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WI-18 Pulmonary > Dz States 3 > Flashcards

Dz States 3 Flashcards

1
Q

bronchiectasis pathphys

A

severe viral infxn causes inflamed and easily collapsed airways = air flow obstruction, decreased clearance of secretions

therefore chronic bacterial growth resulting in inflammation and damage to bronchioles

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2
Q

bronchiectasis

persistent inflammatory injury causes

A
  1. permanent dilation of proximal and med. sized bronchi
  2. progressive inability to clear secretions and resolve colonization or repeat infection
  3. COPD
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3
Q

etiologies of bronchiectasis (7)

A
  1. infection
  2. bronchiole obstruction
  3. aspiration
  4. CF
  5. allergic bronchopulmonary aspergillosis
  6. AAT
  7. autoimmune/connective tissue
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4
Q

epidemiology of bronchiectasis

A

slender caucasian women, 60+

often cause by MAC

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5
Q

symptoms of bronchiectasis

A

cough and mucopurulent sputum production (months - yrs)

dyspnea, pleuritic chest pain, wheezing, fever, weakness and weight loss

exacerbations: increased and more viscous sputum with would odor

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6
Q

signs of bronchiectasis

A

blood-streaked sputum but few specific signs

rales, wheezing, and rhonchi

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7
Q

evaluation of bronchiectasis

A

discovering cause and tx underlying dz

spirometry irreversible obstruction (no change with bronchodilators)

sputum smear culture (infectious organisms)

HRCT scan of chest with contrast = SOC

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8
Q

tx of bronchiectasis

A

early recognition of bronchiectasis and tx underlying cause

ABX and chest physiotherapy (Abx 1/wk)

+/- bronchodilators, corticosteroid tx, dietary supplementation, oxygen or sx therapies

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9
Q

pulmonary HTN

A

increased resistance thru lung is present = vascular remodeling occurs and pt develops HTN

PA pressure > 25 mmHg

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10
Q

PAH pathophys

A

vascular scarring, endothelial dysfunction and intimal/medial smooth muscle proliferation (decreased lumen size)

vascular remodeling causes RV hypertrophy then RV dilation/RSHF symptoms, decreased preload

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11
Q

etiologies of PAH

A
  1. sporadic/idopathic, hereditary
  2. Pulmonary artery muscle dz (connective tissue dz - scleroderma, SLE, HIV, HTN, anemia
  3. Drug and toxin
  4. LV dysfunction, valve dz
  5. hypoxemia lung dx (COPD, OSA)
  6. PE
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12
Q

drugs that may cause PAH

A

st. john’s wort
SSRIs

cocaine, meth

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13
Q

medical disorders that may cause PAH

A

HIV, liver dz, hemolytic anemia

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14
Q

PAH pathophys

A
  1. high pressure pulm circuit = pulmonary vascular remodeling
  2. RV hypertrophy to maintain output in face of increased resistance
  3. pull remodeling = RV failure
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15
Q

pathogenesis of PAH

A

progressive hypoxemia, hypercapnia, acidemia

excess peripheral oxygen extraction and eventual erythrocytosis

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16
Q

PAH s/s

A

initially vague fatigue, and decreased exercise tolerance

exertional dyspnea

lungs are clear (blood backs up to periphery)

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17
Q

diagnosing PAH (imaging)

A

2D trans thoracic can screen in high risk pts (can tell if increased pressure is there)

R sided cath is GOLD stnd for evaluation

HRCT scan

V/Q scan

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18
Q

anatomy changes of PAH

visible on 2d echo

A

increased pulmonary pressure

dilated RA and RV hypertrophy

R –> L shunt across PFO

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19
Q

R Cardiac Cath

A

specifically quantifies RV and LV function

excludes valvular disease and measure pulmonary vascular resistance

can also det. if reactive to CCB

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20
Q

who do we give a full PAH work up

A

LV dysfunction, COPD = work up stop after confirmation 2D echo

absent or insufficient: Lab eval (HIV, autoimmune, LFTs), PFT, polysomnography, V/Q scan

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21
Q

tx of PAH

A

tx begins early, det. underlying dz

  1. Diuretics (fluid retention, decrease pulmonary and hepatic congestion and edema)
  2. supplemental O2
  3. consideration of anticoagulation
  4. exercise
  5. digoxin (RV EF but more sensitive to dig toxicity)
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22
Q

advanced PAH tx

A

synthetic prostacyclin analog (vasodilators inhibit platelet aggregation)

endothelin receptor agonists (blocks vasoconstriction)

nitric oxide GMP enhancers (Oral PDE-5 , guanylate cyclase)

CCB

23
Q

surgical options for PAH tx

A

atrial septostomy (create the R/L shunt )

transplant

24
Q

diseases of disordered breathing

A

Pickwickan syndrome (sig CO2 retention, can’t take deep breaths)

Central apnea (neural issue causes decreased respiratory drive, tumor/stroke)

obstructive apnea (something wrong when relaxed - ok during day)

25
OSA
relaxed tissue of mouth and pharynx occlude air passage as pt tries to breath
26
causes of OSA
anatomical features (macroglossia, tonsils, hypertrophy, acromegaly, etc) sedatives other risk factors (DM, lung dz)
27
typical OSA pt
men > women, older, younger AA male craniofacial issues, heredity, current smoking, nasal congestion obese male, HTN
28
clinical features of OSA STOP BRAG
Snore loud Tired/fatigued Observed stop breathing Pressure (HTN) Bmi >35 Age > 50 Neck circumference >43 Gender = male
29
diagnosis of OSA
polysmonography/sleep study CBC exclude drug use study findings: decreased pulse ox, tachycardia, arrhythmia (VTACH), increased BP
30
mild OSA
asymptomatic, report sedentary sleepiness noted only in retrospect respond to tx
31
moderate OSA
take steps to avoid daytime sleepiness likely HTN but no co pulmonate manifestations respond to tx
32
severe OSA
freq. manifestations of car pulmonate all need tx not benefit for symptoms and dz
33
tx of OSA
weight loss, avoidance of alcohol/sedatives CPAP +/- O2 (difficult mask, remind pt that symptoms can be deadly) UPPP
34
what does effective lung function req. ?
patient, dry alveoli small amount of interstitial fluid appropriately perfusion of capillaries
35
diffuse disruption of fluid balance cuisine leaky capillaries and proteinaceous deposit
ARDS/ALI
36
ARDS clinical criteria
1. Acute onset 2. Bilateral infiltrates 3. No decrease in LA pressure (just lungs) 4. PaO2/FiO2 ratio <200
37
etiologies of ARDs/ALI
``` Sepsis aspiration PNA severe trauma drug overdose massive tranfusion/transplant EtOH ```
38
pathophysiology of ARDS
1. inciting event 2. pro inflammatory cytokines released (TNF, IL-1, IL-6, IL-8) and neutrophil recruited to lungs = damage to capillary and alveolar endothelium 3. protein escapes from vascular space 4. osmotic gradient for reabsorption is lost and fluid pours into intersitium 5. alveoli fill with bloody, proteinaceous fluid and cellular debris 6. surfactant loss, alveolar collapse 7. V/Q mismatch and hypoxemia 8. loss of lung compliance 9. respiratory failure
39
clinical picture of ARDS
acutely ill within 48-72 hrs after inciting event tachypnea, tachycardia, refractory hypoxemia, acute respiratory alkalosis intubation/ventilation
40
diagnostic eval of ARDS
ABG shows hypoxemia despite 100% O2 and alkalosis CXR - diffuse, fluffy infiltrates, air bronco grams Lab studies - leukocytosis, DIC, lactic acidosis
41
initial course of ARDS
IF survive initial: severe pulmonary edema that slowly improves req. prolonged mechanical ventilation due to hypoxemia * some pts do not improve = honeycombing
42
subsequent ARDS course
prolong ventilation req and patients are at risk for many complications Barotrauma, pneumothorax (stiff lung = tension pneumothorax) noscocomial PNA DVT/PE GIB sedation and paralysis
43
mortality from ARDs
mortality improved with better supportive care death form respiratory distress is uncommon precipitating event causes death in first few days, nosocomial infection and sepsis cause death
44
respiratory distress syndrome
neonatal equivalent of ARDS deficiency of surfactant production either due to premature infant or genetic/birth
45
alveolar development
lungs grow in late gestation and 2+ yrs after brith zero alveoli at 32 weeks, 50-150 million at term , 300 million adult
46
surfactant development
Type II growth begins at week 20, surfactant production during weeks 34-36 amniotic fluid tested for present of lectin to determine lung maturation
47
fetal stress and surfactant production
decreased due to hypoveolmia (mother), hypothermia, acidosis, hypoxemia, genetic disorder
48
pathophys of respiratory distress syndrome
1. instability at end exhalation, decreased compliance, low lung volumes = atelectasis 2. lung inflammation and epithelial injury, extravasation of fluid and pulmonary edema 3. pulmonary shunt and hypoxemia - lung perfused but not ventilated
49
risk factors respiratory distress syndrome
prematurity previous premie, fetal distress, maternal FM, asphyxia
50
respiratory distress syndrome exam
``` cyanosis tachypnea nasal flaring intercostal/sternal muscle retraction grunting ```
51
respiratory distress syndrome CXR
atelectasis | ground glass haze
52
clinical course respiratory distress syndrome
during first 72 hrs increasing respiratory distress and hypoxemia edema, apnea, respiratory failure uncomplicated show spontaneous improvement
53
prevention and tx of respiratory distress syndrome in MOM
prevent pre term delivery neonatal cold stress, asphyxia and birth , hypovolemia if unavoidable - antenatal corticosteroid, stimulates surfactant
54
tx of baby respiratory distress syndrome
exogenous surfactant administration warm O2 + monitoring empiric IV ABx

WI-18 Pulmonary (11 decks)

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