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CSI > respiratory > Flashcards

respiratory Flashcards

1
Q

obstructive lung dis.

A

obstruction air flow–>air trapping
airways close premat. at high lung vols–>inc. RV and dec. FVC
v. low FEV1 and low FVC–>dec. FEV1/FVC ratio (

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2
Q

air flow directly prop to…

indirectly prop to…

A

dir. prop to driving pressure

inv. prop to resistance

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3
Q

obstructive lung disease

A

airway narrowing w/ inc. airway resistance +/- dec. elastic recoil w/ dec. driving pressure (emphysema)

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4
Q

*pathophys: what defines asthma?

A 
airway inflammation (current med tx)
*mucosal edema*
inc. mucus production
airway narrowing
hypersensitivity/hyperreactivity
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5
Q

asthma

A

hyper reactivity of lungs causes mucosal edema, airway inflammation
why we don’t just give B2s, but steroids–>target inflammation not just dilation

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6
Q

B2 receptors, smooth muscl

A

adr: dilates
chol: constricts

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7
Q

work of breathing is inc. as air-trapping occurs:

A

diaphragm flattened

inspiratory musc. fibers shortened, so little opportun. for further contraction

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8
Q

asthma

A 
industrialized country disease (pollution) 3-5%
chronic airway inflammation maj. mech
hyperreactiv. to triggers
sm. musc hypertrophy (extra work)
can be fatal
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9
Q

asthma: rev or irrev airway narrowing?

A

reversible airway narrowing, bronchospasm, bronchoconstr. (type 1 hypersens. rxn of airways)
COPD is not reversible!!

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10
Q

asthma incidence: increasing?

A

YES: inc. mold, roaches (poop), and pollution

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11
Q

dec. asthma risk with

A

breastfeeding

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12
Q

Curshcmann’s spirals

A

spiral shaped mucus plugs in sputum
desquamated/shed epithelium forms whorled MUCUS PLUGS (see pic)
think asthma

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13
Q

Charccot-Leyden crystals

A

asthma
eosinophilic (allergy related), hexagonal, double pointed needle-like crystals
formed by breakdown of eosinophils in sputum

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14
Q

asthma triggers

A

infections** (URI, pneumonia)
stress
environ.: insects, pollen, mold, pollution, weather changes, air temp/humid.**
allergens (roach droppings, allergies)
subsets of asthma pts: hypersensitivity to Aspirin, NSAIDS (inc. react. w/ motrin, naprocen, etc.) aspirin as well

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15
Q

symptoms of asthma

A

persistent wheeze (may be audible (pretty bad) or with auscultation)
need to be able to tell if asthma pt. is sick or not sick!!
chronic episodic dyspnea
cough
CP, tightness, inc. sputum prod, tachypnea, hypoxemia, dec. I/E ratio, pulsus paradoxus, mucus plugging

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16
Q

pulsus paradoxus

A

systolic will drop during inspiration by =>10mmHg

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17
Q

timeline of wheezing

A

expiratory wheezes –> add inspiratory when more severe (entire phase is wheezing)

  • *end expiratory wheezing** is beginning of asthma
    dec. expiratory phase (3-4 sec–>2-3 sec)
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18
Q

asthma: if no wheezing??

A

usually there is NO air movement

VERY SEVERE

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19
Q

asthma dx

A

Pulm. Func tests: dec. FEV1 which IMPROVES w. bronchodilator
inc. serum IgE and eosins
allergy testing

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20
Q

asthma: CXR

A

hyperinflation (hyperexpansion) w/ flat diaphragms

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21
Q

asthma dx studies

A

measu. of airway reactivity after graded challenge w. inhaled METHACHOLINE or HISTAMINE
bronchoconstriction occurs at LOWER doses in asthma

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22
Q

findings in sev. asthma

A

-speech difficulty
diaphoresis: implies they are sick!!**
-**fatigue: worrisome when become conversationally dyspnic (“are you feeling ok?”)-check in
-hypoxia: attempt to rip off mask; ominous during breathing tx
orthopnea: can’t lay down, diff. to intubate
agitation, somnolence, confusion

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23
Q

acid/base imbalance with asthma

A

respiratory acidosis from not blowing off CO2

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24
Q

accessory muscle use in asthma

A

“belly breathing”, retractions (gut sucks in, ribs stick out)
take shirt off!
tracheal tugging: ant. portion of neck pulls in and out (type of retraction, suprasternal notch)
nasal flaring

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25
Q

questions to ask every pt having an asthma attack

A

ever been intubated? red flag-high risk how many times?
last ED visit? how often?
last attack?
for you, is this a mild, mod, sev. attack compared to previous? -det. baseline
trigger? document

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26
Q

obstructive lung diseases

A 
asthma
bronchiectasis
emphysema
chronic bronchitis
bronchiolitis
CF
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27
Q

albuterol inhaler

A 
rescue inhaler! acute tx
why use? to quickly bronchodilate, NOT a maintenance program, should not be used every day 
B2 agonist, relaxes bronch sm. musc
SE: tachycardia, tremors
inhaler or nebulizing tx
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28
Q

chronic asthma tx

A

peak flow monitoring: >500 is GOOD (200s is worrisome)

  • inhaled corticosteroids: aerobid, azmacort, flovent pulmicort, advair
  • B2 agonist-Albuterol
  • antichol-Atrovent
  • Leukotriene inhib.-singulair
  • mast cell stabilizer-cromolyn
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29
Q

salmeterol (serevent), formoterol

A

B2 agonist
LONG ACTING PPX agent, not for acute
SE: tremor, arrhythmia
inhaled, inc. in deaths in asthmatics???

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30
Q

Methylxanthines

A

older drug, Marshall dislikes
theophylline: :
bronchodilator,
narrow therapeutic index: SE: cario and neuro tox: arrhythmias, seizures
blocks adenosine*
metab. by P450
inhib. phosphodiesterase–>lowers cAMP hydrolysis–>inc. cAMP

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31
Q

Muscarinic antagonist

A

atrovent-(ipratropium)
anticholinergic, comp. block competitive block of musc rec, prev. bronchoconstr.
often used simultaneously w. albuterol
DUONEB

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32
Q

Tiotropium

A

long-acting musc. antagonist

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33
Q

Cromolyn sodium

A

prev. rel. of mediators from mast cells (mast cell stabilizer, prev. mast cell degranulation)
pox only, QID dosing?? dec. compliance
largely repl. by leukotriene rec. antagonist

34
Q

corticosteroids

A

fluticasone, budesonide, prednisone*
(today give out like candy)
can give IV: Solumedrol, about 6 hours to work

35
Q

corticosteroid action

A

inhib. syn. of virtually all cytokines
* FIRST LINE THERAPY* for chronic asthma
- txs inflammation, reduces narrowing, most important
- takes about 6 hrs to work

36
Q

what really helps people

A

inhaled corticosteroid: prevents asthma attacks

take 1-2x day

37
Q

antileukotrienes

A

Zafirlukast, montelukast
-v. expensive, blocks leuk rec, v. good for aspirin-ind. asthma
Zileuton
-v. expensive, liver toxic SE, 5-LOX pathway inhibitor, blocks conversion of arachidonic acid to leukotrienes
prevent attack, do not tx symptoms

38
Q

cure for asthma?

A

NO

if using albuterol inhaler few times a week: uncontrolled

39
Q

Omalizumab

A

MoAb anti IgE Ab
binds mostly unbound serum IgE
used in allergic asthma resistant to inhaled steroids and long acting B2 agonists

40
Q

real life management

A

albuterol +/- atrovent neb: all pts

-if using often, need inh. corticosteroid

41
Q

asthma pt presents to ER

A

DUONEB: albuterol + atrovent: all pts
prednisone PO or Solumedrol IV: all pts (95% pts)
Mag 2 gs IV over 20 min (mod–>sev. pts)
-sm. musc relaxer
terbutaline (bronchodil.-B2) SQ, or EPI SQ (v. severe pts) (Marshall dislikes cardiac effects of EPI)
last ditch effort!
O2: all pts
Bipap: sev. and worse pts
Intubation worst cases: difficult, will desat. very fast!
Heliox: combo of helium and oxygen: makes air thinner, into airways w/ less resistance

42
Q

Bipap

A 
like Cpap: used for sleep apnea
control inspiratory and expiratory pressures
lets O2 in, sucks CO2 out
be careful about barotrauma
pts. need to be cooperative!
43
Q

dx test to consider

A

consider CXR, ABG (Marshall already knows results)
ensure no pneumonia, no dropped lung, etc
-if following pts, consulting pulmonology

44
Q

peak flow

A

how bad is asthma? improving? can take home, know what zone they are in

45
Q

COPD

A

emyphsema
chronic bronchitis

will usually co-exist in same pt!** same: PE (lung sounds), etiology, tx, phys. tx and imaging

46
Q

COPD etiology

A

SMOKING (if stop: 0% of damage done will be reversed :( )
slowly progressive, pts. blow off bc they get used to sym
-dec. abs response to bronchodilators
-inc. prevalence with age
4th leading cause of death in US!

47
Q

COPD: rev. or irreversible obstruction?

A

IRREVERSIBLE obstruction

48
Q

first sign of COPD

A

DOE: dyspnea on exertion

49
Q

COPD is how serious

A

4th leading COD in US!

50
Q

COPD signs

A 
pulmonary HTN
inc. AP diameter of chest
(cough, SOB, wheezing)
access. musc use
dec. breath sounds
prolonged expiratory phase inc. A-P diameter
cyanosis (ends up on home O2)
51
Q

COPD causes

A

a1-antitrypsin deficiency
smoking accounts for up to 90% (a lot of times called asthma)
air pollution
airway hyperresponsiveness (Dutch hypothesis) : unclear mechanism

52
Q

COPD lab findings

A

polycythemia (chr. hypoxemia) (not for asthma)
a1-antitrypsin level (when younger than 40 yo)
sputum: S. pneumo, H. flu most common during exacerbation

53
Q

ABG shows

A

hypoxemia, with or without hypercapnia

54
Q

lung CT shows:

A

alveolar walls breakdown–>non-func airspace coalesce–>bullae
LONG, DARK AIR COLUMNS : dark: not much long tissue left, air trapping, hyperinflation
flattened diaphragm
narrow hear shadow

55
Q

COPD PFT’s

A

essential to dx
FEV1 forced expiratory volume in 1 sec; most common used index of airflow obstruction
TLC, FRC, RV all increased

56
Q

COPD walking distance

A

how far can you walk in 6 minutes?
good predictor of mortality
-desat/hypoxic, higher risk

57
Q

emphysema

A

distinction does not matter as much clinically
“Pink puffer”
air spaces enlarge as alveolar walls are destroyed
air pockets (non-functioning)
loss of elastic recoil-can’t exhale
inc. air trapping
inc. compliance due to loss of elastic fibers
-lose natural recoil that helps you exhale

58
Q

bullae in emphysema

A

alveoli can coalesce to form bullae that compress normal lung, can compress on normal, functioning lungs

59
Q

emphysema: less alveoli cause

A

dec. diffusion capacity

60
Q

inc. elastase activity–>loss of elastic fiber

A

increased compliance

61
Q

centriacinar emphysema

A

smoking

62
Q

panacinar emphysema

A

think a1-antitrypsin def.

more diffuse, involving entire acinus

63
Q

chest shape in emphysema??

A

barrel shape

64
Q

emphysema pts breath how

A

pursed lips : self-taught or learned

increases airway pressure and prevents airway collapse during respirations

65
Q

why are emphysema pts slender?

A

takes more work to breathe,

also sit forward

66
Q

a1-antitrypsin deficiency

A

principal endogenous antiprotease: protects from elastase: uncont. elastase–>lose elasticity of lungs
-genetic, premature

67
Q

emphysema CXR

A
  • hyperinflated lung (may see bottom of heart)-low flattened diaphragm
  • “arterial deficiency”: don’t see many arteries
  • hyperinflation
  • bullous disease
  • may be mistaken for pneumothorax!*
  • ->if not sure, get a CT scan
68
Q

emphysema lung

A

pockets of non-func space

-cigarrette tar: carbon deposits

69
Q

Bullae

A

pocket of non-func. tissue

may need to be surg. removed

70
Q

Chronic Bronchitis

A

“blue bloater”
airway walls become deformed (not “eaten away* like emphysema) and structurally altered due to atrophy, inflammation, smooth muscle hypertrophy, mucus hypersecretion in airway lumen
Productive cough for MORE THAN 3 MONTHS per year, for at least 2 YEARS—does not have to be consecutive
-Small airway disease
-Mucus gland enlargement, (hypertrophy of mucus gland) is histologic hallmark
-Hyperplasia of mucus secreting glands in bronchi

71
Q

Reid index

A

gland layer depth/total bronchial wall thickness:

>50% ind. COPD (need to be dead!!)

72
Q

symptoms of bronchitis

A 
Wheezing
Crackles
Cyanosis
Early onset hypoxemia due to shunting
Late onset dyspnea (not as quick as emphysema pts)
CO2 retention
polychythemia
73
Q

COPD tx

A 
education
oral and inhaled meds (same as asthma..)
stop smoking
pulm. rehab
BiPaP
surg (vol. reduction, bullectomy, lung txp)
O2
74
Q

COPD tx: bronchodilators

A

Beta 2 agonist (albuterol inhaler)
Anticholinergics (atrovent/ipratropium inhaler)
Long acting

75
Q

COPD tx: anti-inflammation

A

Steroids (solumedrol, prednisone)

Inhaled corticosteroids

76
Q

COPD tx: abx?

A

MAYBE; pot. to be inf-related

77
Q

COPD O2 therapy

A

-for supplementation in acute disease, home O2 for chronic lung disease

78
Q

COPD:chronic hypoxic pt: CAUTION**

A

**O2 can worsen hypercapnia
**dec. hypoxia resp. drive (“CO2 retainers”)-chronically elevated, small subset of COPD pop
CO2: 50-60! (should be 30-40)
lost ability to breathe due to high CO2 levels (no longer acts as trigger, chron. elevated)–>if goes higher, CO2 narcosis
-need for O2 only stimulation to breathe
never withhold O2 for hypoxic pt
-if give O2: fall asleep slowly, hypoventilate–>resp. arrest

79
Q

how can you tell if pt. is retaining CO2??

A

ABG:

  • non-CO2 retainer: if elevated CO2, IF ACUTE: low pH, bicarb will be normal (kidneys cannot respond/adapt that quickly! takes days)
  • if CO2 retainer: elevated CO2, NORMAL (typ.) pH, bicarb will be HIGH (chronically elevated to comp. for CO2) -corrected resp. acidosis
80
Q

how to give O2 if CO2 retainer

A

titrated O2, can’t handle too much, will hypoventilate

BiPaP is awesome for this takes CO2 out

81
Q

other things about asthma

A

B blockers can worsen (also COPD)

consider GERD if adult onset asthma

82
Q

restrictive lung disease

A

dec. TLC

CSI (75 decks)

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