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Pulm > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

Berlin criteria

A

measure of acute lung injury severity

  1. PaO2/FiO2 less than 300 (normal: 100/.21 = 476)
  2. no evidence of volume overload
  3. acute onset of respiratory failure
  4. bilateral infiltrates on CXR (WHITE OUT)
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2
Q

asthma

A

airway hyper responsiveness: OBSTRUCTION, inflammation, epithelial injusry, neural mechanisms, intrinsic airway smooth muscle function
CD4 T cells, TH2
eosinophils, basophils, mast cells, eosinophilic cationic protein, major basic protein, histamine, leukotrienes, PG, PAF
IgE, IL-5
inflammatory, episodic, reversible bronchospasm
exacerbation: neutrophilic
reduce: FEV1, FVC, and FEV1:FVC ratio (reverses with bronchodilators)
NORMAL TLC
REVERSIBLE
Dx: SOB, WHEEZE, diurnal variation of PEFR greater than 20%, reduction of FEV1/FVC that is reversible, hyperinflation
NORMAL DLCO

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3
Q

COPD

A 
CD8 T cells
IL-8, macrophages (CD68+), neutrophils
exacerbation: eosinophilic
reduced: FEV1, FVC, and FEV1: FVC ratio 
FEV1: FVC less than 70
PARTIALLY reversible
Sx: cough, dyspnea, sputum
risk: tobacco, pollution, occupational
Dx: SPIROMETRY
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4
Q

emphysema

A

permanent abnormal enlargement of air spaces distal to the terminal bronchioles, occurs in the lung parenchyma in COPD
PINK puffer
V/Q mismatch, LOW DLCO
HYPERVENTILATION (maintain normal PCO2), tachypnea, thin

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5
Q

centriacinar emphysema

A

SMOKING
dilatation and destruction of respiratory bronchioles
UPPER lobe process

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6
Q

panacinar emphysema

A

alpha-1 antitrypsin deficiency
destruction of entire acinus
LOWER lobe

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7
Q

resorption atelectasis

A

airway obstruction by mucous plugs, tumor
resorption of trapped O2 in dependent alveoli
mediastinum shifts TOWARD affected lung

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8
Q

compression atelectasis

A

filling of pleural cavity by tumor, blood, air
compression of pulmonary tissue
mediastinum shits AWAY from affected lung

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9
Q

contraction atelectasis

A

fibrotic lung or pleura
prevention of full expansion
NOT reversible

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10
Q

paraseptal emphysema

A

underlies spontaneous pneumothorax in young adults

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11
Q

A1 anti-trypsin deficiency

A

liver biopsy: pink PAS positive hyaline globules
misfolded protein accumulates in the ER
PiZZ homozygotes: liver cirrhosis and panacinar emphysema
PiMZ heterozygotes: ok unless smoker

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12
Q

chronic bronchitis

A

persistant cough with sputum at least 3 months in at least 2 consecutive years
Reid index > 50%
BLUE bloater, hypoxemia and hypercapnia
V/Q mismatch
long term hypoxemia: polycythemia, pull HTN, cor pulmonale (right heart failure causes edema)
HYPOVENTILATION

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13
Q

Charcot-Leyden crystals

A

disintegration of eosinophils

ASTHMA

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14
Q

Curschmann spirals

A

ASTHMA mucous forms tight coils

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15
Q

cystic fibrosis

A

chloride transport defect

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16
Q

immotile cilia syndrome

A

dynein arm defective

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17
Q

Tracheoesophageal (T-E) fistula

A

failure of fetal respiratory tract to separate from the GI tract

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18
Q

When do fetal lungs begin to make surfactant?

A

26-32 weeks

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19
Q

Allergic Bronchopulmonary Aspergillosis (ABPA) criteria

A 
asthma due to Aspergillus
type III IgE response
1. poorly controlled ASTHMA
2. EOSINOPHILIA
3. IgE > 1000ng/ml
other
4. Aspergillus Fumigatus positive skin antigen test, IgG Ab
5. proximal bronchiectasis
6. fleeting chest infiltrates
7. peripheral eosinophilia with chest infiltrates
Tx: PREDNISONE
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20
Q

positive end expiratory pressure (PEEP)

A

increase FRC and recruit atelectatic alveoli

improves oxygenation in patient with ARDS already on 100% O2

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21
Q

Why would increasing VT in a patient with ARDS increase mortality?

A

increasing tidal volume causes too much stretch and more inflammation

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22
Q

high peak pressure and high plateau pressure

A

compliance issue

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23
Q

high peak pressure and low plateau pressure

A

resistance issue

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24
Q

mechanisms underlying airway limitation in COPD

Irreversible vs Reversible

A

Irreversible
1. fibrosis and narrowing of airway
2. loss of elastic recoil
3. destruction of alveolar attachments that keep airway open
Reversible
1. inflammation, exudate, mucus accumulation
2. sm. muscle contraction of airway
3. hyperinflation (increased WOB and reduced exercise intolerance)

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25
Q

irreversible airflow limitation in COPD

A
  1. fibrosis
  2. loss of elastic recoil
  3. destruction of alveolar attachments
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26
Q

COPD Tx for each stage

A

I: mild: reduction of risk factors (pneumococcal and flu vaccine) and short acting bronchodilator when needed
II: moderate: ADD long acting bronchodilator and rehabilitation
III: ADD inhaled glucocorticoids if repeated exacerbations
IV: very severe: ADD longterm O2 if chronic respiratory failure; consider Sx

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27
Q

methacholine challenge test

A

high negative predictive value
Negative: you don’t have it
Positive: inconclusive
Pos: FEV1 decreased by 20% with 8 mg/dL dose

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28
Q

asthma Tx

A
  1. intermittent: as needed short acting beta2 agonist or short acting anticholinergic
  2. mild: add inhaled corticosteroid
  3. moderate: add long acting beta agonist
  4. severe: add leukotriene modifiers
    other: systemic steroids, anti-IgE
    IMPORTANT: LABA associated with increased mortality
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29
Q

extrinsic asthma

A 
MOST COMMON
IgE mediated
response to allergen
acute: minutes
late: hours
Family Hx
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30
Q

intrinsic asthma

A

triggered by respiratory infection
ADULT
NO IgE, Fam Hx doesn’t matter, skin antigen test neg.

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31
Q

drug-induced asthma

A

ADULT

ASPIRIN, NSAIDs

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32
Q

Samter’s syndrome

A
  1. asthma
  2. aspirin sensitivity
  3. nasal polyps
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33
Q

occupational asthma

A

ADULT
occurs after repeated exposure and sensitization
fumes, dusts, chemicals, gasses at work
IgE and non-IgE

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34
Q

exercise induced asthma

A

IMMEDIATELY after EXERCISE (5-10 min)
Cooling and drying of mucosal airways
Tx: pretreat with B agonist, slow warm up period

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35
Q

cough variant asthma

A

Sx: cough (possibly without wheezing); chronic cough with irritants
Dx: positive clinical response to treatment, methacholine inhalation challenge by aid in diagnosis

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36
Q

nocturnal asthma

A

Sx midnight to 8 am

decline of circulating catecholamines and cortisol

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37
Q

signs of life-threatening asthma

A
  1. accessory muscle use on
  2. presentation
  3. pulsus paradoxus
  4. right heart strain: P-pulmonale on EKG
  5. hypoxemia
  6. hypercapnia
    death: usually DIFFUSE MUCOUS PLUGS
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38
Q

reversibility criteria for Dx of asthma

A

uses bronchodilator
12% improvement AND 200cc increase in FEV1 and/or FVC
OR
15% from basal FEV1

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39
Q

triggers of asthma

A
  1. humidity/ change in pressure
  2. allergens: dust mites, pollen, cockroach, food, NSAIDS
  3. occupation
  4. URI, sinusitis
  5. GERD
  6. hormonal
  7. psychological
  8. cigarettes
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40
Q

intrinsic restrictive lung disease

A

alterations in lung

  1. interstitial lung disease
  2. resection of lung tissue
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41
Q

extrinsic restrictive lung disease

A

alteration in the structures surrounding lung

  1. disease of pleura
  2. disease of chest wall
  3. neuromuscular disorder
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42
Q

interstitial lung disease

A

diffuse inflammatory process involving the lung parenchyma resulting in excess growth of connective tissue with dysfunction of lungs

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43
Q

drugs that induce interstitial lung disease

A

bleomycin
amiodarone
nitrofurantion
external radiation

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44
Q

granulomatous interstitial lung disease

A

berylliosis
hypersensitivity pneumonitis
sarcoidosis

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45
Q

list of interstitial lung diseases

A 
berylliosis
hypersensitivity pneumonitis
asbestos, coal, silica
drug induced
sarcoidosis
unknown etiology:
idiopathic interstitial penumonias
ILD with connective tissue diseases
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46
Q

Interstitial lung disease (ILD)

A

hypoxemia, HYPOcapnea, wide A-a gradient, exercise induced hypoxemia
Sx: DYSPNEA (most common), tachypnea, crackles, CLUBBING
late: cor-pulmonale, cyanosis
Dx: Hx, Sx, imaging, PFT, BAL (broncho-alveolar lavage) and lung biopsy
MACROPHAGES mostly, lymphocytes, few PMN

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47
Q

radiologic finding of end stage ILD

A

Honeycomb

48
Q

radiologic finding of early stage ILD

A

ground glass

49
Q

CFTR

What happens when it is mutated?

A

cystic fibrosis gene
cell surface: regulated chloride channel
normal: inhibits ENaC
mutant: ENaC not inhibited: Na absorption increased and water follows: low airway fluid and Cl- not secreted
mucus is dehydrated: impairs mucociliary clearance

50
Q

cystic fibrosis

A

white
autosomal recessive
chromosome 7
bacterial airway infections, nasal polyps, pancreatitis, elevated sweat electrolytes, hepatobiliary disease, meconium ileum, obstructive azoospermia, portal HTN, clubbing
suspect if see: non-TB mycobacterial infection, allergic bronchopulmonary aspergillosis
most infected with P. aeruginosa by 18

51
Q

what is the most common CF mutation?

A

FD508

52
Q

What is the sweat chloride level of a CF patient?

A

greater than 60 mmol/liter

53
Q

complications of CF

A

osteoporosis, hypertrophic pulmonary osteoarthropathy, allergic aspergillus, hempoptysis, spontaneous pneumothorax

54
Q

systemic inflammatory response syndrome (SIRS)

A 
due to infection proven or suspected
NOT a positive culture
1. Temp: greater than 38 or less than 36
2. heart rater greater than 90 bpm
3. tachypnea (RR greater than 20)
4. white blood count greater than 12,000 or less than 4000 with greater than 10% bands
55
Q

sepsis

A

SIRS + infection
profound immune activation
inflammatory cytokines elevated, NEUTROPHILIC leukocytosis
lacks sensitivity and specificity

56
Q

severe sepsis

A

sepsis + organ dysfunction (or evidence of hypoperfusion)
MENTAL status change, increases MINUTE VENTILATION, not tolerating feeds
other: fever, tachycardia, tachypnea, hypotension, N/V, loss of appetite

57
Q

septic shock

A

sepsis + hypotension not responding to fluid resuscitation

Tx: VASOPRESSORS

58
Q

crystalloids

A

saline/LR

resuscitation fluid of choice for septic shock

59
Q

early goal directed therapy (EGDT)

A

improves mortality of sepsis
two or more of:
1. central venous pressure 8-12 mmHg
2. mean arterial pressure greater than 65 mmHG
3. urine output greater than O.5 mL/kg/hr
4. central venous O2 saturation greater than 70%
Tx: underlying cause

60
Q

afebrile infections

A
  1. very young or old
  2. CKD
  3. DM
  4. steroid use/NSAIDS
  5. immunocompromised
  6. neurologic: stroke or brain malformation
61
Q

preventative measures in sepsis

A
  1. DVT prophylaxis: early ambulation
  2. stress ulcer prophylaxis
  3. remove foley catheter and central lines
  4. target glucose less than 150 mg/dL
  5. chlorhexidine mouthwash
    other: hand washing, head of bed elevation to prevent VAP/HAP
    FASTHUG: feeds, analgesics, sedation, thromboembolism, head of bead, ulcer, glucose
62
Q

GM-CSF

A

can cause SIRS

63
Q

What lab work should be done before giving antibiotics to someone with sepsis?

A

GET antibiotics EARLY or DIE

  1. gram stain and culture of appropriate body fluids
  2. TWO blood cultures: vascular device and peripheral
  3. imaging
  4. good H&P
64
Q

levophed

A

NE for septic shock
BETTER than dopamine
add vasopressin
then wean levophed first then vasopressin

65
Q

Factors that play a role in pleural effusion

A
  1. hydrostatic pressure
  2. oncotic pressure
  3. tissue pressure
  4. lymphatic drainage
66
Q

Which pleura has lymph drainage?

A

parietal

67
Q

What condition is indicated if a pleural effusion is due to increased hydrostatic pressure? Transudate or exudate?

A 
MOST COMMON
heart failure
transudate
see cardiomegaly
PWP greater than 24 mmHg
visceral pleura shifts from fluid absorption to fluid formation
Tx: diuretics
68
Q

What condition is indicated if a pleural effusion is due to decreased hydrostatic pleural pressure? Transudate or exudate?

A

atelectasis
transudate
visceral and pleural formation of fluid

69
Q

What condition is indicated if a pleural effusion is due to decreased systemic oncotic pressure? Transudate or exudate?

A

low albumin: malnutrition, renal loss, decreased production in liver
transudate
visceral and pleural formation of fluid

70
Q

What condition is indicated if a pleural effusion is due to increased oncotic pressure in pleural space? Transudate or exudate?

A

inflammation (increased vascular permeability): infection, cancer
exudate
visceral and pleural formation of fluid

71
Q

Sx of pleural effusion

A

dullness to percussion
decreased tactile remits
increased RR
decreased breath sounds

72
Q

indication for thoracentesis of pleural fluid

A

greater than 10 mm on lateral decubitus Xray

73
Q

How do you differentiate between transudate and exudate in pleural effusion?

A

exudate:

  1. pleural/serum protein ratio greater than 0.5
  2. pleural/srum LDH ratio more than 0.6
  3. serum LDH greater than 200 U/L
    transudate: ABSENCE of all 3
74
Q

What does a pleural fluid with greater than 5% mesothelial cells EXCLUDE?

A

TB pleurisy

75
Q 
What does a WBC of 
a. less than 1000/ ul
b. greater than 5000
c. greater than 10,000
d. greater than 50,000
indicate?
A

a. transudate
b. Chronic: TB, CA
c. parapneumonic, pancreatitis, pulm. infarct
d. parapneumonic ONLY

76
Q

What could low pleural fluid glucose be due to?

A 
decreased transport:
1. rheumatiod
2. CA
increased utilization: infection
1. empyema 
2. TB
3. esophageal rupture
77
Q

What can you suspect if pleural fluid is acidotic?

A
  1. esophageal rupture
    2, empyema
  2. rheumatoid
    other: CA, TB, lupus
78
Q

What can you suspect if pleural fluid amylase/serum amylase is greater than or equal to 1?

A 
acute pancreatitis
pancreatic pseudocyst
esophageal rupture
CA
ruptured ectopic pregnancy
79
Q

What is the most likely cause of lymphocytosis in pleural effusion?

A

TB

other: CA

80
Q

primary pulmonary artery hypertension (PAH)

A
  1. mean PAP greater than 25 mmHg at rest (30 with exercise)
  2. mean PCWP and LVEDP less than 15 mmHG (rules out heart failure as a cause)
    Sx: fatigue, exertion dyspnea, chest pain, syncope, edema
    need HIGH INDEX of SUSPICION
    Dx: apical impulse shifts OUT, parasternal HEAVE, accentuated and palpable P2, widely split S2, SEM L 2nd ICS
    can have: RHF signs: JVD, bilateral leg edema, prominent central arteries on CXR, mild decreased DLCO, EKG: R axis deviation
    POOR PROGNOSIS without Tx
81
Q

causes of secondary PAH

A
  1. parenchymal lung disease
  2. chronic thromboembolic disease
  3. left sided valve disease
  4. myocardial disease
  5. systemic connective tissue disease
82
Q

what are the 5 groups of PAH

A
  1. primary PAH
  2. heart disease
  3. lung disease
  4. CTEPH
  5. multifactorial
83
Q

Factors that play a role in PAH pathogenesis

A
  1. prostacyclin, TXA2
  2. ET-1
  3. NO (reduced nitric oxide synthase)
  4. serotonin
  5. VEGF
  6. ANOREXIANTS (phenphen)
  7. CNS stimulant (COCAINE)
84
Q

conditions associated with PAH

A

SCLERODERMA, HIV, SICKLE CELL

other: HHV-8, SLE, MCTD, RA, portal HTN, thrombocytsis (SEROTONIN), HHT (free heme and iron)

85
Q

BMPR2 (bone morphogenetic protein receptor type II)

A

familial primary pulmonary HTN

86
Q

NO role in PAH

A

PAH: reduced
vasodilation
inhibits sm. muscle growth

87
Q

endothelin 1 role in PAH

A

potent vasoconstrictor

mitogen for Sm. muscle cells

88
Q

VEGF role in PAH

A

speculative role in PAH
endothelial growth stimulate
expressed by endothelial cells in PLEXIFORM lesions

89
Q

serotonin role in PAH

A

high levels in PPH

vasoconstriction and proliferation of sm. muscle cels

90
Q

Kv (voltage gated potassium channels) role in PAH

A

control cell membrane potential and release of Ca

PPH: pulmonary artery sm. muscle has low mRNA for K channels and low channel curren: increase intracellular Ca

91
Q

anorexiants role in PAH

A

appetite suppressant

blocks voltage gated potassium channels

92
Q

What is the first test if PPH is suspected?

A

echocardiograph: good screen

evidence of: right heart enlargement, paradoxical motion IVS, tricuspid insufficiency

93
Q

What indicates a better prognosis in PPH?

A

vasoreactivity with NO: greater than 20 percent reduction in PAP and PVR

greater than 10 mmHg drop in MPAP (should drop to less than 40mmHg)

94
Q

Drugs that improve survival in PAH

A

epoprostenol
bosentan
anticoagulation

95
Q

S1Q3

A

EKG finding in a minority of pulmonary thromboembolism patients

96
Q

pulmonary thromboembolism

A

LOWER extremities
Sx: bronchospasm, wheezing, dyspnea, pleuritic pain, tachypnea, tachycardia, LOUD P2
Tx: initiate as soon as suspected (DON’T wait to prove Dx)

97
Q

Virchow’s Triad

A

predisposing factors for clot formation (PE)

  1. stasis
  2. hypercoagulable
  3. endothelial injury
98
Q

congenital hyper-coagulability diseases

A
  1. factor V Leiden mutation
  2. antithrombin III deficinecy
  3. prothrombin G20210A
  4. protein C and S deficiency
  5. dysfibrinogenemia
  6. homocystinemia
99
Q

acquired hypercoagulability

A
  1. estrogen use
  2. preganancy
  3. malignancy
  4. nephrotic syndrome
    other: thrombocytosis, DIC, HIT (don’t give heparin), antiphospholipid Ab syndrome, PNH
100
Q

physiologic consequences of PE

A
  1. increased PVR: obstruction, neurohumoral
  2. impaired gas exchange:
    a. V/Q mismatch (WIDE A-a)
    b. low DLCO
    c. shunt (massive PE)
  3. hyperventilation (HYPOCAPNIA)
  4. increased airway resistance (wheeze)
  5. decreased compliance
    HYPOXEMIA
101
Q

How does circulation compensate in PE?

A
  1. vasodilation of uninvolved vasculature
  2. helps decrease PVR
  3. improves V/Q in uninvolved areas
  4. improves overall oxygenation
102
Q

EKG findings in PE

A
  1. nonspecific ST-T abnormalities
  2. tachycardia
  3. atrial arrhythmias
  4. MINORITY: S1Q3T3
103
Q

Lab data seen in PE

A

ELEVATED D DIMER (> 500)

low: PaO2, PaCO2
wide: A-a
elevated: BNP, troponin, LDH, bilirubin
normal: WBC (can be elevated), transminases

104
Q

V/Q lung scan meaning in PE

A

high clinical suspicion and high probability lung scan: confirms PE
both low: excludes PE
pitfalls: 15 sec hold breath, observer variability, most are indeterminate

105
Q

GOLD standard for PE

A

pulmonary angiography

106
Q

what is the primary diagnosis modality of choice for PE?

A

helical CT

if PE excluded: provides an alternate Dx in most patients

107
Q

Signs of DVT

A

swelling in one leg

Homan’s only 50:50

108
Q

Best diagnosis measure for DVT

A

real-time (B-mode) ultrasonography

109
Q

Gold standard for Dx DVT and why isn’t it used

A

ascending contrast venography

can dislodge DVT and cause a pulmonary embolism

110
Q

prevention of DVT

A 
1. heparin 5000 units SQ every 8 hours
OR
low molecular weight heparin
2. early mobilization
3. T.E.D. hose stocking
4. intermittent external  pneumatic compression of calf and thigh
111
Q

aPTT

A

activate partial thromboplastin time

monitor heparin

112
Q

PT

A

prothrombin time

monitor warfarin

113
Q

Factor Xa

A

low molecular weight heparin

114
Q

Tx of DVT

A

radiological: disrupt with catheter
surgical: RARE
SHOCK: t-PA for thrombolysis

115
Q

fat embolism triad

A

long bone fractures in elderly

  1. mental status change
  2. thrombocytopenia
  3. petechiae in chest and neck

Pulm (11 decks)

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