Respiratory pathophys. part 2 Flashcards
0
Q
risk factors for asthma
A
Host factors: genetic, gender (F), obesity
Environmental factors: allergens, occupational sensitizers, tobacco smoke, air pollution, respiratory infections (RSV), diet (low Vit. D)
1
Q
asthma (defn)
A
chronic inflammatory disorder of the airways,
(typically eosinophilic inflamm)
–> recurrent episodes of wheezing, chest tightness, cough,
*usually reversible, BUT can get remodeling(!)
2
Q
Th1 vs. Th2 asthma phenotype
A
Th1: get Sx young, but go away (rural, have siblings, go to daycare, etc)
Th2: get asthma older & it stays (urban, more antibiotics, less trigger exposure when young)
3
Q
Major cell types involved in asthma
A
Inflammatory: Eosinophils, mast cells, Th2
Structural: epithelial, sm. muscle, and endothelial, etc.
4
Q
low V/Q vs. shunt
A
Low V/Q: decreased ventilation to that alveolus, but may be normal elsewhere. CAN correct PCO2 AND PO2 with adding O2.
Shunt: completely blocked ventilation to that alveolus, but may be normal elsewhere. CanNOT correct PO2 (but can PCO2) with adding O2.
5
Q
Acute Respiratory Distress Syndrome
A
- Acute (within 7 days)
- bilateral infiltrates on CXR
- infiltrates not fully explained by heart failure of fluid overload
- hypoxia (use PaO2/FiO2 to rate severity)
6
Q
Pathogenesis of pneumonia (4 types)
A
- pneumonia = infection of lung tissue
1. aspiration (most common cause)
2. aerosol
3. hematogenous
4. reactivation
7
Q
Aspiration pneumonia
A
something goes down wrong way & causes infection;
- requires abnormal host or abnormal flora **
from:
- requires abnormal host or abnormal flora **
- oropharyngeal secretions (#1)
- stomach contents
- foreign body
8
Q
respiratory characteristics of abnormal host:
A
- Impaired airway/mucociliary clearance
- poor cough: COPD, EtOH, neuro disease, lung cancer;
- bad cilia: kartagener’s, immotile cilia syndrome, viral inf, CF - medications
- - antipsychotics, antacids, inhaled corticosteroids
9
Q
most common bacteria causing pneumonia (5)
A
(for community-acquired pneumonia)
- S. pneumonia - H. influenzae
- S. aureus - Mycoplasma
- legionella *aerobic gram neg. bacteria
10
Q
Diagnosis of pneumonia
A
1: abnormal CXR (esp. compared to previous x-ray for that person) ** help distinguish from bronchitis **
- or CT scan
- Use history to understand exposures!
- Antigen tests (pneumococcus, influenza, legionella)
- Culture sputum, etc – only if likely severe, should not delay antibiotic start
- Use history to understand exposures!
11
Q
Empiric therapy for pneumonia in OUTpatients
A
Low resistance risk: macrolide (antibiotic)
High resistance risk: macrolide + beta lactam or fluoroquinolone, for 5+ days
12
Q
Empiric pneumonia therapy in Inpatients or non-Psuedomonas ICU
A
Inpt: Fluoroquinolone OR beta lactam + macrolide
ICU: beta lactam + macrolide or fluoroquinolone
13
Q
Empiric therapy in ICU pts w/ possible pseudomonas
A
Anti-pseudomonal + ciprofloxacin
- be wary of other causes of pneumonia-like Sxs!!!
- -> take step back and reassess if not getting better!
14
Q
Virchow’s triad
A
=> increase risk for thrombus formation: (can lead to PE)
- venous stasis
- endothelial damage
- hypercoagulability
15
Q
imaging used to prove DVT
A
- venography (w/ contrast, CT)
- doppler ultrasound
16
Q
Imaging used to prove Pulmonary Embolism
A
- pulmonary angiography (w/ contrast)
- ventilation-perfusion lung scan
- CT angiography
- MRI
- Need clinical insight (Hx, etc) along w/ imaging to make Dx**
17
Q
Common sources for emboli (sites)
A
(usually Deep Vein Thrombosis - DVT)
- External iliac v.
- superficial femoral v.
- deep femoral v.
- popliteal v.
- posterior tibial v.
18
Q
Westermark’s Sign
A
Xray finding indicating pulmonary embolism;
= localized oligemia w/ proximal pulmonary artery enlargement.
(rare, but classic if seen)
19
Q
Hampton’s Hump
A
Xray finding indicative of pulmonary embolism,
= localized pleural triangular density.
–> = visualization of infarcted tissue from PE.
(rare, but classic if seen)
20
Q
type of effusion found w/ pulmonary embolism
A
not always w/ PE, but if so, will be:
small, hemorrhagic exudative effusion.
21
Q
typical ABG (blood gas) levels in Pulmonary Embolism
A
- hyperventilation
- low PaCO2
- PaO2 normal OR low
(WARNING: can have 100% normal ABG w/ PE!)
22
Q
Utility of V/Q scan in diagnosing PE
A
normal V/Q scan EXCLUDES pulmonary embolism;
abnormal is not diagnostic (not specific).
23
Q
Utility of D-dimer test in diagnosing pulmonary embolism
A
if low clinical suspicion of PE: normal D-dimer excludes PE;
otherwise not specific/diagnostic
24
Common ECG findings w/ pulmonary embolism
1. R ventricular dilation & hypokinesis
2. Intraventricular septal shift (bulges away from RV)
(3. "clots en passage" = clots sitting in heart RA, waiting to travel to lungs)
25
Therapies for pulmonary embolism (what, why, when)
#1. Anti-coagulation (Heparin 1st, then warfarin/indraparinux)
*start empirically!
2. Thrombolysis (tPA or urokinase)
- esp. if hypotensive or hemodynamically unstable,
BUT has risk of intracranial hemorrhage!
3. Surgical thrombectomy or umbrella
- if contraindication to anti-coag, or recurrence on anti-coag.
26
Main strategies for prevention of pulmonary embolisms
```
#1: Early ambulation after surgery/hospitalization
2. prophylactic anti-coagulation if moderate risk (ie: after surgery)
```
27
Bronchiectasis
Chronic dilation of bronchi/bronchioles, with airway wall thickening from inflammation or obstruction.
Sx: chronic cough, excess sputum, recurrent chest infections, malaise
Dx: chest CT, obstructive PFT
28
Definition of pulmonary hypertension
mean pulmonary artery pressure > 25 mmHg at rest.
29
2 parts of lung circulation
(dual vasculature)
1. Bronchial circulation (from aorta)
- Pressure: systemic; Compliance: low
2. Pulmonary circulation (from pulmonary a.)
- Pressure: low; Compliance: high
* minimal change in pressures w/ exercise*
30
pathological changes w/ pulmonary hypertension
1. affected pulmonary arteries thicken & constrict
- UNaffected pulmonary arteries dilate bc increased BF
2. R ventricle dilates & hypertrophies (bc increased pressure)
31
5 official types of pulmonary hypertension
1. Pulmonary artery hypertension
2. pulm. htn secondary to L heart disease
3. pulm htn secondary to lung disease/hypoxia
4. Chronic thromboembolic pulmonary htn
5. pulm htn "w/ unclear multi-factorial mechanisms" (idiopathic)
32
Interstitial lung disease (defn)
non-infectious, non-malignant process in the lower respiratory tract causing stiffness and fibrosis.
* in an immunocompetent individual.
33
Main pathophysiologic aspects of interstitial lung disease (4)
1. decreased lung compliance (stiffer, more work of breathing)
- decreased lung volumes, but FEV1/FVC > 80% preserved
2. diffusion impairment (small lungs = decreased surface area)
- low DLCO
3. Impaired gas exchange
- V/Q mismatch & hypoxemia even w/ minimal activity
4. pulmonary HTN ("cor pulmonale")
34
clinical signs of interstitial lung disease
Hx: gradual/insidious dyspnea, dry non-productive cough
| Physical exam: lung crackles, finger clubbing, edema & cor pulmonale
35
occupational & environmental causes of interstitial lung disease
aka: pneumoconiosis
- INorganic: asbestosis, silicosis, coal worker's lung, talc pneumoconiasis, etc.
- ORganic: aka farmer's lung/allergic extrinsic alveolitis
36
3 categories that cause bronchiectasis
- Cystic fibrosis
- non-CF (infection, etc.)
- traction bronchitis (usually w/ interstitial lung disease)
37
pathogenesis of bronchiectasis
1. airway injury --> impair cilia & host defense (immune-mediated)
=> airway obstruction (=> scooped exp. limb on PFT)
2. irreversible airway inflation --> inflammation, mucosal edema, ulceration...
=> recurrent infectious flares (ie: pseudomonas aeruginosa)
38
pathogenesis of Cystic Fibrosis
(mutations in CF gene - encodes chloride channel, which regulates other ion channels)
Ion transport abnormalities --> impaired mucus secretion, poor mucociliary clearance.
39
common non-ciliary causes of bronchiectasis
- Hx of infection: w/ pneumonia, mycobacteria
- allergic bronchopulmonary aspergillosis
- immunodeficiency/autoimmune disease
- inhalational injury
40
techniques for diagnosis of Cystic Fibrosis
#1: Gibson-Cooke sweat test (high [ ] Cl in sweat, trigger w/ pilocarpine)
2. Genotyping
3. Newborn screen
41
primary ciliary dyskinesia
autosomal recessive inherited disorder,
= abnormalities is cilia structure that make them in immobile;
--> chronic sinusitis, bronchiectasis, infertility.
*often w/ Kartagener's syndrome -> also situs inversus.
42
clinical findings w/ pulmonary hypertension
- Hx: Dyspnea, fatigue
- Lungs: clear
- Heart: prominent P2, RV hypertrophy, R heart failure,
- Liver, etc: ascites, peripheral edema
(Histo: intimal fibrosis, smooth m cell hypertrophy)
43
Causes of pulmonary artery hypertension (type I)
- idiopathic
- heritable
- drug-induced
Risk factors: collagen vascular disease, congenital heart disease, cirrhosis/portal HTN
44
changes from endothelial dysfunction for w/ pulmonary HTN
1. decreased NO/cGMP signaling - vasodilation
2. decreased prostacyclin/cAMP signaling - vasodilation
3. increased endothelin signaling --> vasoconstriction & smooth muscle cell proliferation.
45
most common type of pulmonary hypertension (in world)
L heart disease (L systolic OR diastolic dysfunction, valve disease)
--> increase peripheral vascular resistance & L atrial P
46
Causes of Type III pulmonary HTN
(from hypoxia or lung disease)
- alveolar hypoxia (COPD, etc.)
- impaired breathing control (ie: sleep apnea)
- living at high altitude
47
common causes of Type V pulmonary HTN (multi-factorial)
- chronic myeloproliferative disorders
- mediastinal fibrosis
- sarcoidosis
- metabolic disorders
- cancer
48
Steps to diagnosing pulmonary HTN
1. echocardiogram (estimate pulm. a. pressure & ID heart disease)
2. CXR, PFTs (ID lung disease - restriction/obstruction...)
3. Ventilation-Perfusion scan (ID thromboembolic disease)
4. Other: sleep study, HIV test, autoantibody tests, liver f(x) test...
5. Cardiac catheterization (determine severity)
49
Treatment of pulmonary HTN
#1. treat underlying disease
2. give O2 long-term if needed (increases survival!)
3. thromboendarterectomy
4. NEW drugs targeting endothelial pathway signaling
5. anti-coagulation
Last ditch: lung transplant, vasodilators ONLY if no other Tx works
50
Drugs that target endothelial signaling pathways for pulmonary HTN
1. Endothelin R antagonists
2. Increase NO (ie: PDE-5 Inhibitors)
3. promote prostacyclin pathway
51
reticular lung infiltrates on xray
= interlacing linear shadows (mesh-like)
* if also have fine nodules = "reticulonodular"
52
"honeycombing" of lungs on CXR
Coarse reticular shadows w/ cystic changes
| * indicative of chronic inflammation*
53
"ground glass opacity" on CXR
= increased lung density (whitish) which does NOT obscure vessels
54
interstitial lung disease processes associated w/ Upper lung fields
silicosis or Coal workers' lung
| *most others affect the lower lobes more
55
interstitial lung disease processes associated w/ Pleural changes
- asbestosis
- Systemic lupus erythematous (SLE)
- Rheumatoid arthritis (RA)
56
interstitial lung disease processes associated w/ lymphadenopathy
sarcoidosis
57
organic dusts and interstitial lung disease
Causes: birds Ags, mold (farm environment, hot tubs, AC etc.)
when inhaled cause Sx:
- acute (dyspnea, fatigue; patchy infiltrates)
- chronic (interstitial inflammation, immune rxn; diffuse infiltrates)
58
characteristic appearance of CT for hypersensitivity pneumonitis
very diffuse: w/ micronodules and ground glass infiltrates
59
Radiation-induced Interstitial Lung disease
= damage to pneumocytes & vasc. endothelium, appear w/ straight edges on CXR!
- Pneumonitits: subacute (2-6 mo.), cough, fever, dyspnea; can treat w/ steroids
- Fibrosis: chronic (mo - yrs), dyspnea & decreased lung V; NO response to Tx
60
idiopathic pulmonary fibrosis
= most common type of Interstitial lung disease!
Sx: gradual dyspnea, old onset (50-70), crackles, clubbing
Dx: looks like Usual Interstitial Pneumonia ("UIP") on CT... BUT has fibroblastic foci! (histo: temporally heterogenous)
Tx: only lung transplant
61
Hallmark of sarcoidosis
(systemic, but can cause a type of Interstitial Lung Disease)
=> NON-caseating granulomas
*often asymptomatic*
62
Loffgren's syndrome
a type of sarcoidosis w/ 80% spontaneous remission;
| characteristic Sx: dry cough, dyspnea, erythema nodosum, & arthralgias
63
Reactivation of (lung) infections
- mech
- common organisms
is a consequence of impaired T cell function
Common perpetrators:
TB, CMV, Ebstein-Barr virus, herpes-8 virus, toxoplasma, papilloma virus
64
aspergillus infection
= opportunist, cannot infect unless impaired neutrophils
--> causes invasive (acute) or chronic aspergillosis.
Risk factors: neutropenia, corticosteroids
65
Invasive aspergillosis
Acute infection, in patients have severe PMN dysfunction;
(hematopoetic stem cell transplant, solid organ transplant, or AIDS)
==> tracheobronchitis & other organ infection (spreads by blood)
66
neutrophil opportunists that commonly infect lungs
- aspergillus
- mucormycosis (also affects brain; risk w/ Diabetes, Fe overload)
- candidiasis
(mucosal if T cell def., deep tissue/skin if neutrophil def.)
67
HIV pathogenesis in lungs
1. binds to lung cells w/ CD4 Rs
2. lyses & depletes T helper cells
- -> impaired cell-mediated immunity, humoral immunity, and decreased macrophage activation.
68
Impact of HAART on HIV
| Highly Active Anti-Retroviral Therapy
- lower viral loads
- higher CD4 levels (may even reach normal!)
- fewer opportunistic infections
* but: not a cure.
69
histological evidence of pneumocystis infection
foamy alveolar casts ---> w/ pneumocystis organisms inside
| ** almost exclusively w/ HIV or AIDS **
70
pneumocystis jiroveci infection (in lungs)
fungal infection of lungs, causes type I pneumocyte damage;
= ubiquitous, only infectious if immunocompromised.
*does NOT grow in culture! (need bronchial biopsy to Dx)
Tx: bactrim (trimeth-sulf.) & corticosteroids.
*prophylaxis if CD4 <200*
71
norcardiosis
opportunistic infection after solid organ transplant,
--> pneumonia & systemic disease (skin and CNS)
bc lack ability to contain and kill the infection.
72
CMV lung infection
= reactivation of dormant virus,
usually: early after transplant if not on prophylaxis OR w/ HIV
* affects many organs/systems.
73
non-infectious complications from immunosuppression
| or if immunocompromised
* more common bc of longer survival (w/ HAART)
- cancer (lymphoma & kaposi's sarcoma)
- drug toxicity
- airflow obstruction
- pulm. HTN
74
primary histoplasmosis
Common in affected areas, often asymptomatic,
--> Most problems long after initial infection; found bc:
- nodule confused w/ cancer
- complications from location of nodule calcification
- disseminated disease if immunocompromised.
Exposure: Ohio river valley, up into MN & WI
Dx: Serum test = high diagnostic power
75
benign nodule presentation
calcification pattern: central, laminated, total calcification
* not involving hilar nodes
76
treatment of histoplasmosis
1. oral itraconazole for 6 moonths
| - if critically ill: IV for 1st 2 weeks, then #1
77
Blastomycosis
appears as (lobar) pneumonia that doesn't respond to antibiotics, w/ coughing up pus, +/- crusty skin lesions.
* do NOT just pick 2nd antibiotic if "pneumonia" that doesn't respond!
Exposure: similar to histoplasmosis (NW wisconsin/N minnesota + all areas covered by histo too)
* up to 3 month lag period btwn infection & Sx!
Dx: serum test not helpful
