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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
Q

OSA

A

relaxed tissue of mouth and pharynx occlude air passage as pt tries to breath

26
Q

causes of OSA

A

anatomical features (macroglossia, tonsils, hypertrophy, acromegaly, etc)

sedatives

other risk factors (DM, lung dz)

27
Q

typical OSA pt

A

men > women, older, younger AA male

craniofacial issues, heredity, current smoking, nasal congestion

obese male, HTN

28
Q

clinical features of OSA

STOP BRAG

A

Snore loud
Tired/fatigued
Observed stop breathing
Pressure (HTN)

Bmi >35
Age > 50
Neck circumference >43
Gender = male

29
Q

diagnosis of OSA

A

polysmonography/sleep study

CBC

exclude drug use

study findings: decreased pulse ox, tachycardia, arrhythmia (VTACH), increased BP

30
Q

mild OSA

A

asymptomatic, report sedentary sleepiness

noted only in retrospect

respond to tx

31
Q

moderate OSA

A

take steps to avoid daytime sleepiness

likely HTN but no co pulmonate manifestations

respond to tx

32
Q

severe OSA

A

freq. manifestations of car pulmonate

all need tx

not benefit for symptoms and dz

33
Q

tx of OSA

A

weight loss, avoidance of alcohol/sedatives

CPAP +/- O2 (difficult mask, remind pt that symptoms can be deadly)

UPPP

34
Q

what does effective lung function req. ?

A

patient, dry alveoli

small amount of interstitial fluid

appropriately perfusion of capillaries

35
Q

diffuse disruption of fluid balance cuisine leaky capillaries and proteinaceous deposit

A

ARDS/ALI

36
Q

ARDS clinical criteria

A
  1. Acute onset
  2. Bilateral infiltrates
  3. No decrease in LA pressure (just lungs)
  4. PaO2/FiO2 ratio <200
37
Q

etiologies of ARDs/ALI

A 
Sepsis 
aspiration 
PNA
severe trauma 
drug overdose 
massive tranfusion/transplant 
EtOH
38
Q

pathophysiology of ARDS

A
  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
Q

clinical picture of ARDS

A

acutely ill within 48-72 hrs after inciting event

tachypnea, tachycardia, refractory hypoxemia, acute respiratory alkalosis

intubation/ventilation

40
Q

diagnostic eval of ARDS

A

ABG shows hypoxemia despite 100% O2 and alkalosis

CXR - diffuse, fluffy infiltrates, air bronco grams

Lab studies - leukocytosis, DIC, lactic acidosis

41
Q

initial course of ARDS

A

IF survive initial:

severe pulmonary edema that slowly improves

req. prolonged mechanical ventilation due to hypoxemia
* some pts do not improve = honeycombing

42
Q

subsequent ARDS course

A

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
Q

mortality from ARDs

A

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
Q

respiratory distress syndrome

A

neonatal equivalent of ARDS

deficiency of surfactant production either due to premature infant or genetic/birth

45
Q

alveolar development

A

lungs grow in late gestation and 2+ yrs after brith

zero alveoli at 32 weeks, 50-150 million at term , 300 million adult

46
Q

surfactant development

A

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
Q

fetal stress and surfactant production

A

decreased due to hypoveolmia (mother), hypothermia, acidosis, hypoxemia, genetic disorder

48
Q

pathophys of respiratory distress syndrome

A
  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
Q

risk factors respiratory distress syndrome

A

prematurity

previous premie, fetal distress, maternal FM, asphyxia

50
Q

respiratory distress syndrome exam

A 
cyanosis
tachypnea 
nasal flaring 
intercostal/sternal muscle retraction 
grunting
51
Q

respiratory distress syndrome CXR

A

atelectasis

ground glass haze

52
Q

clinical course respiratory distress syndrome

A

during first 72 hrs increasing respiratory distress and hypoxemia

edema, apnea, respiratory failure

uncomplicated show spontaneous improvement

53
Q

prevention and tx of respiratory distress syndrome in MOM

A

prevent pre term delivery

neonatal cold stress, asphyxia and birth , hypovolemia

if unavoidable - antenatal corticosteroid, stimulates surfactant

54
Q

tx of baby respiratory distress syndrome

A

exogenous surfactant administration

warm O2 + monitoring

empiric IV ABx

WI-18 Pulmonary (11 decks)

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