?

Back 310

YES!

Front 311

What 2 interstitial diseases are associated with smoking?

Back 311

DIP and RB-ILD

Front 312

What characterizes Wegener's Granulomatosis?

Back 312

NECROTIZING granulomatous inflammation and vasculitis

Front 313

Key diagnostic finding of Wegener's?

Back 313

ANCA antibodies!!!

Front 314

Key pathogenesis of Sarcoidosis?

Back 314

T-cells mediate inflamm
bilat hilar lymphadenopathy
RESEMBLES TB

Front 315

2 key clinical features of sarcoidosis?

Back 315

skin nodules
eye irritation, i.e. uveitis

Front 316

What do lab tests show for sarcoidosis?

Back 316

hypergammaglobulinemia
hypercalcemia
INC ACE levels

Front 317

How do you Tx sarcoidosis?

Back 317

cortisone or prednisone

Front 318

Where do you see the fibrotic nodules of silicosis?

Back 318

upper lobes

egg shell calcification in the hilar LNs
NO CLUBBING

Front 319

What part of the lungs do you see involved in asbestosis?

Back 319

peribronchiolar fibrosis involving the LOWER lobes

-alveolar spaces may have asbestos bodies and inflamm cells

Front 320

Coal workers pneumonia is seen in what part of the lungs?

Back 320

usually UL zones, with nodular or rounded appearance

Front 321

Rheumatoid arthritis has what finding similar to IPF, what is it?

Back 321

Velcro crackles in the lower lobes

Front 322

What organs does Sjorgen's syndrome affect?

Back 322

eyes
salivary glands

Front 323

Bleomycin toxicity causes...

Back 323

PMNs alveolitis and eosinophil proliferation in hypersensitivity reactions

causes nodular lesions mimicking metastasis due to BOOP

Front 324

Methotrexate toxicitiy shows...

Back 324

T-cell alveolitis and eosinophil prolif

Front 325

Patient presents with lamellar bodies on EM and lipid-containing vacuoles, what's the problem?

Back 325

amiodarone toxicity

Front 326

2 KEY histo findings of Squamous Cell Carcinoma?

Back 326

1) Keratin pearls
2) Intracellular bridges via desmosomes

Front 327

What is the triad of pulmonary embolism?

Back 327

1) dyspnea
2) pleuritic chest pain
3) hemoptysis- occurs later on

Front 328

Most common mutation leading to PE?

Back 328

Factor V leiden

Front 329

How do you treat PE?

Back 329

heparin, then long-term use coumadin, elastic stokcings, pneumatic compression devices, an IVC filter, thrombolytics are RARE and so is a thromboendarterectomy

Front 330

What is defined as Pul HTN?

Back 330

mPAP >25mmHg at rest or >30mmHg during exercise

Front 331

Define ARDS:

Back 331

diffuse alveolar damage, specifically to th e alveolar capillary walls that results in the rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to O2 therapy and may progress to extrapulm organ failure

Front 332

Findings of ARDS

Back 332

Profound dyspnea and tachypnea herald ARDS, but the CXR is initially normal. Subsequently, there are increasing cyanosis & hypoxemia, respiratory failure, and appearance of diffuse bilateral infiltrates on CXR.

Looks like bilateral lung opacity (“white out”). They’re heavy, stiff, non-compliant lungs.

Front 333

Describe ARDS pathogenesis:

Back 333

-Diffuse alveolar damage leads to:
-INC alveolar capillary perm leads to:
-protein-rich leakage into alveoli
leads to:
-formation of intra-alveolar HYALINE MEMB
leads to:
-neutrophilic substances toxic to alveolar wall, activaiton of coag cascade, or oxygen-derived free radicals

Front 334

When does the incidence of lung cancer peak?

Back 334

ages 55-65

Front 335

#1 risk factor for lung cancer?

Back 335

SMOKING

Front 336

#2 risk factor for lung cancer?

Back 336

Passive exposure to smoke

Front 337

#3 risk factor for lung cancer?

Back 337

Occupational exposures:
-asbestos ESPECIALLY
-roofers exposed to coal tars
-railroad workers
-others

Front 338

Local tumor clinical Px:

Back 338

-cough
-hemoptysis
-wheezing due to tumor obstructing airway
-atelectasis or postobstructive pneumonia--> dyspnea, signs of pneumonia

Front 339

What are the Sx's of pancoast syndrome?

Back 339

see Horner's syndrome, which is ptosis and myosis, along with anhydrosis

"a droopy-eyed, constricted people in someone NOT sweating."

Front 340

What are all the paraneoplastic syndromes you could see:

Back 340

-endocrine
-mskel: hypertrophic osteroarthropathy
-neurlogic- Lambert-Eaton, peripheral neuropathy, dementia, cerebellar degen
-hematologic: thrombophlebitis

Front 341

What are the paraneoplastic issues seen with squamous cell carcinoma?

Back 341

PTH-syndrome giving:
-HYPERcalcemia
-lethargy
-polyuria
-polydipsia (excessive thirst)
-constipation
-abdominal pain
-possible coma

Front 342

Why do you typically see SVC syndrome?

Back 342

due to mediastinal LN invasion of the tumor

Front 343

SIADH Sx's

Back 343

hyponatremia leading to:
-irritability
-confusion
-weakness
-poss. seizures

Front 344

Cushing's Sx's:

Back 344

-facial edema
-cachexia
-hypokalemia
-alkalosis
-

Front 345

Hypertrophic osteoarthropathy Sx's:

Back 345

overgrowth of cortical bone and presenting with pain in the lower joints

Front 346

What are the 2 options for Dx of a Small-Cell lung cancer?

Back 346

Limited (30%)

or

Extensive (70%)

Front 347

What are the options for a Non-Small-Cell Lung CA:

Back 347

Can the patient tolerate resection, determined by pul func test

and
is the tumor possibly resected for a cure?

Front 348

When a tumor is more periperal, how do you resect it?

Back 348

Use fluorscopy-assisted percutaneous needle aspiration

Front 349

What are the levels needed to permit a pneumonectomy?

Back 349

FEV1ppo and DLCO >/= 75% predicted

if less, do split pul func test to estimate post-resection FEV1 and DLCO...

If they're greater than 40% then you can still do the pneumonectomy

Front 350

What are the steps of lung CA staging?

Back 350

1) extent of Primary Tumor- T
2) presence and extent of regional metastasis to hilar and mediastinal LNs- N
3) presence/absence of distant mets- M

Front 351

T of TNN:

Back 351

T1 </= 3CM
T2 >3CM
T3 INVADES CHEST WALL
T4 invades VITAL intrathoracic strucs

Front 352

N of TNM:

Back 352

N0- no LNs
N1- ipsilateral peribronchial/hilar LNs
N2- ipsilateral mediastinal/subcarinal LNs
N3- CONTRAlateral mediastinal/hilar LNs and/or supraclav LNs

Front 353

Small Cell Tx:

Back 353

Limited disease:
-do radiation port to Tx, confined to one hemithorax, and only regional LNs, Tx is chemo and radiation!

Extensive disease:
tumor beyond limited limits, Tx is chemo

Front 354

How to be sure a Solitary Pulmonary Nodule is benign?

Back 354

1) No growth on X-ray for 2 years
2) pt. <35 yrs of age AND non-smoker
3) chest radiograph and/or CT shows it's calcified: through and through, target, laminar, or popcorn

Front 355

Which tumor do you Tx with surgery and which is too bad already when Dx'ed?

Back 355

try to treat Non-Small cell with surgery, but small cell is considered already spread by the time the Dx is made so you do chemo and radiation if it's a limited disease, and just chemo if it's an extensive small-cell diagnosis

Front 356

Atypia, dysplasia, and DCIS of bronchial epi imply...

Back 356

invasive squamous cell CA likely assoc with heavy cig smoking.

Front 357

Scar carcinoma is...

Back 357

when pul fibrosis, such as IPF is present and then a tumor arises at the site of prev fibrosis

Front 358

Desmoplasia is when..

Back 358

fibrosis 2ndary to presence of a carcinoma.

Front 359

C-myc is a mutation found in...

Back 359

small cell CA

Front 360

K-ras is seen in...

Back 360

adenocarcinomas

Front 361

What 2 genes are often inactivated in lung CAs?

Back 361

p53 and retinoblastoma

Front 362

Adenocarcinoma definition:

Back 362

malignant epi tumor with GLANDULAR DIFFERENTIATION

-see gland formation or see intracytu mucins!

-usually periph location
-equally frequent in men and women, but most frequent type in the non-smoker population

-sometimes assoc with areas of scarring

Front 363

4 sub-types of adenocarcinoma

Back 363

tubular/acinar
papillary
solid
bronchioloaveolar

Front 364

Squa cell CA definition:

Back 364

-malignant epi tumor charac by presence of keratin prod AND/OR intracellular bridges

-closely assoc with smoking history

Front 365

Large Cell CA is...

Back 365

malignant epi neoplasm undifferentiated
-cells large/polygonal
-nucleolus is prominent and cell borders are well-defined

-see giant cell CA and clear cell CA in this group

Front 366

Adenosquamous carcinoma is...

Back 366

at least 10% of each of the two tumor types combined

Front 367

Small cell definition

Back 367

highly-defined neuroendocrine tumor strongly assoc with cig smoking

-usually close to hilum

-originated in the Kulchitsky cells

-composed of smallc ells with scant cytoplasm and ill-defined cellular borders
-salt and pepper chromatin
-nuclei molding is CHARACTERISTIC

Front 368

Typical carcinoid tumors:

Back 368

-low-grade neuroendocrine tumors
-great survival rate >90% at 10yrs
-salt and pepper chromatin appearance
-mitotic figures scant and necrosis absent

MOST COMMON LUNG TUMOR IN CHILDREN

Front 369

Atypical Carcinoid tumors:

Back 369

-10-yr survival around 55%
-more mitotic figures
-necrosis present
-nuclei tend to be more pleomorphic and nucleoli are conspicuous

slightly more agressive

Front 370

What's the best way to Dx as an adenocarcinoma?

Back 370

mucin-stains!

Front 371

What's clearly indicative of a Squamous cell carcinoma diagnosis?

Back 371

KERTAIN!!!

-also see intracellular bridges

Front 372

Where do you see the Azzopardi effect?

Back 372

in small cell carcinoma, it's a liberation of nucleic acids from the cells

Front 373

Which tumors have APUD?

Back 373

neuroendocrine tumors, which are Typical and Atypical Carcinoid and Small cell

APUD: Amine Precursor Uptake and Decarboxiylation
These cells take up amino acids and modify them into amines and peptides. APUD cells synthesize most of the hormones in the body.

Front 374

Carcinoid tumor CHARAC:

Back 374

Low grade malignant tumors demonstrating endocrine microscopic pattern admixed with abundant blood vessels
It usually involves large bronchi with an endobronchial growth pattern.
Affects patients under 45 years of age.
It is the most common lung tumor in children

Front 375

Where do you see lamellar bodies in an interstitial lung disease?

Back 375

amiodarone toxicity

"lipid-containing vacuoles"

Front 376

What is amiodarone used for?

Back 376

treat tachyarrhythmias

Front 377

Bleomycin can cause...

Back 377

BOOP

Front 378

NSAIDs can cause...

Back 378

pulmonary eosinophilia

Front 379

Ara C and Aspirin can be associated with which disease?

Back 379

ARDS

Front 380

What's a key hallmark of cancer chem agent drug-induced lung disease?

Back 380

-almost always assoc with fever, but they are a Dx of exclusion

-Tx limited to discontinuing the drug and considering ADDITION OF CORTICOSTEROIDS

Front 381

Changes as a result of drug-induced lung disease?

Back 381

-vascular damage- endo swelling with exudation of fluid
-type I destruction and type II prolif

Front 382

What are some possible findings from a BALF?

Back 382

-T-lymphocytes alveolitis- methtrxate
-PMNs alveolitis- bleomycin
-eosinophils in hypersensitivty rxns- MTX, Bleomycin, Procarbazine

Front 383

Bleomycin toxicity increases with...

Back 383

age

and

dosage

Front 384

Bleomycin facts:

Back 384

-DLCO predicted subsequent disease
-toxicity reversible if changes only minimal
-anticancer drug
-synergistic toxicity with cyclophosphamide
-if O2 and radiation included, plus the drug, mortality is 50-75%
-up to 20% mortality after cisplatin infusion
-see nodular lesions mimicking metastases due to BOOP

Front 385

What's the cardinal symptom of radiation pneumonitis?

Back 385

-2-3 months post-Tx
-see 93% dyspnea, but also dry cough and/or less-so fever
-due to local cytokine prod
-usually confined to field of irradiation
-generally self-limited, but may become progressive fibrosis

CAN ACCEL REPAIR PROCESS WITH CORTICOSTEROIDS

Front 386

Malar rash, polyarthritis, rapid onset of a cough, fever, and some rapidly progressive dyspnea

-see also lung crackles and severe hypoxemia

Diagnosis?

Back 386

Systemic Lupus, it was a black female, but I left that out.

Front 387

What's a hallmark of diagnosing lung disease as a result of rheumatoid arthritis?

Back 387

-pleurisy with effusion, an exudate that shows SUPER LOW SUGAR content, like less than 10

Front 388

Rheumatoid arthritis lung effects may be seen as what in the bronchioles:

Back 388

-bronchiolitis obliterans organizing pneumonia (BOOP)
-bronchiolitis obliterans

Front 389

2 possible manifestations of rheum arthritis intrathoracically?

Back 389

Poly/Dermatomyositis:
-fibrosing alveolitis or BOOP
-pul vasculitis or HTN
-aspiration pneumonia
-respiratory muscle weakness

Systemic Sclerosis
-fibrosing alveolitis
-BOOP
-pul HTN
aspiration pneumonia
CHEST WALL RESTRICTION

Sjorgen's Syndrome:
LYMPHOCYTIC infiltration, esp. in lungs

Pul Fibrosis and Autoimmune DIsease
-Myasthenia gravis
-chronic active hepatitis
-thrombocytopenic purpure
-hemolytic anemia
primary biliary cirrhosis

Front 390

LNK- what disease?

Back 390

Lungs, Nose, and Kidneys

Wegener's Granulomatosis

Front 391

Saddle-nose deformity, what disease?

Back 391

Wegener's!

Front 392

What are 2 major presentations in blacks > whites for sarcoidosis?

Back 392

skin sarcaoidosis

and

ocular Sx's, i.e. uveitis

Front 393

Inherited coagulopathies involve...

Back 393

Protein C and S
Factor V Leiden
antithrombin III deficiency

Front 394

Where do you get the majority of PEs from?

Back 394

DVTs
-with most coming from the popliteal fossa to the pelvis

-start as platelet aggs on valves in the venous sytem

Front 395

If you see infarcts from PE, what type will they be?

Back 395

red infarcts

Front 396

What's the classic triad of Sx's in PE?

Back 396

hemoptysis
pleuritic chest pain
dyspnea

Front 397

What is in Virchow's triad?

Back 397

1) stasis
2) hypercoaguability
3) venous injury

Front 398

4 Signs of PE:

Back 398

tachypnea
tachycardia
accentuated 2nd heart sound
fever- due to infarct

Front 399

With a PE, what vent/perfusion do you expect to see?

Back 399

It will create more deadspace, so if anything you would expect an elevated pCO2, but the person hyperventilates, so it's normal or low if anything

Front 400

What happens to the pO2 in PE?

Back 400

V/Q mismatch with hypoxemia due 2 bronchoconstriction
-DEC alveolar PCO2, and there's mediators giving clinical wheezing and bronchoconstriction

Front 401

What are the expected pO2 and pCO2 VALUES in PE?

Back 401

hypoxemia
AND
hypOcarbia

Front 402

What would be an ECHO finding indicative of PE?

Back 402

right vent dilation due to quick onset of INC press

Front 403

Westermark's sign...

Back 403

shows area of poor perfusion in a PE, but Salathe has never even seen one!

Front 404

What happens on a V/Q scan when you have a PE?

Back 404

see bronchoconstriction, so the radioisotopes have delayed washout in those areas, so there will be an area of no mottling, and an area of prolonged washout

Front 405

What's diagnostic for PE when using a V/Q scan to examine the patient?

Back 405

2 or more segmental deficits that are MISMATCHED, i.e. no perfusion, BUT ventilation

Front 406

What 2 things can duplex measure?

Back 406

1) compressibility, or in the case of a DVT, NON-compressibility


2) flow measurements can be done too

Front 407

Cannot diagnose patients with Protein S and C deficiencies if they're on...

Back 407

coumadin

Front 408

What can cavitate in the lung?

Back 408

1) squamous cell carcinoma
2) Wegener's
3) Aspergillosiss

Front 409

What is the most common cavitator in the lung?

Back 409

squamous cell carcinoma

Front 410

Popcorn lung is associated with what disease?

Back 410

BOOP

Front 411

Where do you see the Golden S-sign?

Back 411

-simple collapse of a lung/lobe would give a straight line

here, collapsing AROUND A MASS
-not a straight line b/c this mass is seeing lung drape over the mass

Front 412

When do you see the air bronchgram sign?

Back 412

When you have consolidation in the alveoli so it outlines the bronchi which are the only spots left with air in them

Front 413

Where do 95% of pul thromboembo come from?

Back 413

DVT from popliteal or larger

Front 414

How many PEs affect the lower lobes?

Back 414

75%

>50% are multiple
and
30% recurrence rate

Front 415

Small emboli account for what % of PE?

Back 415

70-95%

-60-80% are clinically silent.
-they're in a patient with adequate cardiorespiratory function

-10-15% lead to infarction, which means there was some sort of cardiorespiratory compromise

Front 416

Steps of SMall Emboli in the Lungs:

Back 416

1) ischemia of endothelial cells
-see pul hemorrhage with adequate cardioresp status and dual blood supply
2) Once there's compromised cardiorespiratory status, you'll get red infarct, which is coagulative necrosis of the parenchyma PLUS hemorrhage
3) RBCs will lyse and see red/brown hemosiderin deposits
-wedge shape formation, apex will be at the occluded vessel, the base will be at the pleural aspect
4) org of embolus, gray/white shrunken peripheral scar, so now it's FIBROTIC

Front 417

What are the other conditions associated with having a PE?

Back 417

pul HTN
chronic cor pulmonale
vascular sclerosis

Front 418

3 Ways to get pul HTN

Back 418

1) DEC cross-sectional area of pul vasc bed leading to inc vasc resistance
2) INC pul BFlow
3) INC in left heart resistance

Front 419

How do you get secondary pul HTN?

Back 419

-chronic obstructive or interstitial lung disease- destroying the parenchyma and there will be fewer alveolar capillaries
-recurrent pul emboli reduce the cross-sectional area
-heart disease with a Right --> Left shunt will INC flow across the lungs

Front 420

What grades of pul HTN are reversible?

Back 420

Grades 1-3

Front 421

Grades IV/V of Pul HTN look like...

Back 421

an organizing thrombus with re-canalization
-can't tell the diff b/n the 2!!

Front 422

Grade VI Pul HTN presents as...

Back 422

Necrotizing arteritis
AND
fibrinoid necrosis (vessel wall is now acellular, amorphous material)

Front 423

Classic sign of pleural effusion?

Back 423

meniscus sign

Front 424

As you go down a lateral CXR, the spine should....

Back 424

get DARKER, but if it gets lighter at all, then there is something there, some infiltrate is present.

Front 425

How do distinguish between pleural effusion and pleural thickening on CT?

Back 425

pleural thickening has an irregular border, whereas pleural effusion will appear pretty smooth. This was especially discussed in reference to a CT.

Front 426

How distinguish a DDx of pleural effusion and pleural thickening?

Back 426

POSITIONAL CHANGES
-put patient in the lateral decubitus position

Front 427

Does the trachea deviate with pleural effusion?

Back 427

if there's a large amount of fluid it'll get pushed away from the side with the effusion

Front 428

What are 2 possible consequences of pleural effusion?

Back 428

1) diaphragm can do gown
2) lung can get compressed even to point of atelectasis

-excess fluid in pleural space can compress lungs

Front 429

If you see an opacity with a straight line, what do you think?

Back 429

without the meniscus, think of a HYDROPNEUMOTHORAX, where the air-water interface ends up being a straight line!

Front 430

If the pleural effusion is a transudate, what are the possible problems?

Back 430

1) CHF
2) liver problem
3) renal problem

pleural fluid protein >3g/dl to be exudate

Front 431

When is pneumothorax more apparent?

Back 431

during expiration because the lung retracts more from the chest wall, so ORDER CXR at EXPIRATION

Front 432

Bloody pleural effusion, think...

Back 432

possible malignancy

Front 433

What are the 3 most common causes of pleural effusion?

Back 433

1) CHF
2) pneumonia- bacterial
3) malignant disease

Front 434

Usually what gives only transudate will not give exudate, but...

Back 434

what gives exudate may also give transudate
-part of why exudate is a more complicated DDx

Front 435

Meig syndrome is the triad of...

Back 435

1) right-sided hydrothorax
2) ascites
3) ovarian fibroma

Front 436

What could cause serofibrinous pleuritis?

Back 436

it's serous fluid plus fibrinous exudates

-inflamm in adjacent lung due to pneumonia, TB, an infarct, or abscess
-collagen vasc diseases like rheum arthritis or lupus
-uremia
-radiaiton
-systemic ifxs

Front 437

Which is more common, metastases or primary PLEURAL TUMORS?

Back 437

metastases
-coming from LUNG, BREAST, ovary, and GI tract
-see desquamated tumor cells in serosanguineous fluid

Front 438

Solitary Fibrous Tumor, aka pleural fibroma:

Back 438

CD34+Keratin-
-attached to pleural surface by a pedicle
-white, filmy mass

Front 439

How often is malignant mesothelioma related to asbestos exposure?

Back 439

90% of the time!
-25-45yr latency
-GROSS- diffuse grayish pink tumor, spreads widely in pleural space

CD34-Keratin+

-epithelial mesotheliomas may be difficult to DDx from mets of adenocarcinoma to the pleura

Front 440

How to disting b/n Adenocarcinoma and mesothelioma

Back 440

Adeno:
EMA + in CYTO, CEA+, Calretinin-

Mesothelioma:
EMA+membrane, CEA-, Calretinin-

Front 441

How do you Dx diffuse pul interstitial fibrosis?

Back 441

see "asbestos bodies"- golden brown rods containing asbestos fibers coated with iron-containing proteinaceous material
-pul macrophages attempt ti ingest asbestos fibers and are activated to release chemotactic factors and fibrogenic mediators that lead to a diffuse interstitial fibrosis

Front 442

serpentine/chrysotile asbestos looks like...

Back 442

curly and flexible

BOTH FORMS ARE FIBROGENIC

Front 443

amphibole asbestos looks like...

Back 443

straight and stiff

BOTH FORMS ARE FIBROGENIC

Front 444

Asbestos inc. risk of bronchogenic CA...

Back 444

5-fold
smoke too, see 55-fold increase in the risk of it!!!

Front 445

How do you Tx mesothelioma?

Back 445

pneumonectomy, radiation, and chemo

Front 446

90% of mesotheliomas are related to asbestos exposure, BUT...

Back 446

asbestos workers have GREATER chance of getting bronchogenic CA

-remember Goljan said Bronchogenic CA develops faster, so it's gonna come before mesothelioma has a chance to develop, that's why it's more prevalent

Front 447

If see a malignant cytopathology, what's the DDx?

Back 447

mesothelioma vs. adeno, so need IHC

Front 448

If malignant cytopath, and determine by IHC it's adenocarcinoma...

Back 448

use IHC cell markers like estrogen receptor for 70% of breast carcinomas, or TTF-1 for 70% of lung adenocarcinomas

Front 449

Hypoxic respiratory failure:

Back 449

Low paO2 (<50-60mmHg)
Normal/low pCO2

Front 450

Hypercapnic hypoxic respiratory failure:

Back 450

Low paO2 (<50-60mmHg)
PLUS
Elevated PaCO2 (>49mmHg)

Front 451

Kussmaul breathing is...

Back 451

very deep breathing that is used to correct for acidosis

Front 452

paCO2 is NOT affected by...

Back 452

age
OR
position

Front 453

CO2 ventilation equation

Back 453

VCO2 = paCO2 * Valv * k

Front 454

What are the ALI criteria?

Back 454

paO2/FiO2 < 300mmHg


only difference from ARDS is that ARDS is <200

Front 455

ARDS is NOT a homogeneous disease. Giving PEEP will...

Back 455

affect parts of the lung differently.

Front 456

4 Causes of Type I Respiratory Failure:

Back 456

This is hypoxic failure:

1) R-->L Shunt
2) V/Q MISMATCH
3) low piO2
4) diffusion problem, which almost never occurs at rest

Front 457

Causes of Type II Respiratory Failure:

Back 457

Alveolar ventilation insufficiency, leading to HYPOXIC-HYPERCAPNIC Resp Failure

-central resp drive is low
-INC work of breathing
-resp. muscle dysfunction
-hypOventilation
-can be combined with INC CO2 production

Front 458

Does shunting respond to supplemental O2?

Back 458

NO!

Front 459

Shunting can be caused by...

Back 459

-alveolar collapse- atelectasis
-intra-alveolar filling process, pneumonia or edema
-intracardiac- platypnea possible (Difficulty in breathing when erect, relieved by lying down.)

-vasc shunt w/in lung- AVmalformation

When seeing air bronchograms, MOST CONSISTENT with alevolar filling process and likely pneumonia

Front 460

In a situation where you hypOventilate because of a drug overdose/neuro or muscle disease or injury/excessive load on resp. sys, then...

Back 460

can see abnormal lungs WITH V/Q mismatch, and since patient can't INC alveolar vent sufficiently, then have hypoxia PLUS INC dead space, leading in total to HYPERCAPNIA

Front 461

Hypoventilation is defined as...

Back 461

HYPOXEMIA with a NORMAL A-a gradient.

Front 462

Does hypoxemia respond to supplemental O2?

Back 462

YES!

Front 463

What happens to the body with an acute rise in acidosis?

Back 463

1) DEC cardiac contractility
2) DEC resp muscle contractility
3) INC arterial vasodilation to compensate for cerebral BFlow
4) loss of conciousness

Front 464

In a depressed drive patient, such as one with sedative and a prev. present resp. insufficiency, see that there is an increase...

Back 464

in paCO2 with oxygen therapy
-due to V/Q mismatch
and
-depressed drive

Front 465

Aminoglycoside SE leading to poss. resp. effects:

Back 465

curare-like effects--> could paralyze resp. centers

also consider procainamide

Front 466

Assist-Control Ventilation

Back 466

-ventilator delivers set tidal volume when triggered by patient's inspiratory effort or independently if not patient effort occurs within a certain amount of time

Front 467

Intermittent mandatory vent:

Back 467

mandatory # of fixed volume breaths, pt. could also do own breaths in between

Front 468

Pressure support:

Back 468

graded assistance, physicians sets the level of pressure to augment every spontaneous resp effort

Front 469

Controlled mech vent:

Back 469

completely dependent upon rate and tidal volume set
-patients resp efforts have no effect

Front 470

Peak Inspiratory pressure depends on...

Back 470

compliance

Front 471

Anosmia top 2 causes:

Back 471

1) Viral URI
2) Trauma

RULE OUT: brain tumor/other neoplasm

Front 472

Rhinosinusitis top 2 causes:

Back 472

1) Viral URI
2) Allergic Rhinitis

Front 473

Nodule
vs.
Polyp
vs.
Cyst

Back 473

fix with speech therapy and it'll go away
vs.
so big it won't resorb
vs.
usually won't go away, esp. fluid-filled issues

Front 474

Who gets pulmonary venous hypertension?

Back 474

-left-sided atrial or vent. disease

-left-sided valvular heart disease

Front 475

Definitive pul HTN dx?

Back 475

Use right heart catheterization to measure right vent press

Front 476

Idiopathic pul HTN typically seen in what age population?

Back 476

age 30-50

progressive disease- survival is 2.8 years w/o therapy

Front 477

What disorder is most commonly associated with pul HTN?

Back 477

Systemic sclerosis

Front 478

What's the other HTN assoc with pulmonary HTN?

Back 478

PORTAL

Front 479

When seeing PoPH, which presents first?

Back 479

portal HTN

Front 480

What happens to cardiac output when the pulHTN gets SEVERE?

Back 480

starts dropping, a BIG problem

Front 481

epoprostenol

Back 481

IV med given through central line, and needs specialized pump and to be given on continuous basis due to a short half-life

-w/o the med see rebound and the pul art press shoots way up

Front 482

What is Bosentan?

Back 482

-aka tracleer
-oral endothelin dual receptor antagonist
-oral twice daily
metabo by liver
-teratogenic

DOES IMPROVE SURVIVALS

Front 483

3 main pathways to impact in pul HTN?

Back 483

1) endothelin pathway
2) NO pathway
3) prostacyclin pathway

Front 484

Acute exacerbation of COPD, what do you do?

Back 484

give ABx and Glucocorticosteroids (IV/oral) for FOURTEEN (14) days

Front 485

Do you give steroids in hypersensitivity pneumonitis?

Back 485

-DO NOT prevent the development of fibrosis
-they DO, however, reduce the time to recovery after exacerbation


MOST IMPT: Allergen Avoidance