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NU734 Acute Care I > NU 735 Pulmonary > Flashcards

NU 735 Pulmonary Flashcards

1
Q

**Ventilator Associated PNA
Overview **

A

Community Rate VAP
- Ventilated >/= 30 days, 70 % acquired
- VAP >/= 48 HRS after Intubation

**Mortaligy **
- 50 to 70%
- Underlying disease plays a role

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2
Q

VAP : Etiology AKA
Bacteria

A

MDR & non-MDR bacterial pathogen

  • **Non-MDR like CAP /gm negative : **
  • Pseudomonas aeruginosa ,
  • E.coli;
  • klimseala pneumonia )
    **MDR /gram positive
    MRSA or Steph aurous

Atypical Bacteria: Lower incidence
Accept Legionella

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3
Q

VAP
Three factors to Pathogenies of VAP

A

* Colonization of the oropharynx (from pathogenic organisms )
* Aspiration of these organisms (lower respiratory tract )
* Compromise of the normal host defense
*

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4
Q

Ventilator Associated Pneumonia
Risk Factors

A

* Endotracheal tube : Prolonged intubation
**Bypass normal mechanical factors to prevent aspiration **
- Macro Aspiration: High air flow
- Micro aspiration can occur exacerbation by secretion above the cuff
**Oropharynx flora replaced by pathogenic microorganisms
Glycocalyx biofilm
Protect bacteria
Risk for inoculation

Immunoparalysis: Corresponds with VAP

**Antibiotic selection pressure: Poses Greater Risk **
* Cross infection
* Contaminated equipment
*** Malnutrition **

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5
Q

Ventilator Associated Pneumonia
**Complications **

A
  • **Prolonged Ventilation and ICU Stay **
    *** Nectrotizinet Pneumonia **
    - Pulmonary Hemoragged
    - Bronchietasis
    - Parenchymal Scarring
    *Result i Catabolic State:
    -Nurtitional Risk muscle waist Rehab
    **Permanently Impact the Elderly: **
    Unable to return to Independent Living
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6
Q

PNA
Clinical Manifestations

A

***** Symtoms ca indolent or Fulinant
* Febrile, ST, Chills, Night Sweats, HA, Malgias, and or arthragias

  • Caugh
    - Nonproductive
    - Productive mucoid, Purulent, or Blood tinged Sputum
    Gross Hemotysis: CA-MRSA
    Pleural Chest Pain: Pleural Involvement
    GI: N/V/D
    Dull to flat percussion
    Crackles, bronchial breath sounds and pleural friction rub
    Elderly Display AMS and few other manifestations
    AMS may be 1st
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7
Q

Hospital & Ventilator Acquired Pneumonia
Empiric Treatment Plan

A

** Importance of antibiogram ( consult pharmacy _ **
* Plan treatment based on risk factors
** Risk factors: **
* prolonged hospitalization,
* recent antibiotic use,
* intubation,
* immunocompromised,
* ARDS,
No MDR risk factors <10%

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8
Q

VAP TX Empirical
No MDR Risk Factors

A
  • **Treat with single agent **
  • Zosyn 4.5 mg Q 6 hrs ,
  • Cefepime 2gm Q 8 hrs or
  • Levofloxacin
  • Zosyn and Cefepime ( more common for TX b/c of gr negative coverage)
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9
Q

VAP TX Empirical
MDR

A

**Antibiotic coverage: 3 different antibiotics
2 will be directed for Pseudomonas ariginosis and
1 MRSA ) **

  • Cover for P. aeruginosa & MRSA
  • P Aeruginosa: Zosyn, Cefepime or Merrem
  • Consider double coverage if severely ill
    Aminoglycoside or Fluoroquinolone
    +/- Zyvox or Vancomycin for MRSA**
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10
Q

VaP
Specific Treatment Plan

A
  • Narrow Down ABT
  • Negative Tracheal Aspirate Culture or Growth
    -Consider Stoping ABT
    - look for Alternative Dx
  • D/C Combo Therapy for most Pseudomonas Pneumonia
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11
Q

Lung Abcess
Overview

A
  • Necrosis and Cavitation of Lung
    -Caused By Microbial Infection
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12
Q

Lung Abscess
Microbes

A
  • Anaerobs Associated with** Aspiration **
  • Ca-MRSA
  • Pseudomonas Aruginosa: Worsen Prognosis in Community
  • Strepntococcus Pneumonia
    *
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13
Q

Lung Abcess
**Risk Factors **

A

**Aspiratin is major risk factor contributed by **
* AMS
* ETOH
* Drug overdose
* Seizures
* Stroke
* Neuromuscular Disease
* Esophageal Dysmotility

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14
Q

Lung Abcess
Decreased Incidence

A

Significan
Mortality and Morbidity

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15
Q

Lungs Abcess
Characterization

A
  • Primary VS Secondary
  • Acute vs Chronic
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16
Q

Lungs Abcess
Acute

A

Less <4 to 6 wks

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17
Q

Lung Abcess
Chronic

A

40% cases

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18
Q

Lung Abscess
Typically Single dominant

A

> 2cm (can be single or multiple )

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19
Q

Lung Abcess
Primary

A
  • **Anaerobic Bacteria **
  • Produce extensive Tissue Necrosis
  • **Absence of underlying pulmonary or sytemic Condition **
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20
Q

Lung Abcess
Primary /clinical Manifestation

A
  • Pneumonitis (Gastric acid )
  • Parencymal necrosis and vaitatio develop 7 tp 14 days
  • Posterior Upper
  • Superior lower
  • Right lung field (effective more b/c Rt bronchi less angulated )
  • Putrid Abscess: Foul smelling breath, sputum or empyema
  • Anaerobic Etiology
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21
Q

Lung Abscess
Secondary

A

*** Underlying Condition **
- Post obstruction process (bronchial foreign body or tumor )
- Systemic process (HIV or other immune compromised conditions )

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22
Q

Lung Abcess
Secondary /Organisms

A
  • Pseudomonas aeruginosa & GNR (other gm – rods) most common
  • Staphylococcus aureus (septic Emboli)
  • Legionella spp.
  • Pneumocystitis jirovecii
    • Fungal (imuno compromised like bone marrow or organ transplant pt )
      *
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23
Q

Lung Abcess
DX

A
  • CT chest: Air fluid levels with Development Abcess
  • Putrid Sputum Odor: Virtually dx for Anaerobes
  • **Sputum Culture and Gram’s Stain:
    - Failure of treatment b/c does not show anerobic culture
    Yield Polymicrobial
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24
Q

Lungs abcess
Secondary Abscess specific

A

present and Faile of tx to Epirical Therapy
* Sputum and BC : Need for target therapy in addition to serologic study for opportunistc pathogenns
* Bronchoscopy with Bronhoaveolar Lavage
* CT guided percutaneous needle aspitration

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25
Q

Lung Abcess TX
Primary Lung Abcess

A
  • **Clindamycin 600 mg IV TID **
  • Duration TX
    -Clinical Improvement
    -No Fever
    **Transition to Clindamycin 300 mg PO QID **
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26
Q

Lung Abcess TX
Primary Lung Abcess

Alternative: Bat Lestin Combination

A

Unasyn
Transitio to Augmentin
Duration : 14 wks
3 to 4 wks or 14 wks duration

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27
Q

Secondary Lung Abscess

A

Specific Coveragr for pathogens
Abcess: > 6 to 8 cm diameter
Less likely to respond to aBX alone
Surgical resection
Percutaneous drainage

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28
Q

Pleural Effisin

A

Starts Here

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29
Q

Pleural Effusion
Overview

**What is Pleural Space ?
What is Pleural Effusion ?

A

**Pleural Space **
-Lies between **lung **and **chest wall
- Normally contains thin layer of fluid
**Fluid enters pleural space from capillaries **
- Removed from lymphatics in parietal pleura
The pleural fluid formation exceeds pleural fluid absorption
-Excess quantity of fluid in pleural space
Pleural effusion occurs

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30
Q

Pleural Effusion
Initiating Treatment Plan

A

Suspect pleural effusion
- Chest imaging to diagnose the extent
-Chest ultrasound,
-CT scan (no contrast ) or
-chest x-ray (Pick up sometimes 1st )

Significant pleural effusion
-Thoracentesis: Bedside or IR
-Chest tube or
VATs: (video assistant **thoracotomy ) : **
Late treatment or difficult cases

-** Pleural fluid analysis** : once pleural fluid obtained

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31
Q

Pleural Effusion
Etiology

A

Transudate
VS
Exudate

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32
Q

TEST

** Trasudate **

Effusion develop when change in** systemic factorss such as increase in capillary Hydrostatic pressure or decrease collide pressure

A
  • CHF (left Ventrical Failure )
  • Cirrhosis
  • Nephrotic Syndrome
  • Peritoneal Dialysis
  • SVC onstruction
  • Myxedema
  • Urinothorax (urine in pleural due to retropinnind leaking of urine occumulation
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33
Q

**Exudate **

Result of pleaural inflammation, Infection, injury, or Lymphatic obstruction

A
  • Neoplastic diseases
  • Infectious disease: TB, , pNA
  • Inflammation :
  • Pulmonary embilism or infarction
  • Trauma
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34
Q

**Normal Pleural Fluid **

Pleural Effusio Fluid Analysis

A
  • Appears Clear
  • PH: 7.60 to 7.64
  • Protein: <2% (1-2)
  • WBC <1000
  • Glucose : Similar to Plasma
  • LDH: <50% plasma concetration
  • Amylase: 30 to 110
  • Triglycerides: <2
  • Cholesterol : 3.5 to 6.5
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35
Q

Light’s Criteria

Pleural Effusio Fluid Analysis

A

**Light’s Criteria

Exudate vs TRAnsudate
- Exudate = meet at least one -

  1. Pleural fluid protein/serum **protein >0.5 **
    • Pleural fluid LDH/serum **LDH >0.6 **
    • Pleural fluid LDH >2/3 normal upper limit for serum
  • **Serum protein/pleural fluid protein differnts **
    Gradient >3.1 g/dL: Transudate
    Exudated ruled out It will be Transudate
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36
Q

Trasudate

A

** **Serum protein/pleural fluid protein differnts **
Gradient >3.1 g/dL: Transudate

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37
Q

EXudate

A

Light Criteria 1 out 3
**Serum protein/pleural fluid protein differnts
Glucose < 60
Protein : <3.0

38
Q

Pleural Effsuon
Diagnostic Approach

A

**Transudate:
- TP >3.1;
- due to disease like CHF, Cirrhosis,
- Treat underlying condition (CHF, Cirrhosis….. )
- —————————————————————————–

**Exudate
- Less 3.0;
-glucose <60
- Inflammation, Bacteria (TB), Immune (HIV )

Further diagnostic procedures needed
* Pleural fluid glucose, cytology, cell count, culture & stain, TB marker
-Glucose <60 mg/dL
* Consider malignancy vs bacterial infections vs rheumatoid pleuritis

  • Work up coming back negative
    -Consider PE work up ( CT contrast of + TX as PE result to fluid 2/2 escemia )
  • Work up negative again
    -Consider tuberculosis
  • Work up still negative
    -Consider thoracoscopy or pleural biopsy
  • Absolute Findings
    pH <7.2, Glucose <60 mg/dL, LDH >1000 U/L, bacteria cultured
    -Complete drainage needed MUST
39
Q

Absolute Findings

Must complete drainage : Bacteria

A

PH: <7.2
**Glucose: <60
**LDH: >1000 **
Bacteria Culture
Must Complete drainage needed Must

40
Q

Pleurla Effusion
Due to Heart Failure

A
  • Most common cause of pleaural effusion: Left Ventricular HF
  • Abnormal Presentation
          ** -Throacetesis needed**
                   Not Bilaterial and Comparable
                   Febrile 
                   Pleuritic chest Pain
  • Treat Underlying heart Failure
    -Failure of therapy (Lasix not helping )
    Thoracentesis
  • Fluid Analysis :
  •         **NT-proBNP >1500 (this case you DX Pleural effusion                                                                                 secondary CHF) **
41
Q

Pleural Effusion
Due to Hepatic Hydrothorax

A

*** Cirrhois **
-5% develop effusion exudated ruled out it al be *
*TRansulate **
* Predominant Mechanism
- Direct Movement of peritoneal fluid into pleural space thru diaphragm
* Right Sided Effusion (predomi) : large enougth to produce SOB

42
Q

**Pleural Effusion

**Due to Parapneumonic (should be consider with pt Bacteria PNA )
Overveiw

A

**Most common exudative pleural effusion USA
- Should consider Bacteria

  • **Underlying Causes: **
    -Bacterial pneumonia, lung abscess, or bronchiectasis
43
Q

Parapneumonic
Clinical Presentation

Aerobic Infectio

A
  • Acute Febrile Illness
  • Chest Pain
  • Sputum Production
  • Leukocytois
44
Q

Parapneumonic
Clinical Presentatio :
Anaerobic Infection

A

Subacute illness
Weight loss
Mild Anemia
Aspiration factor

45
Q

Parapneumonic: Clinical Presentation
Grossly Purulent Effusion

A

Refer to Empyema (puss )

46
Q

Pleural Effusio
Parapneumonic Treatment

A

Management Considerations

-** Free fluid serparting lung frm chest wall >10mm**

                              -Throracentesis needed -Loculated Pleural fluid -PH<7.20, Glucose<60 mg/dl, Gram's stain (+) or pus pleural space
                                   Invasive approach needed ( Get Cardothoraci)
  • Reoccurrence Effusion after initial thoracentesis then
    -Thoracentesis (repeat thoracentesis should be done)
    -Chest tube & instilling **fibronolytic agent (if pleaural fluid cannot be remvoed with Thoracentesis )
    -Tissue Plaminogen Activator (tPA )10 mg
    Deoxyribonuclease (DNASE)5mg**Further Meausres : **
    -Thoracoscopy with breakdown of adhesions (chest tube insertion )
    -Decortication ( remove fibrous tissue )
47
Q

Pleural Effusion
Due to Malignansy (Due to Metastatic Disease )
Overview

A
  • **Second most common exudate effusion type (poor prognosis ) **
  • Malignancy progress: Not going to be curable by chemotherapy
  • Tumor Causes (3 Tumor 75% lead to Malignant effusions)
    -Lung cA
    -Breast CA
    -Lymphoma
  • Clinical Findings
    -Dyspnea out of propotion (SOB)
    -DX supported by cytology
    if Cytologic exa are : **Negative Results **
    -Consider throacoscopy like **west procedure **
    -West Procedure: when malignancy suspected
    -Cardithorsurgery on board
48
Q

**Pleural Effusion
Due to **Malignancy **
Treatment

A
  • Confirming DX:
  • -**Thoracoscopy **
  • Pleurodisis (result in adhesion ….
    -CT or US guided needle biopsy of pleural space or nodels

***Treatment **
- Symptomatic relief
- Thoracostomy tube
* **Sclerosis Agent **
- Docxycycline 50 0 mg (can cause inflammation )
- Just symptomatic recommendation Hospice

49
Q

Pleural Effusio
Chylothorax > Etiology

A

-Discrutpion of thoracid duct

-**Chyle (mily fluid that contain fat drops in lymph)accumulatio in pleural space **

50
Q

Pleural Effusio
Chylothorax
Most Common Cause

A

-Trauma
Thoracis surgery

**Madeastinal Tumors ** :
Lymphangiogram and dediastinal CT Scan

51
Q

Pleural Effusion
Chylothorax
Clinical Findings

A

Need Thoracentesis
-Dyspnea
-Large Milky effusion
Trigceride >110

52
Q

Pleural Effusion
Chylothorax
Treatment

A

Medical management
* Chest tube
Avodi prolog insertion
* **Octreotide 50 to 100 mcg SW TID **
* Ocreotide Function By
- Minimizes Lymphatic fluid Excretion
- Do not keep chest tube bor long time b/c excess drainage lead to malnutrition immunologic
* Nutriton: TPN VS Oral feeding
* Surgical Approach:
-Percutaneous transabdominal throracid duct blockage (will control chyle thoresc
-Ligation of throracid duct

53
Q

TB: Overview

A

Bacteria: Mycobaterium Tuberculosis
Common amongs HIV
Main Cause of all HIV infeted Population and Main cause of death
Foreign born Population
Disadvantaged or Marginalized Population

54
Q

TB : Primary

A

Limited to no Clinical Findings
Limited infection and spread of the disease

55
Q

TB
Progressive -Primary

A

Inadequate immune response to contain the primary infection
1/3 of new cases of TB caused by person to person

56
Q

TB Laten

A

Do not have Active disease
Cannot transmit to other

57
Q

Active TB

A

**Can occur within 2 yrs following primary infection
Reactive to diseases
laten not adequately treatment
contagius

58
Q

COPD

A

Start Here

59
Q

COPD : Statistics

A

6th leading cause of death in US
10 mil dx USA

60
Q

COPD
what is that

A

***** Persistent respitory Symptoms and Airlow Limitation
-Not fully reversible (problem happen no going back )

Airlow limitation is major physiologic changes in COPD that result in :
- Small airway disease > **Emphysema **
- Narrowed ariways : **Mucus and Fibrosis **
- Hallmark of Advanced CoPD: Exensive Small airway destruction

COPD: persistent RR symptoms > Airway Limitation .> Extensive Small Airway Detruction

61
Q

COPD
Airway obstruction (chronic )
Determine?
Cause ?

A

Determined by Spirometry
Usually caused by Smoking

62
Q

COPD Classification

A

**Ephysema
Chronic Bronchitis
Small airway disease
Gentic Consideration **

63
Q

COPD : **Enphysema **

A
  • Lung Alveoli destruction
  • Airway Elargement
  • smoking
    *
64
Q

Chronic Bronchitis

A

Chronic Cough and
Phlem

65
Q

Small Airway Disease

A

Narrowed Smal Bronchioles
Reduced in Number

66
Q

Genetic Considerations

A

Alpha 1 Atitrypsins Deviciensy

67
Q

COPD : Emphysema
4 Charatetistics

A
  • Chronic exposure t Cigarette smoke
  • Compromised Airway Vasculature and Gas exchange
  • Structural cell death
  • Disordered repair and other component
68
Q

Emphysema “ Primary Mechanism

A
  • Elastin degradation and disordered Repair
  • Auto Immune : promotes progression
69
Q

COPD
Small Airway Disease

A

**Major stie of Increase Resistance: **Small airway <2mm

**Characteristics: **
-Cellular Changes: Goblet cell Metaplasia
-smooth muschle Hypertrophy
-Luminal Narrowing: Firbrosis, excessive mucous, edema and cellular infiltration
-Hallmark of advanced COPD: Extensive small airway destruction

70
Q

COPD
Chronic Bronchitis

A

**Characteritics **
-Mucus Gland Enlagement
-Goblet cell Hyperplasia
Leading t cough and mucouse production

Bronchi undergo Squamous Metaplasia **
- Predisposed to carcinogenesis and mucociliary clearance
-
- Smooth muschle herptrophy and brochial hyperactivity**
- Lead to air flow limitation

Neutrophil influx: Associated wiht purulent Sputum

71
Q

COPD
Clinical Manifestations

A

Prologned Expiratory Phase
Expiratory Wheezes
Barrel chest
Accessory Muschle use
Tripod POstion: Faciliates accessory mushcle use
Cyanosis in the lips and nailbeds
Digital clubbin - CA
Hyperinflation of the chest Xray

72
Q

COPD
Lab Test

A
  • ABG
  • Resting or Exertional Hypoxemia
    -** pCO2 >45** ( norm 35 to 45)
  • Presence /impending acute exacerbation
  • Elevated Hcg and RVH: Chronic Hypoxia
73
Q

COPD
Lung Studies

A

CXR: increase lung volumes and flatten diaphragm
CT scan of chest
Definitive to establish presence /absence of **ephysema **
Determine any coexisting diseases

74
Q

COPD
TX Goal

A
  • Systemic Relief
  • Reduce Future risk
  • Quit smoking most improtant
75
Q

Articholinertic Muscartinit agent

A

SAMA (Atrovent )
LAMA (Spiriva)

76
Q

Inhaled Beta Agonist

A

SABA (Albuterol )
LABA (Brovana )

77
Q

Inhaled Corticosteroids

A

Pulmicort

78
Q

Combo Therapy

A

Advair
Symbicort
or Trelegy

79
Q

Severe COPD

A

Theophilline
and
Daliresp

80
Q

Acute Exacerbation
COPD TX

A

Dual SABA/SAMA (Duoneb)
Brovana 15mcg Nebs Q 12 HRS and
Pulmicort 0.5 Neb Q 12

**Solumedrol: **
Transtiton to oral dosing 24 hrs prior to d/c
Avoid chronic use

Long Acting Muscarnic Anagonist (Seebri Neoinhaler )

Zyrtec and dingulair

81
Q

Asthma

A
  • Syndrome Aiflow Obstruction
  • Occur any age
  • Adult onset usually permanent
  • Severty does not vary for patients
    - Mild asthma rarely progresses to more severe disease
82
Q

Asthmatics Inflammation Airway different from
NON Asthmatics

A

Narrowing with consequent reduced air flow
usualy reversible
chronic asthma with irreversible airway obsutrucion

83
Q

Asthma
Risk Factors

A

**Major Risk Factor **
-Atopy major RF
Allertic Rhinitis
Atopic deramatitis
Genetic Predispostion
Environmental: Sulfur Dioxide, OZone, Diesel
Obesity: BMI >30

84
Q

Asthma Clinical Findings

A

Eosinophil Infilaration

85
Q

Asthma DX

A

Symptoms
Confirmed : PFT
Spirometry: **Confirme Air flow Limitation **
-Reduced FEF1 and FEV 1/FVC
-Reduce Peak Expiration flow (PEF)

86
Q

Asthma Treatment
Maintenace

A
  • **Maintenance **
    -Bronchodialtors
    -Anticholinergic
    *** LAMA **
    Inhaled Corticosteroids
    Most effective controler
87
Q

Asthma Exacerbatio

A

Duonebs
Solumedrol
Ihaler : Brovana and Pulmocort
singular and Zyrtec
O2 Ensure no mucus plug

88
Q

Bronchiectasis

A

IIrreversible airway dilation : Focal Or Diffuse
**Classic Categorization: **
- Cylindrical, tubular, varicose, cystic
- Most common is tubular

Focal Bronchiectasis
Changes in localized area
* **Consequence of airway obstruction **: Extrinsic vs intrinsic
* **Diffuse Bronchiectasis: **
- Widespread bronchiectasis
- Underlying systemic or infectious disease
Etiology
Infectious or noninfectious
Nontuberculous mycobacteria (NTM) infection
Affects non-smoking women >50 years
Cystic fibrosis
Late adolescence or early adulthood
Mutation in cystic fibrosis conductance regulator (CFTR)
Leads to infections, inflammation, respiratory failure

89
Q

Bronchietasis
Etiology

A

Infectious or noninfectious

Nontuberculous mycobacteria (NTM) infection
- Affects non-smoking women >50 years
**Cystic fibrosis **
* Late adolescence or early adulthood
* Mutation in cystic fibrosis conductance regulator (CFTR)

Leads to infections, inflammation, respiratory failure

90
Q

Bronchiectais
Causes and Risks

A

Poor Mucciliary clearance
Microbial colonization of bronchial treee
Damage larger Airway
**Upper LUngs **: post radiation
**Middle lungs ** Non TB Mycobacteria
**Lower Lung field ** chronic Espiration

91
Q

Bronchiectais
Clinical Findigns

A

SOB, Productve Cough, Thick tenacious sputum
Crackels and Wheezing
Clubbin g
Detected PFT

NU734 Acute Care I (25 decks)

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