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CCP 2 Review > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What structures are in the upper Respiratory tract?

A 
Nasal Cavity
Pharynx
- nasopharynx
- Oropharynx
- Laryngopharynx
Larynx
Glottis
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2
Q

Lower Respiratory Tract

A 
Trachea
Primary Bronchi
Bronchioles
Alveolar Duct
Alveolar Sac
- Alveoli
- Capillary
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3
Q

Inspiratory Muscles

A

Chest, Back, Scalenes, Pectoralis major and minor, serrated anterior, latissmus dorsi

Sternocleidomastoid

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4
Q

Expiratory Muscles

A

Abdominal Muslces,

Recurs Abdomomos. Obliques. Transverse abdomen is

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5
Q

Functions of Respiratory System

A 
Gas Exchange
Acid base balance
Phonation
Pulmonary defence and metabolism
- cough mucus clearance
- lung filter
- vasoactive substance metabolism

Lungs also phagocytosis by alveolar macrophages, filter emboli and leukocytes and excrete volatile substances

It modifies or uptake of serotonin, prostaglandins, norepinephrine, bradykinin, (does not metabolize epinephrine or histamine as it is a major source of histamine release)

Converts angiotensin 1- Angiotensin 2

Synthesize of surfactant

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6
Q

Alveolar Gas Equation

A

PA02=Fi02(Pb-PH20)-(PaC02)/RQ

PA02= 0.21 ( 760-47)- (40/0.8)

PA02= 100mmHg

Increasing PaC02 alone will decrease PA02 (and thus Pa02)

Important of preoxygenation

PH20 is saturated vapour pressure of water at body temperature and is normally 47 at atmospheric pressure

Pb= atmospheric pressure is 760mmHg

This equation is the method for calculating the partial pressure of alveolar oxygen (PA02). Assesses lungs are properly transferring oxygen into the blood.

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7
Q

Daltons Gas’s Law

A

Pt= P1+P2+P3

- Partial pressure of one gas increases the other must decrease

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8
Q

Causes of Hypercapnea

A

1) Won’t breath
- Drugs OD
- CNS lesion, SPinal cord lesion

2) Can’t Breith
- Chest wall injuries, kyphoscoliosis

  • Neuromuscular
  • Myasthenia Crisis, GBS< Muscular dystrophy ALS

Obstructive
- COPD, ASTHMA

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9
Q

Kyphoscoliosis

A

Deviation of the normal curvature of the spine in the Sagital and coronal planes

  • caused by congenital abnormalities including spina bifida, infections and vertebral tuberculosis
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10
Q

What is Low Venous Admixture

A

Normal SV02 70 percent

  • Patients in shock with decreased Sv02 will exacerbate hypoxemia
  • Abdnormal high Aa gradient
  • importance of optimizing oxygen delivery in hypoxemia failure

Intubation and MEchanical ventilation will remove WOB

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11
Q

Hypoxemia and Hypoxia definition

A

Hypoxemia= Low Arterial P02

Hypoxia = Low tissue 02

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12
Q

What is Diffusion limitation

A

Disruption of oxygen diffusion across the alveolar capillary interface

  • interstitial lung disease will have abnormal diffusion processs
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13
Q

Cabins are normally pressurized to?

Can this cause hypoxia in a healthy patient

Explain

A

8000 ft

Barometric pressure at sea level 760 mmHg Pi02 150

At 8000 ft barometric pressure 565 mmHg which Pi02 Inspiratory partial pressure of oxygen is 109 which correlates to a Pa02 62 mmHg

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14
Q

What is oxygen extraction equation

A

Sa02-Sv02

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15
Q

What is oxygen delivery to the tissues determined by

A

1) oxygen content in blood= oxygen bound to Hgb + oxygen dissolved
2) Cardiac output

D02= C0 (1.34xHbxSa02)+(0.003)xPa02)

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16
Q

Define

1) Inspiratory Reserve Volume
2) Inspiratory Capacity
3) Expiratory Reser Volume
4) Residual Volume
5) Functional Residual Capacity
6) Vital Capacity
7) Total Lung Capacity

A

1) Inspiratory reserve volume is the amount of air that can be forcibly inhaled after a normal tidal volume
2) Inspiratory Capacity is the sum of the tidal volume and the inspiratory reserve volume
3) Expiratory reserve volume is the amount of air that can be forcibly exhaled after a normal exhaled tidal volume
4) Residual volume is the amount of air left over in the lung after a full exhalation.
5) Functional Residual capacity is the amount of air left in the lungs after Vte exhalation
6) Vital Capacity is the amount of air the lungs can hold minus the residual volume
7) Total lung capacity is the full amount of air in the lungs maximal inhalation

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17
Q

Define Functional Residual Capacity

What is the importance what can cause increased FRC and decreased FRC

A

Residual volume + expiratory reserve volume
- amount of air left in the lungs after a normal expiration

  • Determined when alveolar pressure = 0 no airflow point where inwards recoil of lung is balanced by outwards recoil of the chest wall
  • usually around 2-3 L
  • It acts as a reserve oxygen allowing continued oxygenation

It is affected by

  • lung size- age, height, sex
  • lung and chest wall disease- ARDS, pleural disease ie pneumo/effusion, abdominal pressures, obesity, anesthetics pneumonia and body position

Decreased FRC Causes

  • Increased WOB, AIrway resistance, decreased lung compliance atelectasis/collapse
  • decreased ventilation and oxygenation
  • increased Pulmonary vascular resistance and increased Afterload
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18
Q

Pulmonary Function Tests AKA Spirometry

Definition and how does it help

A

Measures lung volumes and flow

Helps with diagnosis and grade of severity of obstruction and restrictive lung disease

Obstruction= asthma COPD

Restrictive Lung Disease= interstitial lung disease (ARDS, CHF), Obesity, neuromuscular disease

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19
Q

Interpretation of Pulmonary Function Tests

Restrictive VS Obstructive

A

Restrictive
- Low lung volumes and capacities
- Lung or chest wall compliance curves shifted to the right
- FEV1/FVC normal or elevated
DLCO= diffusion capacity for carbon monoxide normal or low

Obstructive

  • Variabile Expiratory
  • Low FEV1/FVC ratio
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20
Q

Asthma Pulmonary Function Tests interpretation

A
  • Episodic
  • FEV1/FVC is the forced exhalation volume in once second to forced vital capacity.
  • Asthma equals increased FEV1 to FVC in severe disease

Asthma FEV1/FVC ratio will improve with bronchodilator therapy

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21
Q

COPD and Pulmonary Function Tests

A

Chronic Bronchitis

  • increased mucus production from goblet cells
  • damaged cilia increase risk of bacteria and pnemonia
  • DLCO normal
    RV, FRC high secondary to air trapping
  • Low Pa02 with cyanosis
  • High PaC02

Emphysema

  • Low DLCO
  • Lung compliance shifts to the left ( increased compliance from loss of elastin and collagen)
  • Total lung capacity, Residual Volume , FRC all increased secondary to air trapping
  • PaC02 slightly increased.
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22
Q

Pulmonary Function Tests Numbers to remember

A

FEV1 < 50 percent sever for obstructive airway disease

FVC<50 percent significant restrictive airway disease.

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23
Q

What is tactile and Vocal Fremitus

A

Palpating of chest wall to detect changes n the intensity of vibrations created by phonation

Decreased in ( lots of air)

Increased in FLUID ( sound vibrates of Fluid) Think of ultra sound sounds vibrates of fluid.

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24
Q

Breath sounds

A

Vesicular- normal
Bronchial higher pitched seen in consolidation
Absent concerning

Crackles
Wheezes
Rhonchi
Strider

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25
Q

What is a VBG VS ABG

A

VBG good for C02 HCO3 (PH will be 0.02-.004 units lower than arterial)

ABG good for PH, Pa02, Sa02

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26
Q

What are Limitations of pulse Oximetry

A

Does not distinguish between oxy Hgb at 940nm
- does not distinguish between COhb and Methb from OxyHb

MetHb classically reads as 85 percent
- intravascular presence of dye - e.g methylene blue

  • Interference with ambient light, skin tone, nail polish or peripheral shut down

Calibrated from healthy volunteers

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27
Q

Difference between ETC02 and PaC02

A

ETC02and PaC02 difference is normally about 2-5mmHg due to normal dead space

Larger discrepancy can get worse secondary to Dead Space
- PE/ SHOCK

ETC02 is lower because of dead space

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28
Q

Types of Respiratory failure and Definitions

A

Type 1 Hypoxemic
- Pa02 < 60mmHg, Sa02 92%

Consider 6 mechanisms of Hypoxemia

Type 2= Hypercapnc
- PaC02 > 50mmHg

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29
Q

Decision to Intubated in Weakness

GBS, MG

A

VC <20 cc/kg

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30
Q

Definition of ARDS ( Berlin Definition)

A

1) Acute= <1 week
2) bilateral opacities on radiograph
3) non cardiogenic
4) P/F ratio of 300 with at least a peep of 5cm H20

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31
Q

ARDS Severity

A

Mild P/F 200-300

Moderate PF 100-200
Severe P/F <100

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32
Q

Stages of ARDS

A

Stage 1= Early Exudative stage
7-10 days

Stage 2= Fibroproliferative stage
- 2-3 weeks

Stage 3+ Fibrotic stage
- Abdnomral lung architecture- fibrosis cyst formations

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33
Q

Complications with ARDS and treatment

A

Ventilator can cause Barotrauma, Volutrauma, Biotrauma, Electotrauma

VAPS

Disease process can cause fibrosis, RV dysfunction and pulmonary Hypertension which can worsen with PPV

Stress ulcers, Delirium, VTEs, Critical illness myopathy

Organ dysfunction, kidney,liver

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34
Q

When is Prone and ECMO indicated for ARDS

A

PRONE P/F Ratio <150

Severe PF < 80
- ECMO

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35
Q

What is Supportive Management for ARDS

A 
Pain management
Sedation
Nutrition
VTE prophylaxis
Stress ulcer prophylaxis 
- drier fluid management
Hemodynamics monitor end organ perfusion, arterial lines, central lines
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36
Q

What is a good assessment prior to transporting patients with high pressures, air trapping, ARDS

A

POCUS looking for barotrauma

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37
Q

Definition of Aspiration

A

Pneumonitis- generally inflamed reaction to the lower airway caused by chemical irritation from gastric acid

Pneumonia active bacterial infection

38
Q

Define Emphysema

A

Structural changes distal to the terminal bronchioles, destruction of airspace wall floppy alveoli are prone to hyperinflation.

Loss of elastin and collegian,

Cause by smoking and anti-trypsin 1 deficiency

39
Q

Definition of Chronic Bronchitis

A

Chronic productive cough for 3 months in each of 2 successive years in which all o other causes of chronic cause have been excluded

40
Q

Difference between Asthma and COP

A

Asthma has reversibility to its airflow obstruction

41
Q

Pathophysiology of Obstructive Airway Disease

A

Distal airway- goblet cell and muscular gland hyperplasia, fibrosis, narrowing and collapsed airway

  • Lung parenchyma- dilation destruction of respiratory bronchioles alveolar ducts and alveoli

Pulmonary vasculture- smooth muscle hypertrophy hyperplasia

Increased pulmonary hypertension, in creased RV afterload,

42
Q

Staging of COPD

A

Gold Guidelines

Pulmonary Function Tests
- Spiromatry airflow limition

  • FEV1, FVC, FEV1/FVC ratio. Pre and post bronchodilator

Post brocnhoddilator <0.7 = obstruction

Staging/Severity

Mild FEV1 >80 percent
Moderate 50-80
Sever 30-50
Very sever FEV <30

43
Q

What is the Haldane Effect

A

With COPD patients DoxyHb binds to C02 more than OxyHb which increasing OxyHb = more c02 disosolved in blood as HCO+ more PaC02

So more oxygen will bind to hemoglobin in COPD which causes less C02 removal as there is less room for C02 to bind and results in increased C02 in blood PaC02

Will also decrease Hypoxic pulmonary vasoconstriction which can lead to more dead space.

44
Q

What is Hyperventilation Syndrome

A

Inappropriate minute ventilation resulting in respiratory alkalosis

Associated with anxiety, panic attaches

45
Q

How much Cerberal blood flow is reduced with 1mm decrease inPaC02

A

2 percent

46
Q

What causes tetany and parasthesia in hyperventilation syndrome

A

Call in carbon dioxide tension leads to respiratory alkalosis..

Alkalosis produces hypocalcemia which induces the tentany of muscles and parasthesia.

Muscle spasms.

In Alkalosis calcium binds more to albumin decresing ironized calcium

47
Q

What are different transudative Plerual effusions

A 
Heart failure
Hypoalbuminemia 
Nephrotic syndrome ( protein loss)
Liver Failure ( decreased albumin and portal hypertension
Peritoneal Dialysis
Atelectasis
48
Q

Examples of Exudative Effusions

A

Infection
Malignancy
Chylothorax ( lymphatic fluids leaks in the pleural space ) - sever cough and lymphatic flow disorder

49
Q

How much fluid does the pleural lining produce

A

10ml daily production and absorption produced by serious membrane

Can see on chest X-ray with 200ml Ap and 50ml PA

CT ultrasound nor sensitive

50
Q

What are Contraindications for thoracocentesis

A

Overlying infection
To small of an effusion / Unsafe
Coagulopathy

51
Q

Different types of Effusion

A

Simple = fee flowing aka uncomplicated

Complicated= infectious with loculations

Empyema ( infections)
- low glucose, low PH High Protein

52
Q

Define Pneumona

A

Infection of the lung parenchyma
- from a bacterial, viral or fungal infection

CAP, VAP HAP important for anti-microbial

53
Q

Definition of HAP timeline

A

> 48 hours after admission to hospital

54
Q

Definition of VAP

A

> 48 hours after being on a ventilator

55
Q

Definition of CAP

A

Less than 48 hours or presented with

56
Q

Antibiotics for CAP and VAP

A

CAP
- Ceftriaxone and Azithromycin

HAP/VAP
- Piptaz and Vancomycin (pseudomonas, ESBL , Fungal

Cultures poorly sensitive

57
Q

What is Cardiogenic Pulmonary Edema and some causes

A

Increased Hydrostatic pressures from high filling pressures of the left atrium and thus high pulmonary capillary pressures

Caused by Systolic Dysfunction HFrEF EF<40percent
- can be ischemic or nonischemic

Diastolic Dysfunction HFpEF EF<60 percent
- HTN, Renal failure, restricted cardiyopathy

Valvular disease
- mitral regurgitation and mitral stenosis ect

58
Q

What can precipitate Heart failure

A

1) Increased Preload
- Fluids, Salt intake, non compliant medications
- Acute Aortic Regurgitation or mitral regurgitation

2) Decreased Contractility
- ischemia/infarct

3) Increased Afterload
- HTN
- Aortic stenosis
- non compliance to meds

4) Tachyarrhythmias
- Rapid Afib

5) Dynamic LVOT obstruction (SAM) systolic anterior motion

59
Q

When level is helpful for BNP in diagnosing heart failure

A

<100 pg/ml BNP helpful to rule out HF

100-400 not helpful what the heck

> 400 Likely HF

60
Q

What are some findings of Heart Failure on a CXR, Ultra Sound

A

Cardiomegaly, Pleaural effusion, vascular redistribution, central opacities, Kerley A lines

POCUS

  • Decreaed EF
  • FULL IVC
  • diffuse B lines

Don’t forget PA catheter with Increaed Wedge pressure is surrogate for LVEDP and LA

PW Pressure greater than 20-25mm Hg= cardiogenic

61
Q

Pulmonary Embolism Scoring systems

A

PERC
WELLS
YEARS (for pregnancy)

62
Q

Work up For PE

A 
D-DImer to help rule out patieints
- Troponin, BNP
- CBV- leukocytosis is non common
- lactate, mixed venous, renal and liver ailure, ABG coats
ECG
CXR
CT Angio (gold standard ( VQ scan
ECHO
63
Q

Most common ECG Changes

A 
Sinus tachycardia= most common
RAD
RBBB- complete or incomplete
- TWI- V1-V4, inferior leads 
- Rapid AF
- non specific it T wave changes
Right Arial Enlarchment
S1Q3T3
64
Q

Define massive PE and Submassive PE

A

MASSIVE= SBP<90 for 15 minutes or longer or requiring inotropic support
- not caused by bradycardia or pulseless

Submassive PE- HD stable but no signs RV dysfunction
- Troponin 
- ECG
ECHO
- BNP
65
Q

Treatment for Massive and Submassive PE

A

Massive can get fibrinolytics

Submassive antioagulatons

Both can get catheter direct fibrinolytic or surgical embolectomy

66
Q

How to Manage Acute RV Failure

A

1) Optimize Preload
- passive leg raise small IV blouses

2) Minimize RV afterload
- Avoid Hypoxia/Hypercarbia, Acidosis ( will cause pulmonary vasoconstriction by activation voltage baited calcium channels and increases cytotoxic calcium)
- Keep alveoli recruited but not overdistened which can compresses capillaries
- Minimize sympathetic activation
- Vasopressin and Milrinone won’t have as much direct affects on pulmonary vascular use
- inhaled nitric oxide (pulmonary vasodilator)
- DEL WITH CLOT

Optomize LV afterload
- - Cornary and end organ copper fusion, norepinephrine vasopressin

Contractility
- Milrinone, dobutamine, epinephrine

Rate and Rhythm
- Sinus, not to fast (need diastolic filling)

67
Q

Definition and pathophysiology of Asthma

A

Reactive Airway disease associated with airway inflammation, intermittent airflow obstruction and bronchial hyper responsiveness

Hyper reactivity and inflammation associated with IGe, Mast Cell and eosinophils activations (degranulations) releasing histamine

68
Q

What is a Respiratory Antibiotic Resistant Pathogen

A

Bacteria that develop defence mechanisms again these drugs making them less effective

Examples are beta lactate antibiotic are penicillins and cephalosporins

  • bacteria produce beta lactamases= enzymes that break the beta lactate structure of the antibiotic
  • ESBL extended spectrum beta lactamase

Need to use antibiotics like carbapenems

69
Q

What are the 4 different Bacteria

A

1) Gram Positives
2) Gram Negatives
3) Atypicals
4) Anaerobes

70
Q

Describe Gram Positive Bacteria

A

Colonized in Oral, nasal, ( Staph and strep

Skin- Staph corynebacterium

GI- Colostridium, enterococcus

Disease of ORAL, Upper airway, CAP, HAP , SKIN, Soft Tissue , GI/ GU

71
Q

Gram Negatives. (KEEPS)

A
  • Kleibsiella
  • Enterbacter - E. coli
  • Enterococci
  • Proteus
  • Serratia

GI/GU, UTI, Appendicitis, Cholecycitis.

72
Q

Atypicals

A

Don’t stain with gram stain

Chlamydia, legionella, mycoplasma
- no normally colonized

Cause cause CAP

Responded well to macrolides - azithromycin

Does no grow easy in cultures treated empirically

73
Q

Anerobes

A

Need special medium to grow cultures

Can be gra positive or negative

GI GU bugs

CDIF, Bcteroids, fusobacterim

74
Q

CAP/ HAP/VAP antibiotics

CAP
- Ceftriaxone, Azithromycin to cover gram positives and Atypicals
(Strep Pneumonia)

HAP/VAP- Piptazo for gram negative,

Consider antibiotic resistant pathogens. MRSA, ESBL, Psudomona, Strentoprhomonas

A

Same as above

75
Q

MRSA pneumonia Antibiotic

A

Vancomycin and Linezolid

76
Q

Definition of Pulmonary HTN

A

Mean pulmonary arterial pressure of > 20mmHG

Normal 10-15 mm Hg

77
Q

What is LaPlaces Law

A

Wall Tenson (T)= Transpural Pressure (P)xRadius(r)/ 2x H. Wall thickness

78
Q

How to Treat RV Failure

A

1) Monitor IV, 02,
2) arterial line
3) CVC can be used for mixed venous measurements

CRAP approach
Contractility
Rate and Rhythm
Afterload 
Preload

Contractility

  • IF RV Failure secondary to Inferior MI get right side ECG
  • suspect RV involvement with STE V1, STD V2, III>II

ACS Managment
1) DAPT, 60units/kg Heparin followed 12U/kg infusion

Inotropic support

  • EPI if bradycardia
  • Milrinone 0.125mcg/kg start Pulmonary Vasodilator
  • Dobutamine 2.5mg/kg start will decrease afterload and give contractility

Want to optimize diastolic filling time( helps perfuse Coronary Arteries (80-100)

Amiodarone go to for antiarrythmic
150g IV/10 min followed by 1mg/min

79
Q

How to minimize Pulmonary Vascular resistance and Optomize afterload for RV failure

A

1) Hypoxia, hypercarbia, acidosis, derecruitment, overdestention, and sympathetic stimulation can all INCREASE AFTERLOAD
2) Vasopressor of choice= Vasopressin spares pulmonary vascular but will still need norepinephrine

MAP GOAL 65 to ensure coronary perfusion

Pulmonary vsoldialtors iNO,

IF PE- FIx clot- thromboylysis
ACS Inferior MI RV involvement- PCI/Thrombolysis

80
Q

PRELOAD for RV FAILURE AND PULMONARY HTN

A

RV more Preload Dependend (more than LV)- also sensitive to overload

1) use gentle BOLUS 250 CC

POCUS ( look for Septal bowling during diastole suggestive of volume overload
- patient may need diuresis

81
Q

How to Ventilate and Intubated RV Failure

A

1) Minimize peep to allow adequate venous return and Preload
2) Minimize airway pressures and tidal volumes
3) Minimize hypoxemia, hypercarbia and academia
4) Try to avoid intubation and if you do all your medications will cause hypotension
5) Ideally awake intubation to minimize recruitment, Apneic time
6) As RICO says defend the MAP

82
Q

Define Cystic Fibrosis

A

Autosome recessive process, common in Caucasian population

It is cased by mutation in CF tranmembrane conductance regulator (CFTR) protein
- deranged transport of CL- which causes thickened sections in lungs, pancreas, liver, intestines, sweat glands, reproductive system

Screened in Newborn

83
Q

What are Complications with Cystic Fibrosis

A

Thick, viscous secretions> very difficult to clear= airway obstructions, airway destruction, bronchiectasis
- cough, wheeze, SOB

Patients are usually on chronic antibiotics- often resistant to pathogens, pseudomonas MRSA

Chronic lung disease = PULMONARY HTN

Can have Pneumothorax, hemoptysis, allergic bronchopulmonary aspergillosis

84
Q

Treatment for Cystic Fibrosis

A

Secretion Clearance

  • chest physiology
  • saline nebulizers

Bronchodilators/Corticosteroids, Azithromycin, nsaids

Antibiotics, vaccinations and transplant

85
Q

Define Interstitial Lung Disease

A

Also known as diffuse parenchyma lung disease

1) DPLD caused by drugs or associated or rheumatic disease
2) Idopathic interstitial pneumonia
3) Granulomatus

All these lung disorders can cause fibrosis, interstitial pneumonia bronchiolitis

SOBOE, cough, associated with connective tissue disease (sarcoidosis, vascultitis)
- exacerbated by smoking, drugs (restrictive lung disease)

86
Q

Treatment for interstitial lung disease

A

Steroids, support care, Antibiotics

ARDS ventilation strategy

87
Q

What are some disease of the chest wall

A

Kyphosis, scoliosis (cerebral palsy Muscular dystrophy), Ankylosing spondyltitis( arthritis/inflammation of spine

Trauma
- flail chest, rib fractures

Obesity, acute abdomen, burns, ascites

88
Q

What do chest wall disease do to your

FRC

Total lung capacity

A

Decrease them both

89
Q

Difference between primary and secondary spontaneous pneumothorax

A

Primary spontaneous pneumothorax that happens with a normal lung ie smoking, genetic, young mails

Secondary spontaneous pneumothorax is secondary to a diseased lung
Ex COPD, TB, Cystic fibrosis, Interstital lung disease lung diseae

90
Q

What is Tuberculosis

A

Myobacterium tuberculosis
- leading infectious cause of death worldwide

can be latent, subclinical or active

Can be pulmonary or extra pulmonary in the CNS, Lymph nodes, bones, abdomen pericardium or urogenital

Latent phase asymptomatic,

Symptoms fever cough pleuritic chest pain LNA malaise

HIV< immunocompromised, IVDU, CKD DM( chronic disease) Asia affairs South American immigrations, jails

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