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HD 1 > Respiratory pathophys. part 2 > Flashcards

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)

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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(!)

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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)

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3
Q

Major cell types involved in asthma

A

Inflammatory: Eosinophils, mast cells, Th2
Structural: epithelial, sm. muscle, and endothelial, etc.

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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.

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5
Q

Acute Respiratory Distress Syndrome

A
  1. Acute (within 7 days)
  2. bilateral infiltrates on CXR
  3. infiltrates not fully explained by heart failure of fluid overload
  4. hypoxia (use PaO2/FiO2 to rate severity)
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6
Q

Pathogenesis of pneumonia (4 types)

A
  • pneumonia = infection of lung tissue
    1. aspiration (most common cause)
    2. aerosol
    3. hematogenous
    4. reactivation
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7
Q

Aspiration pneumonia

A

something goes down wrong way & causes infection;

    • requires abnormal host or abnormal flora **
      from:
  • oropharyngeal secretions (#1)
  • stomach contents
  • foreign body
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8
Q

respiratory characteristics of abnormal host:

A
  1. Impaired airway/mucociliary clearance
    - poor cough: COPD, EtOH, neuro disease, lung cancer;
    - bad cilia: kartagener’s, immotile cilia syndrome, viral inf, CF
  2. medications
    - - antipsychotics, antacids, inhaled corticosteroids
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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
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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
    1. Use history to understand exposures!
      1. Antigen tests (pneumococcus, influenza, legionella)
      2. Culture sputum, etc – only if likely severe, should not delay antibiotic start
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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

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12
Q

Empiric pneumonia therapy in Inpatients or non-Psuedomonas ICU

A

Inpt: Fluoroquinolone OR beta lactam + macrolide

ICU: beta lactam + macrolide or fluoroquinolone

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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!
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14
Q

Virchow’s triad

A

=> increase risk for thrombus formation: (can lead to PE)

  1. venous stasis
  2. endothelial damage
  3. hypercoagulability
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15
Q

imaging used to prove DVT

A
  • venography (w/ contrast, CT)

- doppler ultrasound

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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**
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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.
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18
Q

Westermark’s Sign

A

Xray finding indicating pulmonary embolism;
= localized oligemia w/ proximal pulmonary artery enlargement.
(rare, but classic if seen)

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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)

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20
Q

type of effusion found w/ pulmonary embolism

A

not always w/ PE, but if so, will be:

small, hemorrhagic exudative effusion.

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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!)
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22
Q

Utility of V/Q scan in diagnosing PE

A

normal V/Q scan EXCLUDES pulmonary embolism;

abnormal is not diagnostic (not specific).

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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

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24
Q

Common ECG findings w/ pulmonary embolism

A
  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)
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25
Q

Therapies for pulmonary embolism (what, why, when)

A

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.
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26
Q

Main strategies for prevention of pulmonary embolisms

A 
#1: Early ambulation after surgery/hospitalization
2. prophylactic anti-coagulation if moderate risk (ie: after surgery)
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27
Q

Bronchiectasis

A

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

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28
Q

Definition of pulmonary hypertension

A

mean pulmonary artery pressure > 25 mmHg at rest.

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29
Q

2 parts of lung circulation

A

(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*
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30
Q

pathological changes w/ pulmonary hypertension

A
  1. affected pulmonary arteries thicken & constrict
    • UNaffected pulmonary arteries dilate bc increased BF
  2. R ventricle dilates & hypertrophies (bc increased pressure)
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31
Q

5 official types of pulmonary hypertension

A
  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
Q

Interstitial lung disease (defn)

A

non-infectious, non-malignant process in the lower respiratory tract causing stiffness and fibrosis.
* in an immunocompetent individual.

33
Q

Main pathophysiologic aspects of interstitial lung disease (4)

A
  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
Q

clinical signs of interstitial lung disease

A

Hx: gradual/insidious dyspnea, dry non-productive cough

Physical exam: lung crackles, finger clubbing, edema & cor pulmonale

35
Q

occupational & environmental causes of interstitial lung disease

A

aka: pneumoconiosis
- INorganic: asbestosis, silicosis, coal worker’s lung, talc pneumoconiasis, etc.
- ORganic: aka farmer’s lung/allergic extrinsic alveolitis

36
Q

3 categories that cause bronchiectasis

A
  • Cystic fibrosis
  • non-CF (infection, etc.)
  • traction bronchitis (usually w/ interstitial lung disease)
37
Q

pathogenesis of bronchiectasis

A
  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
Q

pathogenesis of Cystic Fibrosis

A

(mutations in CF gene - encodes chloride channel, which regulates other ion channels)
Ion transport abnormalities –> impaired mucus secretion, poor mucociliary clearance.

39
Q

common non-ciliary causes of bronchiectasis

A
  • Hx of infection: w/ pneumonia, mycobacteria
  • allergic bronchopulmonary aspergillosis
  • immunodeficiency/autoimmune disease
  • inhalational injury
40
Q

techniques for diagnosis of Cystic Fibrosis

A

1: Gibson-Cooke sweat test (high [ ] Cl in sweat, trigger w/ pilocarpine)

  1. Genotyping
  2. Newborn screen
41
Q

primary ciliary dyskinesia

A

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
Q

clinical findings w/ pulmonary hypertension

A
  • 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
Q

Causes of pulmonary artery hypertension (type I)

A
  • idiopathic
  • heritable
  • drug-induced
    Risk factors: collagen vascular disease, congenital heart disease, cirrhosis/portal HTN
44
Q

changes from endothelial dysfunction for w/ pulmonary HTN

A
  1. decreased NO/cGMP signaling - vasodilation
  2. decreased prostacyclin/cAMP signaling - vasodilation
  3. increased endothelin signaling –> vasoconstriction & smooth muscle cell proliferation.
45
Q

most common type of pulmonary hypertension (in world)

A

L heart disease (L systolic OR diastolic dysfunction, valve disease)
–> increase peripheral vascular resistance & L atrial P

46
Q

Causes of Type III pulmonary HTN

A

(from hypoxia or lung disease)

  • alveolar hypoxia (COPD, etc.)
  • impaired breathing control (ie: sleep apnea)
  • living at high altitude
47
Q

common causes of Type V pulmonary HTN (multi-factorial)

A
  • chronic myeloproliferative disorders
  • mediastinal fibrosis
  • sarcoidosis
  • metabolic disorders
  • cancer
48
Q

Steps to diagnosing pulmonary HTN

A
  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
Q

Treatment of pulmonary HTN

A

1. treat underlying disease

  1. give O2 long-term if needed (increases survival!)
  2. thromboendarterectomy
  3. NEW drugs targeting endothelial pathway signaling
  4. anti-coagulation
    Last ditch: lung transplant, vasodilators ONLY if no other Tx works
50
Q

Drugs that target endothelial signaling pathways for pulmonary HTN

A
  1. Endothelin R antagonists
  2. Increase NO (ie: PDE-5 Inhibitors)
  3. promote prostacyclin pathway
51
Q

reticular lung infiltrates on xray

A

= interlacing linear shadows (mesh-like)

  • if also have fine nodules = “reticulonodular”
52
Q

“honeycombing” of lungs on CXR

A

Coarse reticular shadows w/ cystic changes

* indicative of chronic inflammation*

53
Q

“ground glass opacity” on CXR

A

= increased lung density (whitish) which does NOT obscure vessels

54
Q

interstitial lung disease processes associated w/ Upper lung fields

A

silicosis or Coal workers’ lung

*most others affect the lower lobes more

55
Q

interstitial lung disease processes associated w/ Pleural changes

A
  • asbestosis
  • Systemic lupus erythematous (SLE)
  • Rheumatoid arthritis (RA)
56
Q

interstitial lung disease processes associated w/ lymphadenopathy

A

sarcoidosis

57
Q

organic dusts and interstitial lung disease

A

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
Q

characteristic appearance of CT for hypersensitivity pneumonitis

A

very diffuse: w/ micronodules and ground glass infiltrates

59
Q

Radiation-induced Interstitial Lung disease

A

= 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
Q

idiopathic pulmonary fibrosis

A

= 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
Q

Hallmark of sarcoidosis

A

(systemic, but can cause a type of Interstitial Lung Disease)
=> NON-caseating granulomas
often asymptomatic

62
Q

Loffgren’s syndrome

A

a type of sarcoidosis w/ 80% spontaneous remission;

characteristic Sx: dry cough, dyspnea, erythema nodosum, & arthralgias

63
Q

Reactivation of (lung) infections

  • mech
  • common organisms
A

is a consequence of impaired T cell function
Common perpetrators:
TB, CMV, Ebstein-Barr virus, herpes-8 virus, toxoplasma, papilloma virus

64
Q

aspergillus infection

A

= opportunist, cannot infect unless impaired neutrophils
–> causes invasive (acute) or chronic aspergillosis.
Risk factors: neutropenia, corticosteroids

65
Q

Invasive aspergillosis

A

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
Q

neutrophil opportunists that commonly infect lungs

A
  • aspergillus
  • mucormycosis (also affects brain; risk w/ Diabetes, Fe overload)
  • candidiasis
    (mucosal if T cell def., deep tissue/skin if neutrophil def.)
67
Q

HIV pathogenesis in lungs

A
  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
Q

Impact of HAART on HIV

Highly Active Anti-Retroviral Therapy

A
  • lower viral loads
  • higher CD4 levels (may even reach normal!)
  • fewer opportunistic infections
  • but: not a cure.
69
Q

histological evidence of pneumocystis infection

A

foamy alveolar casts —> w/ pneumocystis organisms inside

** almost exclusively w/ HIV or AIDS **

70
Q

pneumocystis jiroveci infection (in lungs)

A

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
Q

norcardiosis

A

opportunistic infection after solid organ transplant,
–> pneumonia & systemic disease (skin and CNS)
bc lack ability to contain and kill the infection.

72
Q

CMV lung infection

A

= reactivation of dormant virus,

usually: early after transplant if not on prophylaxis OR w/ HIV
* affects many organs/systems.

73
Q

non-infectious complications from immunosuppression

or if immunocompromised

A
  • more common bc of longer survival (w/ HAART)
  • cancer (lymphoma & kaposi’s sarcoma)
  • drug toxicity
  • airflow obstruction
  • pulm. HTN
74
Q

primary histoplasmosis

A

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
Q

benign nodule presentation

A

calcification pattern: central, laminated, total calcification
* not involving hilar nodes

76
Q

treatment of histoplasmosis

A
  1. oral itraconazole for 6 moonths

- if critically ill: IV for 1st 2 weeks, then #1

77
Q

Blastomycosis

A

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

HD 1 (9 decks)

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