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Renal-Pulm > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Categorize COPD by airflow obstruction caused by

  • anatomic narrowing of airway
  • loss of elastic recoil
A

Anatomic narrowing of airway

  • chronic bronchitis
  • asthma

Loss of elastic recoil
-emphysema

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2
Q

What is used to assess respiratory muscle strength?

A

Maximal respiratory pressures MIP and MEP

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3
Q

What effect do asthma and chronic bronchitis have on diffusing capacity?

A

NONE!

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4
Q

FRC in emphysema vs fibrosis compared to normal

A

Emphysema - higher FRC
-tendency of the lungs to collapse is less than the tendency of the chest wall to expand at normal FRC

Fibrosis - Lower FRC
-the tendency of the lungs to collapse is greater than the tendency of the chest wall to expand at normal FRC

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5
Q

COPD vs asthma in terms of reversibility

A

COPD - NOT reversible

Asthma - reversible

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6
Q

Fill in the blanks for definition of emphysema

(blank) enlargement of airspaces (blank) to terminal bronchioles accompanied by (blank x 3) w/out obvious fibrosis

A
  • irreversible
  • distal
  • alveolar wall destruction
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7
Q

Acinus is defined as

A

respiratory bronchiole and beyond

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8
Q

Clinical definition for chronic bronchitis

A

Clinically defined as persistent cough with sputum production for at least 3 months/ year in at least 2
consecutive years without other identifiable cause

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9
Q

List 4 morphological changes seen with chronic bronchitis

A
  1. Squamous metaplasia
  2. Goblet cell hyperplasia
  3. submucosal gland hyperplasia
  4. chronic inflammation
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10
Q

Loss of what, seen with chronic bronchitis, leads to inc risk of infection?

A

CILIA

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11
Q

List 2 organisms that cause recurrent infections in chronic bronchitis

A
  • H. influenzae

- S. pneumoniae

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12
Q

5 A’s for smoking cessation

A 
Ask
Advise
Assess
Assist
Arrange
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13
Q

What are side effects of Varenicline? What is it used for?

A
  • Crazy dreams
  • Shouldn’t be used in patients at increased risk of suicide

3 fold inc in smoking cessation

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14
Q

Which class of emphysema is associated with spontaneous pneumothorax in young adults?

A

Paraseptal

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15
Q

Lobe predominance for centriacinar vs panacinar emphysema

A

Centriacinar -> upper lobe

Panacinar -> lower zone

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16
Q

pO2 level indicating hypoxemic respiratory failure? What should be given to the patient?

A

pO2 < 55 (<60 w/ evidence of RHF)

O2 therapy!

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17
Q

List 4 radiographic manifestations of COPD

A
  • Inc # of ribs -> hyperinflation
  • Lung parenchyma attenuated in UPPER lung zones
  • On lateral view - flat shape of diaphragm
  • Should be dome shaped
  • Retrosternal airspace due to hyperinflation
  • Sign of air trapping
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18
Q

Single most effective and cost-effective, intervention to reduce risk of developing COPD and its progression

A

SMOKING

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19
Q

Which vaccine can reduce morbidity and death in COPD?

A

Influenza vaccine

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20
Q

List 4 effects associated with use of systemic corticosteroids

A
  • myopathy
  • osteoporosis
  • diabetes
  • immunosuppression
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21
Q

Long term administration of what has been shown to increase survival in COPD patients with resting hypoxemia? What should be checked before starting this tx?

A
  • OXYGEN

- check pCO2 -> don’t want to suppress ventilation and make them even more hyercarbic

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22
Q

COPD bronchodilator tx

A
  • Inhaled tx preferred
    1. SABA
  1. Anticholinergic
    - tiotropium - LAMA (preferred)
    - ipratropium - SAMA
  2. LABA
    - formoterol
  3. Inhaled corticosteroid
    - Budesonide

LABA + ICS may improve adherence

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23
Q

COPD other pharmacological tx

A
  1. PDE inhibitors
    - Theophylline
    - Roflumilast (specific for PDE4) -> good for patients w/ bronchitic phenotype
  2. Macrolides -> azithromycin, erythromycin
    - anti-inflammatory; not antibiotics
    - may inc antibiotics resistance
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24
Q

Bronchiectasis

  • what’s destroyed
  • due to what?
  • end result?
A
  • muscular and elastic tissue of bronchi and bronchioles
  • chronic necrotizing infection
  • permanent dilation of airways
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25
Q

Why can hemoptysis occur with bronchiectasis?

A

extension of airway inflammation into adjacent artery

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26
Q

What is the defect in primary ciliary dyskinesia? what lung problem can it lead to?

A
  • defect in dynein arm

- bronchiectasis

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27
Q

Classic radiographic sign of bronchiectasis?

A

Signet ring sign

-dilated bronchus compared to artery

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28
Q

When should surgical resection be considered for bronchiectasis?

A

ONLY for localized, non-progressive disease

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29
Q

Chronic inflammatory disorder characterized by airway hyperreactivity that leads to episodic bronchoconstriction (reversible bronchospasm) and hypersecretion of mucus

A

What is asthma?

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30
Q

What are 2 cytological findings of asthma?

A
  1. Curschmann spirals - coiled basophilic plugs of mucus and detached epithelial cells
  2. Charcot-Leyden crystals - eosinophil membrane protein
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31
Q

Most common chronic disease of childhood?

A

ASTHMA

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32
Q

Death rates in asthma are highest in which group?

A

Young adult african americans (15-24)

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33
Q

What are the 2 types of asthma

-describe pathogenesis of each

A
  1. ATOPIC (allergic/extrinsic)
    - Type 1 IgE mediated HSR
    - skin tests positive
    - genetic predisposition -> allergic rhinitis + eczema
    - environmental antigens -> dust, pollens, animal dander, foods
  2. NONATOPIC (nonallergic/intrinsic)
    - lacks allergen sensitization
    - skin test negative
    - family hx less common
    - triggers -> viral infections, air pollutants, drugs (e.g. aspirin), chemical irritants
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34
Q

Describe the sensitization phase of atopic asthma. Discuss role of:

  • T cells
  • Interleukins
  • Mast cell
  • eosinophils
A

-allergens induce TH2 phenotype in CD4+ T cells of genetically susceptible individuals

  • TH2 cells secrete IL-4, IL-5, IL-10
    • IL-4, IL-5 -> class switching to IgE
    • IL-5 -> calls in EOSINOPHILS
    • IL-10 -> ability to inhibit production of Th1 helper T cells and induce production of Th2 T cells

-Mast cells bind IgE using at the Fc component -> sensitized to next allergen encounter

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35
Q

Early phase atopic asthma (minutes)

A

MEDIATORS

  • leukotrienes
  • prostaglandins
  • acetylcholine
  • histamine
  • platelet activating factor

EFFECTS

  • inc permeability of vessels -> edema
  • smooth muscle constriction -> bronchoconstriction
  • release of mucous
  • loss of integrity of epithelium
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36
Q

Late phase atopic asthma (hours)

A

Inflammatory cells come in

Eosinophils -> release major basic protein which can aggregate to form charcot-leyden crystals
-promotes bronchoconstriction

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37
Q

viral induce inflammation may enhance (blank) mediated bronchoconstriction and edema

A

VAGAL

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38
Q

Describe aspirin intolerant asthma

  • mechanism
  • triad
A

Blocking COX will shunt arachidonic acid down LIPOXYGENASE pathway -> inc production of leukotrienes -> bronchospasms

Triad

  • asthma
  • bronchospasm
  • nasal polyps

NOTE: this is NOT T1HSR

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39
Q

What bronchodilator response is expected with asthma?

A

inc of >12% AND 200ml in FEV1 or FVC

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40
Q

Bronchoprovocation testing

  • standard
  • positive test
  • how long to wait after viral infection befor testing
A
  • methacholine is standard
  • histamine can also be used

PC20 < 20 mg/ml is positive
-concentration of methacholine required to lower FEV1 by 20%

-wait 8-12 weeks after viral infection to prevent false positive

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41
Q

Describe diurnal variation with asthma

A

Peak expiratory flow rate (PEFR) will show variability b/w AM and PM

> 20% difference b/w AM and PM values of PEFR suggestive of asthma

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42
Q

Radiographic findings with asthma

A
  • can be normal

- hyperinflation w/ preservation of diaphragmatic dome

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43
Q

What is the best question to ask when assessing asthma control?

A

How well are you sleeping through the night?

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44
Q

b-2 receptor agonists

  • best way to administer
  • clinical use
  • adverse effects
  • CI

WARNING: LONG CARD!

A

Administration -> inhalant targeted deliver

CLINICAL USE
1. short-acting agents: mild, intermittent asthma, acute asthma
2. long-acting agents (& LACS): a component of treatment for
moderate to severe persistent asthma (& COPD)

ADVERSE EFFECTS
1. Black Box Warning: Increased asthma deaths occur with single
agent LABA usage

  1. high dose effects: largely β2 atrial & β1 myocardial effects
    - CV: HR and BP increases, tachycardia, arrhythmia
    - CNS: nervousness, anxiety
    - Skeletal muscle: tremors, fasciculations & weakness
    - Metabolic effects:
    a) INC liver & skel. muscle metab.;
    b) INC plasma insulin, glucose & free fatty acids;
    c) hypokalemia

CONTRAINDICATIONS

  • Do not use non-selective β-blockers for Rx of hypertension in asthmatics;
  • also cautious use of β2-agonists alone with diabetes, cardiac disease, hyperthyroidism or seizures
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45
Q

Tx for emergency asthma

A
  1. I.V. epi (alpha, beta 1 and 2 agonist)
  2. Terbutaline (beta-2 agonist)
  3. O2
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46
Q

What are the proposed mechanisms for METHYLXANTHINES

How is metabolized?

Adverse effects?

A

MECHANISMS

  1. Blocks phosphodiesterase
    - inc cAMP levels due dec hydrolysis to AMP
    - bronchodilation and dec inflammatory response
  2. Blocks actions of adenosine
    - dec histamine release

METABOLIZED -> cytochrome P-450

ADVERSE EFFECTS

  • narrow TI index due to
  • cardiotoxicity
  • neurotoxicity
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47
Q

Theophylline

  • class
  • clinical use
  • side effects
  • cautions
  • metabolized
  • contraindications
A
  1. Class -> methylxanthine
  2. Clinical use - oral-slow release
    A) for severe and nocturnal asthma and bronchospasms
    -2nd or 3rd line for asthma
    B) COPD and bronchitis
    -for resp fatigue
    -may improve sensitivity to corticosteroid tx
  3. Side effects
    A) CNS (PDE4) -> headaches, nervousness, anxiety
    B) Cardiac (PDE3) -> PVCs, Palpitations, arrythmias
    C) GI irritation (AD1-R) -> vomiting, abdominal-upset, pain, diuresis

High levels -> seizures, arrhythmias,d death

  1. Cautions
    - MUST MONITOR BLOOD LEVELS
  2. Metabolized -> Cyt P450
  3. CI -> pregnancy
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48
Q

Ipratropium
Tiotropium

  • Class
  • MoA
  • Indications
  • Drug of choice for?
A
  1. Class -> muscarinic/cholinergic receptor antagonist
    - Ipratropium - SAMA (6-8 hour)
    - Tiotropium - LAMA ( >12 hr)
  2. MoA
    - antagonists at M1 and M3 receptors
    - dec IP3, DAG and Ca -> bronchodilation and dec secretion of mucous
  3. Indications
    A) refractory chronic asthma -> add tiotropium (LAMA) to LABA and ICS
    -esp. non allergic airways hyper-reactivity
    -SAMA not so good for chronic asthma tx but can be used in acute severe exacerbations
    B) Drug of choice for COPD -> IMPORTANT
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49
Q

Name 2 corticosteroids used for chronic asthma

A

beclomethasone, fluticasone

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50
Q

Cromolyn sodium

  • MoA
  • uses
  • cautions and concerns
A
  1. MoA
    - stabilizes mast cell -> dec histamine release
    - inhibition of mast cell and sensory nerve Cl- channels
2. Uses
A) PROPHYLACTIC
-before exposure to allergens/exercise 
B) COPD and Asthma
C) Used in combination w/ b2 agonist for PEDIATRIC ASTHMA CONTROL
  1. Cautions
    - FEW; very well tolerated and extremely safe
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51
Q

List 2 leukotriene receptor inhibitors

A

Montelukast and zafirlukast

-first aid says -> specially good for ASA induced asthma

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52
Q

MoA of Zileuton

A

Inhibits 5-lipoxygenase
-blocks conversion of arachidonic acid to leukotriene

-good for ASA induced asthma

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53
Q

Common adverse effect amongst the 3 leukotriene pathway/receptor inhibitors

A

LIVER TOXICITY -> zileuton in particular

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54
Q

Omalizumab

  • MoA
  • use
  • cautions
  • how long does it take to work?
A
  1. MoA
    - monoclonal anti-IgE Ab
    - binds to unbound serum IgE -> blocks binding to FceRI
  2. Use
    - severe asthma resistant to inhaled steroids and LABA
    - positive allergen test
  3. Cautions
    - CRS -> anaphylactic shock
    - rare
  4. Duration for action
    > 3-4 months needed
    -weak response
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55
Q

SABA for asthma

  • name 2 drugs
  • when should they be used/not be used?
  • a parameter to measure?
A

– Examples: albuterol, levalbuterol
– Therapy of choice for acute relief of symptoms
– Should be available to all asthmatics (unless intolerant)
– Use only as needed for acute relief. Scheduled use not advantageous and may be deleterious to some pts.
– Frequency of use is parameter to assess/guide therapy

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56
Q

LABA for asthma

  • name 2 drugs
  • recommended for?
  • how should it be used?
  • black box?
A

– Examples: formoterol, salmeterol
– Preferred adjunctive therapy to add to ICS (Steps 3-6)
– NEVER use as monotherapy in asthma (contrasts with
COPD)
– Not currently recommended for treatment of acute
symptoms or exacerbations
– “Black Box” warning in package insert but benefits likely to outweigh risks for vast majority of pts.

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57
Q

What is the preferred drug for the following in asthma tx and why?

  1. Monotx of mild persistent disease
  2. Control med for persistent disease regardless of severity or control
A

INHALED CORTICOSTEROIDS -> Most potent and effective anti-inflammatory med for asthma

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58
Q

If you had a choice b/w leukotriene modifiers and LABA when adding an adjunct to ICS, which one should you use?

A

LABA

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59
Q

In which cases leukotriene modifiers be considered? (list 3)

A
  • asthmatics w/ rhinitis
  • exercise induced bronchospasm
  • aspirin sensitivity
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60
Q

What can be used as monotx or adjuct when oral tx is indicated for asthma?

A

Methylxanthines (theophylline)

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61
Q

Systemic corticosteroids for asthma

  • when to use?
  • how to administer?
  • risk of what if course > 10 -14 days
A
  1. Use
    - acute exacerbation
    - chronic tx only for the worst cases
  2. Method
    - burst or taper (typically 4-10 days)
  3. Adrenal suppression
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62
Q

Parameters to assess asthma impairment

A
  • Frequency of sx’s
  • Nocturnal awakenings
  • Frequency of SABA use
  • Interference with activity
  • Lung function (spirometry)
  • Questionnaire scores
  • Treatment-related adverse effects
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63
Q

Parameters to assess asthma risk

A
  • Frequency of exacerbations requiring systemic steroids
  • Severity of exacerbations (hospitalization, intubation)
  • Potential for long-term lung impairment or adverse tx effects
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64
Q

What’s the end stage of Interstitial lung diseases?

A

HONEYCOMB LUNG - effacement of normal archictecture

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65
Q

What’s the difference b/w ARDS and acute interstitial pneumonia?

A

AIP is idiopathic

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66
Q

Describe the color changes seen with Raynaud’s phenomenon

Raynaud’s syndrome associated with which 3 conditions?

A

White -> blue -> red

  • conn tissue disease
  • SLE
  • CREST syndrome
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67
Q

List one drug from the following medication classes that is associated with pulmonary fibrosis

  • chemo agents
  • antiarrhythmics
  • antibiotics
  • another cancer treatment (not drug)
A
  • chemo agents -> bleomycin
  • antiarrhythmics -> amiodarone
  • antibiotics -> nitrofurantoin
  • another cancer treatment (not drug) -> radiation

FROM FIRST AID
“Breathing Air Badly from Medications”

Bleomycin
Amiodarone
Busulfan
Methotrexate

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68
Q

Occupational exposures:

  1. Silicosis
  2. Asbestosis
  3. Talcosis
  4. Hard Metal Disease (which metals)
A
  1. Silicosis
    - hard rock mining
    - foundry work
    - sandblasting
    - glass/pottery making (porcelain flour)
  2. Asbestosis
    - Shipyards
    - boilers/HVAC
    - plumbing
    - construction trades
  3. Talcosis
    - latex
    - plastics
  4. Hard metal disease (cobalt, tungsten, beryllium)
    - metal foundry
    - tool/die maker
    - Beryllium -> used in aircraft parts
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69
Q

Beryllium mimics?

A

SARCOIDOSIS

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70
Q

Compare the crackles of usual intersitial pneumonia to heart failure

A

UIP -> inspiratory crackles
-sounds like velcro (crisp)

Heart failure -> expiratory crackles

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71
Q

Compare A-a gradient during exercise in usual intersitital pneumonia vs normal

A

Normal
-TV inc and A-a gradient stays the same or even decreases

UIP

  • inc in rate rather than TV w/ exercise
  • Inc dead space to TV ratio
  • progressive hypoxemia
  • WIDENED A-a gradient
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72
Q

Gold stand for ILD dx?

A

SURGICAL LUNG BX

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73
Q

Bronchoscopic parenchymal bx is limited to?

A

Granulomatous diseases

-due to size and sampling artifact

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74
Q

Interstitial inflammation in usual interstitial pneumonia consists of which cell types?

A
  • lymphocytes
  • plasma cells
  • macrophages
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75
Q

Name 3 systemic autoimmune diseases associated with the same pattern as idiopathic interstitial pneumonia. What is this pattern? Why is it important to understand this?

A

Pattern -> chronic interstitial pneumonia with fibrosis

Autoimmune diseases

  1. Progressive systemic sclerosis
  2. Rheumatoid arthritis
  3. SLE

Important because we can treat the autoimmune diseases!

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76
Q

What is thought to be the major driver in the progression of Idiopathic pulmonary fibrosis?

A

TGF-BETA

  • released from injured pneumocytes as part of healing process (cyclic lung injury is involved with IPF)
  • but can promote fibrosis and predispose to more injury
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77
Q

Interstitial fibrosis in IPF is most pronounced where?

A

Periphery and lower lung zones

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78
Q

List 2 radiographic and 2 gross findings associated w/ IPF

A

Radiographic

  • reticular opacities
  • focal ground glass opacities

Gross

  • honeycombing
  • traction bronchiectasis -> fibrosis causes traction and pulls on the airways
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79
Q

Describe the clinical presentation of IPF

A 
•  Insidiously progressive dyspnea
•  Dry, hacking cough 
•  Less commonly
–  Fatigue
–  Weight loss
–  Myalgias/arthralgias
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80
Q

Currently used tx for IPF?

Potential future tx (ASCEND trial)

A

Current

  • O2
  • lung transplant

Future
-Pirfenidone -> reduces effects of TGF-beta

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81
Q

Hypersensitivity pneumonitis

  • which type of hypersensitivity?
  • which lymphocytes are increased?
  • how does the lymphocytes type compare with sarcoidosis?
A

Type III (immune complex) and Type IV (cell mediated)

-CD8+ T cells

Sarcoidosis -> CD4+ T cell response to unknown antigen

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82
Q

What is the relationship between smoking and hypersensitivity?

A

Smoking seems to protective from hypersensitivity pneumonitis

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83
Q

CXR finding with hypersensitivity pneumonitis

A
  1. Reticulonodular infiltrates
    - UPPER zone predominant (note that IPF is lower lobe)
    - sparing of costophrenic angles
  2. Occasional alveolar opacification
  3. honeycombing (end stage)
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84
Q

Histological findings of hypersensitivity pneumonitis

A
  1. expansion of interstitium with chronic inflammatory cells
  2. ill-defined granuloma
    - no necrosis

-patchy process w/ bronchiocentric pattern

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85
Q

Tx for hypersensitivity pneumonitis

A
  1. REMOVE AND AVOID THE ANTIGEN
  2. Corticosteroids
    - prednisone -> 1mg/kg/d w/ gradual taper over 3-6 months
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86
Q

Sarcoidosis patient population

A
  1. adults < 40
    - peaks at 25-34
  2. Women > men
  3. AA > whites
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87
Q

Describe the heterogeneity in disease presentation of sarcoidosis

Japan
Europeans
Puerto Ricans

A
  1. Japan -> inc ocular and cardiac involvement
  2. Europeans -> erythema nodosum
  3. Puerto Ricans -> lupus pernio
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88
Q

List sarcoidosis organ involvement for most common to least common

A

lung > skin = ocular > neurological = CV > MSK

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89
Q

Lofgren’s syndrome triad

A

acute sarcoidosis

  1. Erythema nodosum
  2. bilateral hilar adenopathy
  3. fever
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90
Q

CV abnormalties seen with sarcoidsosis

A
  1. Electrical
    - dysrhythmias -> sudden death
    - heart block
  2. Infiltrative cardiomyopathy
  3. pericardial effusion -> can turn into tamponade
91
Q

Sarcoidosis ocular invovlement

-which one is an emergency?

A

Uveitis -> EMERGENCY

  • painful, red eye
  • give steroids

Lacrimal glands -> dry eye
-can mimic sjogren’s

Conjunctiva
-granuloma formation

92
Q

Why do sarcoid patients tend to have hypercalciuria and hypercalcemia

A

Non-caseating granulomas makes 1-alpha-hydroxylase -> inc vit D3 -> inc Ca and PO4 absorption from gut -> stones

93
Q

What pattern do sarcoid granulomas follow?

A

Lymphangitic

  • interlobular septate along veins
  • subpleural area
  • along bronchovascular bundles
94
Q

Staging for sarcoidosis pulmonary involvement

A

0 - normal
I - bilateral hilar lymphadenopathy
II - bilateral hilar lymphadenopathy + interstitial infiltrates (start here)
III - interstitial infiltrates; no bilateral hilar lymphadenopathy
IV - pulmonary fibrosis

95
Q

Tx for sacoidosis

A
  1. Coricosteroids
    - systemic
  2. Cytotoxic agents
    - MTX
    - azathioprine
    - cyclophosphamide
  3. antimalarials (hydroxychloroquinine)
    - cutaneous involvement
    - hypercalcemia
  4. Biological modifiers
    - infliximab
96
Q

Sarcoidosis prognosis

  • remission
  • chronic progressive course
  • cause of death
A
  1. remission = 2/3
  2. chronic progressive course = 10-30%
  3. cause of death
    - respiratory involvement
    - cardiac
    - neurological
97
Q

Blood supply to the pleura

-visceral vs parietal

A

Visceral -> bronchial arteries
-low pressure

Parietal -> costal arteries
-high pressure

98
Q

Familial pneumothorax is associated with mutation in?

A

Folliculin gene (birt-hogg-dube syndrome)

99
Q

Pneumothorax physical findings

  • breath sounds
  • percussion
  • fremitus
A

dec breath sounds

hyperresonant to percussion

dec tactile fremitus

100
Q

Where should the thoracostomy tube be placed relative to ribs?

A

ABOVE the rib b/c neurovascular bundle is below

101
Q

Pleural effusion vs consolidation

  • breath sounds
  • percussion
  • fremitus
A

Pleural effusion

  • dec breath sounds
  • dullness to percussion
  • dec fremitus

Consolidation

  • later inspiratory crackles
  • dullness to percussion
  • INC fremitus
102
Q

What are 2 causes of pleural effusion?

-give an example of each

A
  1. Inc pleural fluid formation
    - increases interstitial fluid in the lung
  2. Dec pleural fluid absorption
    - obstruction of lymphatics draining the parietal pleura
103
Q

Transudate vs exudate

what the only 3 things that can cause an exudate?

Light’s criteria for exudate?

A

Transudate

  • low protein
  • due to CHF, nephrotic syndrome or hepatic cirrhosis

Exudate

  • high protein
  • cloudy
  • malignancy, pneumonia, collagen vascular disease, trauma etc.

Light’s criteria - need only 1/3 to classify exudate

  1. pleural fluid to serum protein ratio > 0.5
  2. pleural fluid to serum LDH ratio > 0.6
  3. pleural fluid LDH > 0.6 upper limit of normal
104
Q

Glucose of < 60 in pleural fluid can indicate? (2 things)

A
  1. Complex parapneumonic process/empyema (infection)

2. Rheumatoid pleurisy

105
Q

Complication associated with pleural effusion and pneumothorax?

A

Re-expansion pulmonary edema -> rapid re-expansion of collapsed lung

106
Q

Which type of pleural effusion a person with a kidney stone at risk for getting?

A

Urinothorax

  • pleural fluid Cr to serum Cr > 1
  • due to obstructive uropathy
  • this is uncommon
107
Q

Triglyceride > 110 mg/dL in pleural fluid indicates?

A

Chylothorax

108
Q

describe the path for the thoracic duct from inferior to superior

A

cisterna chyli -> through diaphragm posterior to aorta (T12) -> crosses from right to left b/w T4 and T10 -> drains into left subclavian vein

109
Q

List the paraneoplastic syndromes associated with the following lung cancers

  1. Small cell
  2. Squamous cell
A
  1. Small cell
    - ACTH
    - ADH (SIADH)
  2. Squamous cell
    - PTHrp -> hypercalcemia
110
Q

Asbestos + smoking -> inc risk for???

A

primary lung cancer (50-90x RR)

111
Q

Histoplasmosis vs cancer on CXR

A

look similar but CALCIFICATION more common with histo

112
Q

Mets vs primary neoplasm of lung - what’s more common?

113
Q

Immunostaining for squamous cell vs adenocarcinoma

A
  1. Squamous cell
    p63+, TFF1-
  2. Adenocarcinoma
    TTF-1+, p63-

Goljan trick - just remember one

114
Q

Adenocarcinoma is defined by the presence of???

  • peripheral or central
  • most common lung tumor in?
A

GLANDS OR MUCIN

  • peripheral
  • most common tumor in non-smokers and female smokers (pathoma)
115
Q

Most common tumor in male smokers?

  • peripheral or central
  • characteristics?
A

Squamous cell carcinoma

  • central
  • keratin pearls
  • intracellular bridges
116
Q

If no characteristics of squamous, adeno, or small cell carcinoma what’s the cancer?
-list 2 characteristics

A

large cell carcinoma

  • abundant cytoplasm
  • prominent nucleoli
117
Q

Staging and treatment for lung cancer

  • 0-II
  • III
  • IV
A

0-II -> surgery

III -> chemo/rad and maybe surgery

IV -> chemo/rad

118
Q

What stage if you have mets or malignant effusion?

119
Q

Small cell lung tx

how does this differ from tx for NSCLC?

A

CHEMO/RADIATION - Mets even if can’t see it

NSCLC - tx based on stage and patient status
-could be surgery, chemo/rad or both

120
Q

Carcinoma vs sarcoma incidence in kids vs adults

A

Incidence of carcinomas (epithelium) < sarcomas (hematological) in kids

OPPOSITE FOR ADULTS

121
Q

Standard of care drug in patients with adenocarcinoma?

-what does this drug target?

A

Gefitinib -> targets EGFR which is a commonly mutated in adenocarcinoma

122
Q

SPHERE of complications see with lung cancer:

-first aid

A 
Superior vena cava syndrome
Pancoast tumor 
Horner syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal sxs (hoarseness)
Effusions (pleural or pericardial)
123
Q

What’s a unique site that lung cancer likes to metastasize to?

A

ADRENAL GLAND

124
Q

List 1 pro and 1 con of doing lung cancer screening

A

Pros
-low dose CT in high risk patients can dec mortality by 20%

Cons

  • 96% false positive rate (many are non-calcified nodules)
  • 7% of these have invasive procedure
125
Q

Solitary pulmonary nodule that:

  • peripheral
  • well circumscribed
  • mature tissues in lung (which ones?)

THINK?

A

Hamartoma

  • fat
  • cartilage

most common BENIGN tumor in the lung

126
Q

List 2 epithelioid carcinoma that can involve the pleura

A

Malignant mesothelioma
Adenocarcinoma

Need to do immunohistochemical staining to differentiate

127
Q

Most common marker seen on IH chem for malignant mesothelioma?

A

Calretinin

128
Q

How to tell a sarcomatoid malignant mesothelioma from a sarcoma?

A

MM -> cytokeratin positive

129
Q

Serum marker under study for mesothelioma?

A

Plasma fibulin 3 levels

130
Q

Cystic fibrosis

  • inheritance
  • incidence
  • gene
  • chromosome
A
  • inheritance -> autosomal recessive
  • incidence -> 1:3000 births in U.S.
  • gene -> CF gene codes for cystic fibrosis transmembrane conductance regulator (CFTR)
  • chromosome -> 7
131
Q

Infective organism vs age in CF patients

A

Peds -> staph

Pseudomonas aeruginosa -> later age
-peaks around 25-34

132
Q

What type of pseudomonas infection do we want to avoid in CF patients as long as possible?

A

Mucoid PsA

-forms biofilm -> chronic infection -> rapid drop in FEV1

133
Q

What is the mainstay antibiotic used to manage chronic PsA infection? How about early infection?

A

Chronic -> Tobramycin cycles (TOBI trial)
-inhaled antibiotic

Early -> tobramycin for 28 days -> 90% chance of getting rid of infection (EPIC trial)

134
Q

Management of acute pulmonary exacerbation

  • age difference
  • why is it important to avoid APEx?
A

Young -> oral antibiotics
older -> IV

APEx associated with decline in BASELINE lung fx

135
Q

Which infection do all CF patients worry about (hint: onions)
-why do they worry?

A

Burkholderia cepacia

Cepacia syndrome -> life expectancy drops by 9 years
-can lead to death within weeks

136
Q

What’s used to manage inflammation in CF?

which outcomes are improved with use of this drug?

A

Azithromycin - changes inflammatory response of white cells

Improved outcomes

  • better FEV1
  • greater percentage of pulm exacerbation free days
137
Q

Azithromycin use and outcome in patients with PsA infection?

Patients without PsA infection?

A
  1. PsA +
    Improved outcomes
    -better FEV1
    -greater percentage of pulm exacerbation free days
  2. PsA neg
    - no change in lung fx (b/c it was already good to begin with)
    - weight improvement
    - less cough
138
Q

CF patients tend to have deficiencies in which vitamins?

A 
fat soluble (ADEK)
-think about why each of these are important

vit D - bone disease
vit K - bleeding problems

139
Q

What is the most common CFTR class? what’s the problem?

A

Class II -> folding problem + domain assembly -> protein is degraded

DeltaF-508
-deletion in phenylalanine at position 508

85% of patients have this mutation

Problem with N and Po

140
Q

3 factors that influence CFTR anion transport

A

N x Po x G = total Cl- transport

N - number of channels at plasma membrane

Po - time each channel spends open vs closed

G - size of each Cl channel

Modulators will target these areas to in CF tx treatment

141
Q

What one drug approved for CF tx? Where does it act?

A

Ivacaftor (VX-770)

  • targets GATING mutations in CFTR (e.g. G551D)
  • improves Po
  • approved for ALL gating mutations
142
Q

Phase III trial that improved protein to 30% of normal in patients with F508del combined which 2 modulators

A

VX-770 (ivacaftor) + VX-809 (F508 correction)

VX-770 -> improves Po
VX-809 -> improves N

143
Q

Dornase alpha mech

A

mucolytic

RhDNase -> cleaves DNA and makes the mucous less sticky

144
Q

What’s used to improve hydration in CF patients?

A

7% saline (hypertonic)

145
Q

Histoplasmosis capsulatum

  • geography
  • mimics
A
  • ohio and mississippi river valley

- mimics Tb

146
Q

Which component of histo is infectious?

A

Microconidia

147
Q

List 3 dimorphic fungi that cause systemic disease in humans.
-why are they dimorphic?

A
  1. Histoplasmosis capsulatum
  2. Blastomyces dermatidis
  3. Coccidiodes immitis
148
Q

Blastomyces dermatitidis

  • region
  • gender pref
  • upper or lower lung field
  • key area of dissemination
  • appearance of bud
A

-endemic eastern US, reported from Africa
first aid: east of mississippi and central america

  • males>females
  • lower lung field
  • skin
  • broad based bud (same size as RBC)
149
Q

Coccidioidomycosis

  • region
  • conditions
  • associated with which fever
  • dissemination difference by race
  • how does it infect
  • mould culture
  • life cycle
A
  • southwest U.S., Mexico, central and south america
  • arid, alkaline soil
  • san joaquin valley fever
  • dissemination higher in non-caucasian (may be HLA related)
  • arthroconidia -> easily aerosolized -> highly infectious
  • Mould in culture at room temp AND 37 -> IMPORTANT
  • can grow in routine culture (3-10 days)

-inhaled arthroconidia -> spherules -> endospores -> spherules
NOTE:
-spherules -> induce granulomatous response
-endospores -> attract neutrophils

150
Q

Cryptococcus neoformans vs gattii

  • location and assoc
  • pulmonary disease
  • morphology
  • how is it acquired
A

C. neoformans

  • temperate climates
  • assoc -> bird droppings (pigeons)

C. gattii

  • tropical and subtropical climates
  • assoc -> eucalyptus trees
  • vancouver island/pacific NW outbreak
  • pulmonary disease less likely to be subclinical

BOTH

  • encapsulated yeast
  • not dimorphic -> IMPORTANT
  • acquired through inhalation
151
Q

MCC of mycotic meningitis

A

Cryptococcus

152
Q

Dx for cryptococcus

A

Antigen test for presence of polysaccharide shed from capsule (glucuronoxylomannan)
-HIGH SENSITIVITY AND SPECIFICITY in CSF/serum

153
Q

5 A’s of aspergillus fumigatus

  • is it dimorphic
  • dx?
A

A’s for Aspergillus:

  • Acute Angle < 45 degrees
  • Allergic Aspergillosis/Asthma -> IgE and eosinophils
  • Aspergilloma -> infection in preformed lung cavity “fungus ball”
  • Angioinvasive -> hits all the organs
  • Aflatoxin -> hepatocellular carcinoma
  • Amphotericin B

NOT dimorphic

Dx - antigen test for galactomannan

154
Q

HIV and Tb reactivation association

A

+10% annual risk

155
Q

Primary vs reactivation Tb lung zone

A

Primary
-ghon focus in MID zone of lung

Reactivation

  • apex of lung
  • no ghon focus
156
Q

When is risk of reactivation Tb the highest?

A

w/in 2 years after primary infection

157
Q

First line drugs for Tb (RIPES for tx)

A

R - rifampin -> inhibits DNA-dependent RNA polymerase
I - isoniazid (INH) -> dec synthesis of mycolic acid
P - pyrazinimide
E - ethambutol
S - streptomycin (cidal agent)

INH and rifampin kill intra and extracellular bacilli

158
Q

Out of the bacterial causes of pneumonia discussed in saelinger lecture, which 2 have vaccines?

A

Strep pneumo

  • gm pos cocci
  • community acquired pneumo (CAP)

Haemophilus influenza

  • gm neg coccobacillus
  • CAP in COPD, alcoholics and elderly
159
Q

Most common cause of community acquired pneumonia?

List 2 major virulence factors for this organism

A

Streptococcus pneumoniae

virulence factors

  • capsule
  • pneumolysin -> cytotoxic
160
Q

Haemophilus influenzae

  • morphology
  • serotype which most commonly causes human infections
  • virulence factor
  • vaccine (>6 months vs less)
A

Morphology
-gm neg coccobacilli; fastidious

Serotype
-Hib

Virulence factor
-capsule

Vaccine

  • T-independent antigen -> if > 6 months
  • T-dependent antigen -> if < 6 months; capsular carb conjugated to protein
161
Q

Mycoplasma pneumoniae

  • characteristics
  • age group and spread
  • major virulence factor
  • presentation
  • vaccine
  • tx
A
  1. Characteristics
    - NO cell wall
    - pleomorphic
    - cold agglutinins - IgM
    - requires media w/ STEROLS; fastidious
    - fried egg appearance
    - has BOTH RNA and DNA
  2. Age and spread
    - 5-19 years
    - spread through droplets and requires close prolonged contact
  3. Virulence
    - extracellular
    - adheres to respiratory epithelium
    - no alveolar involvement
    - P1 attachment factor!!
  4. Presentation
    - tracheobronchitis - MC
    - atypical pneumonia
    - walking pneumonia -> mild sxs and lasts weeks
  5. No vaccine
  6. Tx
    - macrolides -> block 50S ribosome
    - fluoroquinolones -> inhibit DNA gyrase and topoisomerase IV
162
Q

Legionella pneumophila

  • characteristics
  • major virulence factor
  • presentation (be specific)
  • vaccine
  • what’s needed to resolve disease process
  • treatment
  • dx
A
  1. Characteristics
    - hard to stain; silver stain+
    - fastidious in lab
    - growth in ameba
    - no human to human contact
    - aerosolized water droplets
    - CAP and hospital acquired
  2. Major virulence factors
    - facultative intracellular -> macrophages
    - virulence factors enhance phagocytosis + intracellular survival and growth
  3. Presentation -> legionnaire’s
    - cough: scant sputum
    - high fever (104+)
    - GI sxs
    - primary manifestation = pneumonia
    - Mortality 16-20%
  4. No vaccine
  5. cell mediated immunity is needed to resolve disease process
  6. Tx
    - macrolides
    - fluoroquinolones
  7. Dx
    culturing on BCYE (slow) + urinary antigen test (rapid; only for serotype 1)
163
Q

What is the most common infectious serotype of Legionella pneumophila? why is this important?

A

SEROTYPE 1 - only serotype for which a rapid lab test is available
-urinary antigen test

164
Q

Pontiac fever

A

Non-pneumonic legionella infection

  • flu like illness
  • may be a HSR
165
Q

Chlamydiaceae

-extracellular or intracellular

A

OBLIGATE INTRACELLULAR BACTERIA

166
Q

Chlamydophila psittaci vs C. pneumoniae with regards to:

  • natural host
  • disease in humans
  • frequency
A

Chlamydophila psittaci

  • host = birds and non-human animals
  • disease = pneumonia
  • frequency = rare

C. pneumoniae

  • host = humans
  • disease = acute respiratory disease
  • frequency = COMMON
167
Q

Klebsiella pneumoniae

  • characteristic
  • which patient population
  • give away keywords
A
  1. characteristics
    - gm neg rod
    - enterobacteriaceae
  2. Patients likely to aspirate
    - alcoholics
    - long term care facilities
    - opportunistic infection
  3. MUCOID capsular material
    - “currant jelly”
168
Q

Pseudomonas aeruginosa

-characteristics

A
  • Gm neg rod
  • oxidase positive (cytochrome oxidase)
  • non-fermenter
169
Q

Chronic vs acute pseudomonas infection and predisposing factors

A

Chronic

  • Cystic fibrosis (mucoid strain)
  • mucoid exopolysaccharide (MEP) -> biofilm production (BAD NEWS!!!)

Acute pneumonia

  • Ventilation acquired pneumonia (VAP)
  • comatose, sedated patients on vent
170
Q

Which virulence factor is shared by pseudomonas and diphtheria?

A

Exotoxin A = diphtheria toxin -> ADP ribosyltransferase -> inactivates ef2 -> stop protein synthesis

171
Q

Which isolates of pseudomonas have the following characteristics:

  • mucoid
  • quorum sensing
  • loss of flagella, pili, o side chains and downregulation of production of toxins
A

Cystic Fibrosis ISOLATES

172
Q

All RNA viruses replicate in the (blank) except for (2 blanks)

A

Cytoplasm except influenza and retroviruses

173
Q

Amantadine and rimantadine block

A

viral uncoating and genome release

-influenza A only

174
Q

Neuraminidase inhibitors prevent

A

sialic acid removal -> no spread of virus

  • influenza A and B
  • zanamivir and oseltamivir
175
Q

what causes a pandemic - drift or shift?

A

Shift -> novel virus due to reassortment of viral genes

176
Q

Systemic sxs from influenza infection are caused by?

A

Endogenous interferon release (not due to the virus itself)

177
Q

Influenza virus is more stable in (cold/warm) air and (low/high) humidity

A

COLD air and LOW humidity

178
Q

Influenza A virus

  • characteristics
  • virulence
  • disease systems involved
  • vaccine
A
  1. Characteristics
    - neg sense, single stranded RNA virus with envelope
    - 8 segmented genome
    - replicates in nucleus
  2. Virulence
    - HA -> viral entry
    - NA -> release
  3. upper and lower respiratory tracts
  4. YES
179
Q

Respiratory syncytial virus (RSV) is a disease of which season?

180
Q

MCC of lower respiratory disease in infants?

A

RSV - major resp pathogen of young children

-bronchiolitis and bronchopneumonia

181
Q

RSV (paramyxovirus)

  • characteristics
  • virulence
  • disease systems involved
  • vaccine
  • tx
A
  1. Characteristics
    - neg sense, single stranded RNA virus with envelope
    - NON-segmented
    - replicates in cytoplasm
  2. Virulence
    - Fusion (F) protein -> syncytia formation
    - attachment proteins
  3. resp tract, bronchioles
  4. NO
  5. Tx -> ribavirin
182
Q

Parainfluenza (paramyxo)

  • characteristics
  • virulence
  • disease systems involved
  • vaccine
A
  1. Characteristics
    - neg sense, single stranded RNA virus with envelope
    - NON-segmented
    - replicates in cytoplasm
    - several serotypes
  2. Virulence
    - Fusion (F) protein
    - attachment proteins
  3. upper and lower resp tract; CROUP
  4. NO
183
Q

Croup also called? what’s the unique presentation?

A

Laryngotracheobronchitis

seal like cough
also stridor

184
Q

Describe mech of pertussis toxin

A

ADP-ribosylation
disables Gi -> over activates adenylate cyclase (inc cAMP)

Leads to

  • immunosuppression
  • inhibition of chemotaxis
185
Q

3 stages of pertussis cough

  • which one is most contagious
  • which one has the worse cough
A
  1. Catarrhal
    - MOST CONTAGIOUS
    - lasts 1-3 weeks
  2. Paroxysmal
    - WORST COUGH (paroxysmal cough)
    - lasts 2-6 weeks
  3. Convalescent
    - lasts 2-3 weeks
186
Q

Bordetella pertussis

  • characteristics
  • virulence
  • disease systems involved
  • vaccine
A
  1. Characteristics
    - gm neg rod
    - fastidious growth (potato agar)
  2. Virulence
    - many
    - pertussis toxin = ADP ribosyltransferase
  3. Disease
    - whooping cough
  4. Vaccine -> YES!!!
    - against adhesins
    - vaccine doesn’t last lifetime -> need booster
187
Q

Should antibiotics be given for aspiration pneumonitis?

A

not usually -> clears up into 24 hours

188
Q

Why is azithromycin added to ceftriaxone for hospitalized patients w/ CAP?

A

Azithro covers:

  • legionella
  • chlamydia
  • mycoplasma
189
Q

Good antibiotic for aspiration pneumonia?

-how about in the hospital?

A

Clindamycin -> good activity against anaerobes

Hospital aspiration

  • vanc + carbapenem
  • piperacillin/tazobactam
190
Q

Tx for chlamydia or mycoplasma

A

doxycycline -> inhibits 30S

Azithromycin or clarithromycin

191
Q

Tx for legionella

A
  • Azithromycin
  • quinolone
  • can combine if severe
192
Q

What antibiotics are good for pseudomonas?

A
  • cefepime -> 4th gen cephalosporin
  • carbapenem ->
  • piperacillin/tazobactam
193
Q

necrotizing bronchiolitis seen with bacterial or viral lung infections?

194
Q

Acute vs chronic rhinosinusitis

A

Acute < 4 weeks

Chronic > 12 weeks

195
Q

Viral URI vs acute bacterial rhinosinusitis

-compare duration

A

viral lasts 5-10 days

bacterial > 10 days

196
Q

Radiography for sinusitis

A
  • usually don’t need to image for acute

- do CT for chronic after giving tx

197
Q

most common organisms for acute bacterial rhinosinusitis in ADULTS

A

Strep pneumo

H. influenza

198
Q

most common organisms for acute bacterial rhinosinusitis in KIDS

A

M. cat

strep pneumo

H. influenza

199
Q

What organisms to consider with chronic bacterial rhinosinusitis

A

staph

pseudomonas -> especially w/ prior sinus surgery

Anaerobes

+ all the ones that cause acute

200
Q

Steroid for sinusitis

  • spray
  • systemic
A

Sprays - only good chronic, NOT acute

systemic (prednisone) - excellent for acute AND chronic

201
Q

Epworth sleepiness scale greater than what should warrant a sleep study for OSA?

202
Q

AHI or RDI classification for mild, moderate and severe OSA

A

mild: 5-15
moderate: 15-30
severe: >30

203
Q

most effect tx for OSA?

A

CPAP - improvement in

  • daytime sleepiness
  • quality of life
  • cognitive fx
  • systolic and diastolic BP
204
Q

Patients with OSA due to what can have fantastic outcome through surgery

A

enlarged tonsils and/or adenoids

205
Q

Mallampati classification is used to assess ease of (blank) but also correlates with severity of (blank). A score of IV means?

A

intubation; sleep apnea

Class IV - only hard palate is visible (worst)

206
Q

Friedman classification used to predict success of?

A

Uvulopalatopharyngoplasty (UPPP)

Class I -> successful

207
Q

Rhinovirus

-characterstics

A

small, naked, ssRNA

MCC common cold

208
Q

Coronavirus

  • characteristics
  • common cold percentage
  • which other disease
A
  • enveloped
  • single stranded RNA, + sense
  • replicates in upper resp and GI tracts

15-30% of common colds

SARS

209
Q

MC bacterial cause of pharyngitis?

  • reservoir
  • transmission
  • M protein
  • pyrogenic exotoxin (SPEA, B, C) responsible for?
  • vaccine?
A

Strep pyogenes

Gm positive beta hemolytic streptococci
-in chains

  • reservoir -> throat (infected humans only)
  • transmission -> person to person
  • M protein -> antiphagocytic; many serotypes
  • pyrogenic exotoxin (SPEA, B, C) responsible for RASH of scarlet fever
  • vaccine -> NO; too many M protein serotypes
210
Q

Corynebacterium diphtheriae

  • characteristics
  • lab culture
  • virulence
  • disease
  • vaccine

ABCDEFG (first aid)

A
  1. Characteristics
    - gm pos rod
    - pleomorphic
    - club shaped
  2. Lab culture
    - black colonies on cystine-tellurite agar
  3. Virulence
    - diphtheria toxin (A/B) -> ADP-ribosylation of elongation factor 2 -> stops protein translation (what else does this?)
  4. Disease
    - pseudomembranous pharyngitis
    - lymphadenopathy
    - myocarditis
    - arrhythmias
  5. Vaccine -> YES
    - DPT
ADP-ribosylation 
Beta-prophage 
Corynebacterium 
Diphtheriae 
Elongation Factor 2 
Granules
211
Q

EBV

  • characteristics
  • virulence
  • disease (list 4 aspects of this disease)
  • vaccine
  • primary infection asymptomatic in?
A
  1. Characteristics
    - enveloped, DNA
    - herpesvirus
  2. Virulence
    - latency in B cells
  3. Disease -> infectious mono
    - fever, pharyngitis, lymphadenopathy (posterior cervical), and splenomegaly
  4. No vaccine
  5. primary infection often asymptomatic in children
212
Q

The atypical lymphocytes seen in infectious mono are?

A

Reactive cytotoxic T cells (first aid)

213
Q

Mumps virus

  • characteristics
  • virulence
  • disease (list 4 aspects of this disease)
  • vaccine

Mnemonic -> POM

A
  1. Characteristics
    - enveloped RNA paramyxovirus
    - humans = sole reservoir
  2. Virulence
    - enter resp tract
    - SYSTEMIC spread
  3. Disease
    - mumps -> parotitis, SYSTEMIC infection
  4. Vaccine
    YES -> MMR

Mumps make your parotid glands as big as POM-poms
P - parotitis
O - orchitis
M - aseptic Meningitis

214
Q

Mumps is contagious before or after parotitis develops?

215
Q

H1-R effect on bronchial smooth muscle

A

CONTRACTION

GPCR -> DAG -> IP3 -> inc Ca++ -> contraction of smooth muscle

216
Q

H2-R effect on gastric parietal cell

A

Inc in H+, pepsin secretion

GPCR -> inc in adenyl cyclase -> cAMP -> PKA -> H+,K+ - ATPase

217
Q

Combined H1/H2-R dependent tissue response

  • on vasculature
  • skin -> triple response
A

H2 -> smooth muscle dilation
H1 -> endothelial cell contraction; edema
-NO release -> vasodilation

Skin -> triple response

  • flush, flare, and wheal
  • inc edema, pain and dilation
218
Q

Dif b/w 1st and 2nd gen anithistamines

A

1st gen -> sedating
-lipophilic -> crosses BBB

2nd gen -> longer half life

219
Q

2nd gen H1R antagonists metabolized by the?

A

P450 enzymes - drug drug ix

220
Q

What should be used instead of antihistamines in the following situations when there’s an emergency

  • anaphylaxis
  • shock
  • acute asthma
  • COPD
A

EPINEPHRINE

221
Q

Which population should use antihistamines with caution?

A

Pregnant women

Heart disease

222
Q

H2-R antagonists are generally very safe drugs

  • where do they act?
  • what’s the exception drug?
A

Act on gastric parietal cells -> reduce H+ and pepsin production

  • lower cAMP
  • inhibit vagal and gastric stimulation of H+ production

Cimetidine - garbage drug

  • inhibits P450
  • inhibits hormone binding to androgen receptors and estradiol metab -> gynecomastia and impotence in men + galactorrhea in women
223
Q

SPIKES for delivering bad news

A

SETUP

i. Have a plan before going into room
ii. Sit down
iii. Make eye contact
iv. Get close to patient
v. Have tissues

PERCEPTION (of the patient)

i. What does the patient know?
ii. Expectations of the patient
iii. Misconceptions or misunderstanding
iv. Is patient in denial

INVITATION
i. How much info does patient want?

KNOWLEDGE

i. Speak at level of patient
ii. Don’t use medial jargon
iii. Be direct
iv. Align patient perception

EMPATHIZE

i. Let them cry
ii. Ask is they have questions or concerns

SUMMARIZE

i. Be concrete about next steps
ii. Make sure they understand

Renal-Pulm (9 decks)

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