Pathophysiology Flashcards
1
Q
Berlin criteria
A
measure of acute lung injury severity
- PaO2/FiO2 less than 300 (normal: 100/.21 = 476)
- no evidence of volume overload
- acute onset of respiratory failure
- bilateral infiltrates on CXR (WHITE OUT)
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
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
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
5
Q
centriacinar emphysema
A
SMOKING
dilatation and destruction of respiratory bronchioles
UPPER lobe process
6
Q
panacinar emphysema
A
alpha-1 antitrypsin deficiency
destruction of entire acinus
LOWER lobe
7
Q
resorption atelectasis
A
airway obstruction by mucous plugs, tumor
resorption of trapped O2 in dependent alveoli
mediastinum shifts TOWARD affected lung
8
Q
compression atelectasis
A
filling of pleural cavity by tumor, blood, air
compression of pulmonary tissue
mediastinum shits AWAY from affected lung
9
Q
contraction atelectasis
A
fibrotic lung or pleura
prevention of full expansion
NOT reversible
10
Q
paraseptal emphysema
A
underlies spontaneous pneumothorax in young adults
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
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
13
Q
Charcot-Leyden crystals
A
disintegration of eosinophils
ASTHMA
14
Q
Curschmann spirals
A
ASTHMA mucous forms tight coils
15
Q
cystic fibrosis
A
chloride transport defect
16
Q
immotile cilia syndrome
A
dynein arm defective
17
Q
Tracheoesophageal (T-E) fistula
A
failure of fetal respiratory tract to separate from the GI tract
18
Q
When do fetal lungs begin to make surfactant?
A
26-32 weeks
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
20
Q
positive end expiratory pressure (PEEP)
A
increase FRC and recruit atelectatic alveoli
improves oxygenation in patient with ARDS already on 100% O2
21
Q
Why would increasing VT in a patient with ARDS increase mortality?
A
increasing tidal volume causes too much stretch and more inflammation
22
Q
high peak pressure and high plateau pressure
A
compliance issue
23
Q
high peak pressure and low plateau pressure
A
resistance issue
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)
25
irreversible airflow limitation in COPD
1. fibrosis
2. loss of elastic recoil
3. destruction of alveolar attachments
26
COPD Tx for each stage
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
27
methacholine challenge test
high negative predictive value
Negative: you don't have it
Positive: inconclusive
Pos: FEV1 decreased by 20% with 8 mg/dL dose
28
asthma Tx
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
29
extrinsic asthma
```
MOST COMMON
IgE mediated
response to allergen
acute: minutes
late: hours
Family Hx
```
30
intrinsic asthma
triggered by respiratory infection
ADULT
NO IgE, Fam Hx doesn't matter, skin antigen test neg.
31
drug-induced asthma
ADULT
| ASPIRIN, NSAIDs
32
Samter's syndrome
1. asthma
2. aspirin sensitivity
3. nasal polyps
33
occupational asthma
ADULT
occurs after repeated exposure and sensitization
fumes, dusts, chemicals, gasses at work
IgE and non-IgE
34
exercise induced asthma
IMMEDIATELY after EXERCISE (5-10 min)
Cooling and drying of mucosal airways
Tx: pretreat with B agonist, slow warm up period
35
cough variant asthma
Sx: cough (possibly without wheezing); chronic cough with irritants
Dx: positive clinical response to treatment, methacholine inhalation challenge by aid in diagnosis
36
nocturnal asthma
Sx midnight to 8 am
| decline of circulating catecholamines and cortisol
37
signs of life-threatening asthma
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
38
reversibility criteria for Dx of asthma
uses bronchodilator
12% improvement AND 200cc increase in FEV1 and/or FVC
OR
15% from basal FEV1
39
triggers of asthma
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
40
intrinsic restrictive lung disease
alterations in lung
1. interstitial lung disease
2. resection of lung tissue
41
extrinsic restrictive lung disease
alteration in the structures surrounding lung
1. disease of pleura
2. disease of chest wall
3. neuromuscular disorder
42
interstitial lung disease
diffuse inflammatory process involving the lung parenchyma resulting in excess growth of connective tissue with dysfunction of lungs
43
drugs that induce interstitial lung disease
bleomycin
amiodarone
nitrofurantion
external radiation
44
granulomatous interstitial lung disease
berylliosis
hypersensitivity pneumonitis
sarcoidosis
45
list of interstitial lung diseases
```
berylliosis
hypersensitivity pneumonitis
asbestos, coal, silica
drug induced
sarcoidosis
unknown etiology:
idiopathic interstitial penumonias
ILD with connective tissue diseases
```
46
Interstitial lung disease (ILD)
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
47
radiologic finding of end stage ILD
Honeycomb
48
radiologic finding of early stage ILD
ground glass
49
CFTR
| What happens when it is mutated?
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
cystic fibrosis
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
what is the most common CF mutation?
FD508
52
What is the sweat chloride level of a CF patient?
greater than 60 mmol/liter
53
complications of CF
osteoporosis, hypertrophic pulmonary osteoarthropathy, allergic aspergillus, hempoptysis, spontaneous pneumothorax
54
systemic inflammatory response syndrome (SIRS)
```
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
sepsis
SIRS + infection
profound immune activation
inflammatory cytokines elevated, NEUTROPHILIC leukocytosis
lacks sensitivity and specificity
56
severe sepsis
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
septic shock
sepsis + hypotension not responding to fluid resuscitation
| Tx: VASOPRESSORS
58
crystalloids
saline/LR
| resuscitation fluid of choice for septic shock
59
early goal directed therapy (EGDT)
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
afebrile infections
1. very young or old
2. CKD
3. DM
4. steroid use/NSAIDS
5. immunocompromised
6. neurologic: stroke or brain malformation
61
preventative measures in sepsis
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
GM-CSF
can cause SIRS
63
What lab work should be done before giving antibiotics to someone with sepsis?
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
levophed
NE for septic shock
BETTER than dopamine
add vasopressin
then wean levophed first then vasopressin
65
Factors that play a role in pleural effusion
1. hydrostatic pressure
2. oncotic pressure
3. tissue pressure
4. lymphatic drainage
66
Which pleura has lymph drainage?
parietal
67
What condition is indicated if a pleural effusion is due to increased hydrostatic pressure? Transudate or exudate?
```
MOST COMMON
heart failure
transudate
see cardiomegaly
PWP greater than 24 mmHg
visceral pleura shifts from fluid absorption to fluid formation
Tx: diuretics
```
68
What condition is indicated if a pleural effusion is due to decreased hydrostatic pleural pressure? Transudate or exudate?
atelectasis
transudate
visceral and pleural formation of fluid
69
What condition is indicated if a pleural effusion is due to decreased systemic oncotic pressure? Transudate or exudate?
low albumin: malnutrition, renal loss, decreased production in liver
transudate
visceral and pleural formation of fluid
70
What condition is indicated if a pleural effusion is due to increased oncotic pressure in pleural space? Transudate or exudate?
inflammation (increased vascular permeability): infection, cancer
exudate
visceral and pleural formation of fluid
71
Sx of pleural effusion
dullness to percussion
decreased tactile remits
increased RR
decreased breath sounds
72
indication for thoracentesis of pleural fluid
greater than 10 mm on lateral decubitus Xray
73
How do you differentiate between transudate and exudate in pleural effusion?
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
What does a pleural fluid with greater than 5% mesothelial cells EXCLUDE?
TB pleurisy
75
```
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. transudate
b. Chronic: TB, CA
c. parapneumonic, pancreatitis, pulm. infarct
d. parapneumonic ONLY
76
What could low pleural fluid glucose be due to?
```
decreased transport:
1. rheumatiod
2. CA
increased utilization: infection
1. empyema
2. TB
3. esophageal rupture
```
77
What can you suspect if pleural fluid is acidotic?
1. esophageal rupture
2, empyema
3. rheumatoid
other: CA, TB, lupus
78
What can you suspect if pleural fluid amylase/serum amylase is greater than or equal to 1?
```
acute pancreatitis
pancreatic pseudocyst
esophageal rupture
CA
ruptured ectopic pregnancy
```
79
What is the most likely cause of lymphocytosis in pleural effusion?
TB
| other: CA
80
primary pulmonary artery hypertension (PAH)
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
causes of secondary PAH
1. parenchymal lung disease
2. chronic thromboembolic disease
3. left sided valve disease
4. myocardial disease
5. systemic connective tissue disease
82
what are the 5 groups of PAH
1. primary PAH
2. heart disease
3. lung disease
4. CTEPH
5. multifactorial
83
Factors that play a role in PAH pathogenesis
1. prostacyclin, TXA2
2. ET-1
3. NO (reduced nitric oxide synthase)
4. serotonin
5. VEGF
5. ANOREXIANTS (phenphen)
7. CNS stimulant (COCAINE)
84
conditions associated with PAH
SCLERODERMA, HIV, SICKLE CELL
| other: HHV-8, SLE, MCTD, RA, portal HTN, thrombocytsis (SEROTONIN), HHT (free heme and iron)
85
BMPR2 (bone morphogenetic protein receptor type II)
familial primary pulmonary HTN
86
NO role in PAH
PAH: reduced
vasodilation
inhibits sm. muscle growth
87
endothelin 1 role in PAH
potent vasoconstrictor
| mitogen for Sm. muscle cells
88
VEGF role in PAH
speculative role in PAH
endothelial growth stimulate
expressed by endothelial cells in PLEXIFORM lesions
89
serotonin role in PAH
high levels in PPH
| vasoconstriction and proliferation of sm. muscle cels
90
Kv (voltage gated potassium channels) role in PAH
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
anorexiants role in PAH
appetite suppressant
| blocks voltage gated potassium channels
92
What is the first test if PPH is suspected?
echocardiograph: good screen
| evidence of: right heart enlargement, paradoxical motion IVS, tricuspid insufficiency
93
What indicates a better prognosis in PPH?
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
Drugs that improve survival in PAH
epoprostenol
bosentan
anticoagulation
95
S1Q3
EKG finding in a minority of pulmonary thromboembolism patients
96
pulmonary thromboembolism
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
Virchow's Triad
predisposing factors for clot formation (PE)
1. stasis
2. hypercoagulable
3. endothelial injury
98
congenital hyper-coagulability diseases
1. factor V Leiden mutation
2. antithrombin III deficinecy
3. prothrombin G20210A
4. protein C and S deficiency
5. dysfibrinogenemia
6. homocystinemia
99
acquired hypercoagulability
1. estrogen use
2. preganancy
3. malignancy
4. nephrotic syndrome
other: thrombocytosis, DIC, HIT (don't give heparin), antiphospholipid Ab syndrome, PNH
100
physiologic consequences of PE
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
How does circulation compensate in PE?
1. vasodilation of uninvolved vasculature
2. helps decrease PVR
3. improves V/Q in uninvolved areas
4. improves overall oxygenation
102
EKG findings in PE
1. nonspecific ST-T abnormalities
2. tachycardia
3. atrial arrhythmias
4. MINORITY: S1Q3T3
103
Lab data seen in PE
ELEVATED D DIMER (> 500)
low: PaO2, PaCO2
wide: A-a
elevated: BNP, troponin, LDH, bilirubin
normal: WBC (can be elevated), transminases
104
V/Q lung scan meaning in PE
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
GOLD standard for PE
pulmonary angiography
106
what is the primary diagnosis modality of choice for PE?
helical CT
| if PE excluded: provides an alternate Dx in most patients
107
Signs of DVT
swelling in one leg
| Homan's only 50:50
108
Best diagnosis measure for DVT
real-time (B-mode) ultrasonography
109
Gold standard for Dx DVT and why isn't it used
ascending contrast venography
| can dislodge DVT and cause a pulmonary embolism
110
prevention of DVT
```
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
aPTT
activate partial thromboplastin time
| monitor heparin
112
PT
prothrombin time
| monitor warfarin
113
Factor Xa
low molecular weight heparin
114
Tx of DVT
radiological: disrupt with catheter
surgical: RARE
SHOCK: t-PA for thrombolysis
115
fat embolism triad
long bone fractures in elderly
1. mental status change
2. thrombocytopenia
3. petechiae in chest and neck
