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Respiratory System > Exam I > Flashcards

Exam I Flashcards

1
Q

Histo: Where does the cartilage stop?

A

Bronchioles

-inc. SM, inc. elastic

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2
Q

True/False: Goblet cells, glands and cartilage are not found in the bronchioles, however, SM and elastic fibers are present

A

True

*SM: diameter

*elastic: expands and contracts

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3
Q

The typical epithelium of the respiratory tract is

A
  • ciliated pseudostratified columnar with goblet cells
  • changes at bronchioles: no goblets, no glands, no cartilage
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4
Q

The paranasal sinuses are blind end cavities in the frontal, sphenoid, ehtmoid and maxillary bones. They are lined by respiratory epithelium and drain into the wall of the nasal fossa. These sinuses are considered the

A

diverticula of the nasal cavity

NOTE: Sinusitis and sinus infections:

  • adults: maxillary sinus
  • children: ethmoid (halitosis)
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5
Q

The mesothelium + thin layer of CT that covers the lung is known as the _____ pleura. The mesothelium covering the wall of the thoracic cavity is known as the ______ pleura.

A

Lung: visceral Wall: parietal *serous membranes **90% of mesotheliomas (mesothelial cells - misplace underlying lung alveoli)

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6
Q

The larynx is made up of several cartilages (hyaline and elastic). Extrinsic muscles provide support and movement (deglutition) while intrinsic muscles provide

A

-phonation and conduit (air flow)

*both are skeletal muscle

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7
Q

The blood-air barrier contains what type of epithelium?

A

simple squamous

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8
Q

Site where respiration begins

A

Respiratory bronchioles

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9
Q

Regions of direct air flow have what type of epithelium?

A

Stratified squamous

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10
Q

Other alveolar cells including endothelial cells, fibroblasts, mast cells, monocytes and macrophages (dust cells) are located in the

A

interstitium or area between alveolar walls

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11
Q

Neutrophils secrete Elastase which attacks what fibers in the bronchi, bronchioles, alveolar ducts and alveoli?

A

elastic fibers

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12
Q

Lymphatic nodules in the lamina propria of the bronchioles

A

BALT

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13
Q

Emphysema is the permanent enlargement of alveoli or air spaces caused by destruction of the alveolar wall. It results from the loss of ____ fibers.

A

Elastic fibers Results: -thickened vessel walls -accumulate macrophages in alveoli 2 sites: Centriacinar and Panacinar A. Centriacinar: air trapped in respiratory bronchioles B. Panacinar: air trapped in entire resp. unit

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14
Q

Describe the normal epithelial transition in the respiratory portion of the lungs

A

-ciliated columnar -to ciliated simple cuboidal -to simple squamous

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15
Q

Describe the features of bronchioles

A

-No cartilage, No glands, -Goblets early -1mm or less in diameter -SM -elastic fibers Terminal portion: Alveoli appear -become respiratory bronchioles

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16
Q

Cystic fibrosis involves production of a defective CFTR (cystic-fibrosis transmembrane conductance regulator), a channel for what ions?

A

Chloride ions

-CFTR degraded due to defective protein folding

Results:

  1. decreased Na/C;- reabsorption in sweat glands
  2. Inc. Na reabsorption (other epithelium) -bronchus, pancreas -Water moves into cells
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17
Q

Differentiate between the conducting portion and the respiratory portion of the lungs

A
  1. Conducting -conduction
    - hyaline and elastic cartilage
    - elastic fibers
    - SM (nasal, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles)
  2. Respiratory portion:
    - elastic fibers
    - SM (respiratory bronchioles, alveolar duct, alveoli)
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18
Q

______ constitute the air passages most often affected in children by measles virus or adenovirus which can cause bronchiolitis (closure of airway due to fibrosis)

A

Bronchioles

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19
Q

Describe the vascular supply to the pulmonary branches

A
  1. Pulmonary artery: deox blood in -travels with conductile and respiratory tree 2. Pulmonary vein: ox blood out -veins: run between septa -Bronchial arteries: taking oxygenated blood to lung tissue (off aorta)
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20
Q

Trachea: True/False: Trachea and Respiratory diverticulum are outgrowths of gut tube

A

True

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21
Q

Trachea: The trachea is a long tube lined by respiratory epithelium. It has goblet cells, a thick basal lamina and ciliated cells. It is often described as a “ciliary escalator lined by mucous”. The trachea is a part of the ____ portion of the respiratory system

A

-Conducting portion (inspired and expired air) -16 generations of divisions -continuation from the larynx (inferior limit of cricoid cartilage)

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22
Q

Trachea: List the cells of the trachea

A
  1. Ciliated (most common) -sweep mucous -trap dust 2. Basal cells: -base of columnar cells -replace other epithelial cells 3. Goblet (mucous) 4. Brush (receptor cells) -sneeze rflex 5. Small granule (DNES cells) –diffuse neuroendocrine system –hormone secretion (endocrine) –secretory granules (peptide hormones) *cause carcinoid tumors
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23
Q

Nasal cavity: The area/epithelium that is located on the roof of the nasal cavity and medial/lateral nasal wall.

A

Olfaction area -bipolar neurons (project to olfactory bulb) -CN 1 *pseudostrat. columnar with goblet

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24
Q

Larynx: Below the epiglottis are two pairs of folds: the _____ vocal cords and the ____ vocal cords

A
  1. False vocal cord (ventricular folds) 2. True vocal cord (vocal folds) –direct air flow -strat. squamous epithelium -vocalis musscle *reverts back to respiratory epithelium (pseudostratified columnar with cilia and goblet cells) as moves into trachea
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25
Q

Bronchioles: Asthma is a type I HSR. Explain the process by which it induces bronchoconstriction.

A

-allergen interacts with IgE receptors (mast cells) 1. recruit eosinophils 2. inc. permeability of vessels 3. SM constriction of bronchiioles 4. Hypersecretion of mucus by goblets 5. Mucous plug 6. Charcot-Leyden crystals accumulate from Eosinophils *TH2 cells involved - IL-5 and IL-13

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26
Q

Bronchioles: _____ cells (formerly called clara cells) are found in the smaller bronchioles (terminal and respiratory). They are non-ciliated cells with dome-shaped surface. They display TEM characteristics of protein-secreting cells.

A

Club cells Secrete: surfactant proteins, mucin, anti-inflammatory protein Function: -proliferation of bronchiolar and alveolar epithelium (replace type II pneumocytes NOTE: Club Cells of the bronchiole = Type 2 Cells of the alveoli

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27
Q

Bronchi: There are 2 primary (mainstem) bronchi that enter the hilum of the lung. ____ bronchi branch off of the primary bronchi, and ____ bronchi branch off of the lobar bronchi

A

-Lobar bronchi (3R, 2L) branch from primary -Segmental bronchi (2) branch off of Lobar NOTE: -primary bronchi: similar structure to trachea: cartilage rings -Lobar onwards: cartilage plates (dec. cartilage) -Inc. SM as go down *typical epithelium w/goblet and glands *pulmonary artery

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28
Q

Bronchi: Foreign material localizes to different portions of the lung based on if they are in a standing or supine position. 1. In a standing position, the foreign material localizes to ______ 2. in a supine position, it localizes _____ 3. When lying on your right side, foreign material is most likey to go to _____ 4. The most common aspiration site is ______

A
  1. Standing: –R. lower lobe (posterobasal segment) 2. Supine: –R. lower lobe (Superior segment) 3. Right sided position: –R. middle lobe (post. segment of R. upper lobe) 4. MC aspiration site –Superior segment of R. lower lobe
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29
Q

Alveoli: Within the wall of the alveolus is the site where O2 and CO2 exchange occurs. This is known as the _______. It involves what cells?

A

Blood-air barrier 1. Type I pneumocytes 2. Endothelial cels Basal lamina of both cells 3. Pinocytotic vesicles in endothelium

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30
Q

Alveoli: These structures are found in the alveolar septum (wall) that help to equalize pressure and allow for air movement in case other ducts are blocked

A

Kohn pores

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31
Q

Alveoli: List the features and functions of Type II alveolar (great alveolar) cells

A

Features: -60% of lining -5% surface area -Secretory by week 28-31 -Lamellar bodies (merocrine) -Foamy cytoplasm Functions: 1. Surfactant secretion – (DPPC - phospholipid) –protein –lipid *lowers alveolar tension 2. Progenitors of type I cells

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32
Q

Alveoli: List the features and functions of Type I alveolar (squamous alveolar) cells

A

Type I: -40% of entire alveolar lining -high surface area (95%) -junctions (ZO and desmosomes) -morphed Thin: permeability of gases (Blood-air barrier) -pinocytotic vesicles in cytoplasm

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33
Q

Alveoli: Alveoli are thin-walled, sacular structures important for ____. The alveolar wall (interalveolar septum) has several cell types with 2 making up the epithelium facing the air side. Name the cell types composing the alveolar epithelium

A

Important for: -gas exchange *hollow Cell types: -Type I alveolar cell (Type I pneumocyte; squamous) -Type II alveolar cell (Type II pneumocytes; great)

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34
Q

Alveoli: Alveolar macrophages, also known as Dust cells pass freely between septum and the alveolar lumen. What are they called when they contain rbc’s or hemosiderin (product of rbc breakdown?)

A

Heart failure cells *Left heart failure of chronic pulmonary edema NOTE: Dust cells are first line of airway defense -remove degraded surfactant -engulf foreign bodies

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35
Q

Diseases of airflow resistance that can involve an obstruction at any level (trachea to respiratory bronchioles).

A

Obstructive lung disease FEC1/FVC < 0.7 *differentiate from REstrictive via pulmonary function test

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36
Q

Diseases with reduced expansion of lung parenchyma and decreased total lung capacity

A

Restrictive *cannot breathe in

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37
Q

Obstructive disease: _______ is a disease that involves the alveolar (acinar) spaces. It causes: 1. airspace enlargement (overinflation) distal to the terminal bronchiole 2. destruction of the alveolar wall It is classified according to the anatomic area affected (centriacinar 95% vs. panacinar)

A

Emphysema Causes: 1. **Cigarette smoke (centriacinar) 2. a1 anti-trypsin deficiency (protease imbalance; panacinar) NOTE: over time, entire alveolar unit (alveoli + capillary vessels) can be destroyed

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38
Q

Emphysema: Several factors contribute to airway obstruction in emphysema. Normally, small airways are held open by the elastic recoil of the lung parenchyma. Loss of elastic tissue in the walls of the alveoli (surrounding the respiratory bronchioles) reduces radial traction and causes the respiratory bronchioles to ______ during expiration.

A

Collapse of respiratory bronchioles *functional airflow obstruction (despite absence of mechanical obstruction)

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39
Q

Emphysema: Smoking is the MC cause of centrolobular (centriacinar) emphysema. Which of the following is correct about smokers and can contribute to development of emphysema? a. smokers have inc. neutrophils and macrophages in their alveoli b. smoking irritates alveolar macrophages, leading to release of IL-8 (neutrophil chemotactic factor) c. smoking can activate alternative complement pathway d. proteases (e.g. elastase) secreted by neutrophils and macrophages degrade lung tissue

A

All of the above *nicotine: chemotactic for neutrophils

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40
Q

Emphysema: True/False: Oxidants and free radicals in smoke inhibit alpha-1 anti-trypsin (anti-protease) = dec. protection in alveoli

A

True

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41
Q

Chronic bronchitis: Chronic bronchitis is a disease associated with excess production of mucous. Smoking interferes with ______ of the respiratory epithelium, and this results in decreased clearance of the mucous.

A

Interferes with ciliary action (resp. epithelium) -can’t clear mucus -predisposal to secondary and repeated infections

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42
Q

Emphysema: True/False - Paraseptal emphysema can occur adjacent to areas of fibrosis. It commonly occurs in the upper half of the lung and may underlie cases of spontaneous pneumothorax in kids

A

True *affects distal acini adjacent to pleura

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43
Q

A patient presents with progressive dyspnea, cough and wheezing. He is barrel chested, with prolonged expiration. He sits forward in a hunched position and breathes through pursed lips. Spirometry indicates impaired airflow on expiration. What is his diagnosis?

A

Emphysema *spirometry = key *classic imaging NOTE: weight loss associated – but can suggest cancer NOTE 2: cough and expectorant are variable (based on extent of associated bronchitis)

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44
Q

The following describes what primary pathophysiology? 1. “pink puffer” 2. FEV1/FVC <0.7 3. destruction of airways distal to terminal bronchiole (including pulmonary capillary beds) 4. decreased ability to oxygenate blood 5. dec. ventilation-perfusion mismatch

A

Emphysema

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45
Q

Emphysema: How does the body compensate for emphysema (loss of ventilation-perfusion?)

A

Hyperventilation (“puffer”) –can have normal arterial blood gases (due to compensation) –appear less hypoxemic (“pink” complexion) NOTE: eventual muscle wasting and weight loss (dec. O2)

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46
Q

Hypoxic drive: Normal respiratory drive is based on CO2 in arterial blood (10% based on O2 levels). In emphysema patients, the body is thought to alter the Va/Q ratio to improve gas exchange via _______.

A

Hypoxic pulmonary vasoconstriction *counteract by O2 therapy *largest inc. of O2-induced hypercapnia

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47
Q

Hypoxic drive: True/False: A titrated oxygen therapy is recommended in patients with an acute exacerbation of COPD to avoid hypoxemia and reduce the risk of oxygen-induced hypercapnia

A

True Haldane effect also contributes

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48
Q

A 43 year old patient presents with persistent cough and sputum production. She claims she has had the chronic, productive cough for at least 3 months in 2 consecutive years. She states she has smoked 1 pack/day for the past 20 years. What is her most likely diagnosis?

A

Chronic bronchitis Other symptoms: -dyspnea -hypercapnea, hypoxemia -cyanosis (“blue bloater”; inc. PaCO2, dec. PaO2) -cor pulmonale *absence of any other identifiable cause Histology: -goblet cell hyperplasia -enlarged mucous secreting glands

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49
Q

Chronic Bronchitis: How does the body respond to increased obstruction in a bronchitis patient?

A

-dec. ventilation, inc. CO -inc. CO2 retention -hypoxemia (V/Q mismatch) -inc. residual lung volume (blue bloater) *blue lips and face

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50
Q

A chronic disorder of the conducting airways that is caused by an immunological reaction. It is marked by episodic bronchoconstriction due to 1. increased airway sensitivity (variety of stimuli) 2. inflammation of bronchial walls 3. increased mucous secretion

A

Asthma -episodic, hyperactive (hyper-responsive), reversible airway disease

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51
Q

Asthma: A 6 year old girl presents to the clinic accompanied by her mother who complains her daughter has had episodic wheezing with cough and shortness of breath. You note hyperexpansion of the chest, rapid pulse and increased mucous production. You suspect

A

Asthma –MC chronic respiratory disease in children –Type I HSR -bronchoconstriction (bronchial walls) *bronchi and terminal bronchioles

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52
Q

Atopic (extrinsic) asthma is due to exaggerated TH2 lymphocytes and _____ response to environmental allergens (in genetically predisposed).

A

IgE –response to harmless Ag -other allergic disorders -may present before 5y/o

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53
Q

Asthma: Early phase involves the stimulation of ______ and release of what interleukins?

A

Stimulation of TH2 -IL-4 (IgE) -IL-5 (eosinophils) -IL-10 (TH2)

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54
Q

Asthma: Late phase reaction occurs 4-8 hours later and involves what cells?

A

Eosinophils -MBP (damages epithelial cells) -Eotaxin = chemotactic for eosinophils -bronchoconstriction

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55
Q

Nont-atopic asthma occurs in patients without other atopic (allergic) disease. It typically manifests later in life (adulthood) or can be associated with cold, exercise or infections (viral). What are typical findings of non-atopic asthma?

A

-no assicated allergies -normal IgE -no family Hx -includes drug-induced type ex: viral infection, exercise, cold air, cigarette smoke, ozone, aspirin (nasal polyps; bronchoconstriction)

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56
Q

Nasal polyps in children under the age of 2 may be associated with what disease?

A

Cystic fibrosis

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57
Q

A type of obstructing disease that is caused by chronic necrotizing infections that destroy SM and elastic tissue leading to permanent dilation of the bronchi and bronchioles. “A patient presents with purulent, foul smelling sputum, and hemoptysis. He has a history of recurrent infections.”

A

Bronchiectasis *purulent sputum (foul smell) *recurrent infections *hemoptysis

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58
Q

Bronchiectasis: The following are common causes of bronchiectasis: 1. Kartagener (sinusitis; dynein arm of cilia) 2. tumor 3. cystic fibrosis 4. allergic bronchopulmonary aspergillosis Of these, what is the most common cause of bronchiectasis?

A

Cystic Fibrosis (AR) *affects lower lobes *pus NOTE: Young patient w/ recurrent infections and malabsorption (cystic fibrosis)

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59
Q

An inherited disorder of ion transport that affects fluid secretion in exocrine glands in the epithelial lining of the respiratory, GI and reproductive tracts. *multi-system disease

A

Cystic fibrosis *abnormally viscous secretions (mucoviscidosis)

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60
Q

Cystic fibrosis is an AR disorder that results from abnormal function of an epithelial chloride channel protein encoded by the CFTR gene on chromosome: 7q31.2. The functions of CFTR are tissue specific, as are the effects. What are the effects in the lungs?

A

-dehydration = defective mucociliary action -accumulation of hyperconcentrated, viscid secretions -obstruct air passages -predispose to recurrent pulmonary infections

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61
Q

With cystic fibrosis, symptoms may appear at any point in life with a wide degree of phenotypic variation. Why is this so?

A

-diverse mutations in the gene associated with cystic fibrosis -tissue-specific effects of the encoded gene product -influence of so-called modifier genes

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62
Q

Cystic fibrosis decreases chloride secretion and increases sodium and water reabsorption. This leads to dehydration of the mucous layer coating the epithelium. As a result, mucociliary action becomes defective and mucus plugs the airways. What is a way to test for cystic fibrosis?

A

Production of hypertonic sweat

*positive sweat chloride test

*altered membrane potential test

*tryptophan

NOTE: CF - Phe508 mutation (7q31.2); ATP binding, protein misfolding (CFTR)

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63
Q

Cystic fibrosis can cause significant pathologic changes affecting numerous systems in the body. Some of these include: 1. unaffected sweat glands 2. azoospermia and infertility 3. congenital bilateral absence of vas deferens Pulmonary changes pose the most serious complications of this disease. Describe respiratory changes associated with cystic fibrosis?

A
  1. secondary changes to viscous mucous secretions –(submucosal glands) 2. obstruction and infection of air passages 3. bronchioles distended w/ thick mucous –marked hyperplasia and hypertophy of mucous secreting cells 4. sumperimposed infections –severe chronic bronchitis/bronchiectasis 5. lung abscesses
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64
Q

True/False: In addition to genetic factors (class of mutation), different environmental factors can influence the severity and progression of lung disease in cystic fibrosis patients. These factors can include: 1. virulent organisms 2. efficacy o ftherapy 3. intercurrent and concurrent infections by other organisms 4. tobacco or other allergens

A

True

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65
Q

What are the three most common organisms for lung infections in cystic fibrosis patients?

A
  1. Staph aureus –gram + cocci in clusters –necrotizing or cavitary (MRSA) 2. Haemoph. influenza 3. Pseudomonas aeruginosa *** NOTE: mucoid form of P. aeruginosa is frequent (chronic inflammation; alginate production)
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66
Q

Severe illness can occur in CF patients with what type of pseudomonas infection?

A

Burkholderia cepacia complex *severe illness

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67
Q

What fungi is commonly associated with lung infections in CF patients?

A

allergic bronchopulmonary aspergillosis

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68
Q

Most common cause of death in patients involves cardiorespiratory complications (persistent lung infections, COPD, cor pulmonale). What are causes of recurrent infections?

A

–indiscriminate use of antibiotic prophylaxis against Staph – led to resistant pseudomonas *most patients with CF harbor P. aeruginosa or B capacia

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69
Q

True/False: Individuals who carry one “severe” and one “mild” CFTR mutation may develop late-onset mild pulmonary disease, another example of nonclassic or atypical cystic fibrosis

A

True

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70
Q

Diagnosis of cystic fibrosis is based upon compatible clinical findings with biochemcial or genetic confirmation. The sweat chloride test is the mainstay of laboratory confirmation. What are the criteria that must be met to confirm CF?

A

Both criteria must be met: 1. Clinical symptoms consistent with CF in at least one organ system, AND 2. Evidence of cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction (any of the following): a. Elevated sweat chloride ≥60 mmol/L (on two occasions) b. Presence of two disease-causing mutations in CFTR, one from each parental allele c. Abnormal nasal potential difference

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71
Q

True/False: Genetic analysis by sequencing the CFTR gene can capture about 90% of the mutations present in general population (higher sensitivity for Ashkenazi Jew population, lowest for Hispanic). Genetic testing also used in pre-conception screening for families with a known history.

A

True

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72
Q

A patient presents with his wife who complains her husband has repeated and chronic cessation of breathing during sleep that lasts >10 seconds. She states he breathes noisily and snores loudly at night. He admits to daytime sleepiness (hypersomnolence) and fatigue. He is at risk of endocrine abnormalities (hormones released at night). You suspect

A

Sleep apnea

*Dx: polysomnography (sleep study)

NOTE: chronic changes 2o to chronic nocturnal hypoxia: -pulmonary HTN

  • systemic HTN (elevated Hb and RBC (polycthemia)
  • 2o to erythropoietin released in response to low O2
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73
Q

Obstructive sleep apnea is associated with elevated body mass index > 30 (obesity). This is due to: a. obesity contributes to hypoventilation (poor air movement) b. respiratory effort obstructed c. diminished diaphgragmatic excursion e. upper airway laxity/excess tissue

A

All of the above e. Excess tissue –post. pharynx mucosal tissue –tonsillar hypertrophy (kids) NOTE: associated with polycthemia, RHF (cor pulmonale) Tx: weight loss, CPAP, surgery, reduce tonsil size, uvula, etc.

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74
Q

Type of sleep apnea caused by injury to the CNS (trauma, surgery, meds - opiates, barbs). It can be seen in heart failure. Common features include:

  1. Cheyne stokes respirations –progressively deeper/faster breathing followed by dec. apneic episodes

–every 30-120 seconds

A

Central sleep apnea

Tx: address underlying condition, CPAP

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75
Q

Obstructive Drugs: Describe the actions of the following on Bronchial Tone: 1. Acetylcholine 2. Epinephrine 3. Histamine & Leukotrienes 4. Prostaglandins

A
  1. Acetylcholine –Muscarinic Receptors (parasympathetic) –CONSTRICTION 2. Epinephrine B2 receptors (sympathetic) –DILATION 3. Histamine & Leukotrienes H-1 & LTD4 and LTE4 Receptors –CONSTRICTION 4. Prostaglandins –PGE2 causes DILATION –PGF2α causes constriction
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76
Q

Obstructive drugs - Bronchodilators: B2 receptor agonists are sympathomimetic, and thus cause bronchodilation of SM. These include:

  1. Epinephrine
  2. Short acting Beta-2 selective agonists (SABA)
  3. Long acting B2 agonist (LABA)

What is their mechanism of action?

A

Increased cAMP = relax SM

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77
Q

Obstructive drugs - Bronchodilators: B2 receptor agonists are sympathomimetic, and thus cause bronchodilation of SM. These include: 1. Epinephrine 2. Short acting Beta-2 selective agonists (SABA) 3. Long acting B2 agonist (LABA) ________ is non-selective (alpha and beta receptors). It is used in EMERGENCIES and will cause CV stimulation.

A

Epinephrine (epi-pen) *B1 - heart -a1 b.v.’s *increase heart rate and b.p.

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78
Q

Obstructive drugs - Bronchodilators: B2 receptor agonists are sympathomimetic, and thus cause bronchodilation of SM. These include: 1. Epinephrine 2. Short acting Beta-2 selective agonists (SABA) 3. Long acting B2 agonist (LABA) _____ include albuterol and Levalbuteral. These act as “rescue” inhalers.

A

SABA’s –oral inhalation for ACUTE bronchospasm *albuterol = okay for pregnancy

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79
Q

Obstructive drugs - Bronchodilators: B2 receptor agonists are sympathomimetic, and thus cause bronchodilation of SM. These include: 1. Epinephrine 2. Short acting Beta-2 selective agonists (SABA) 3. Long acting B2 agonist (LABA) _____ include salmeterol (used for pregnancy). They are useful for: 1. nocturnal asthma 2. exercise induced bronchospasm 3. inhibit late phase allergen-induced bronchoconstriction (after SABA’s wear off)

A

LABA’s *salmuterol NOTE: not for monotherapy (inc. mortality) *not rescue inhalers

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80
Q

Obstruction drugs - Bronchodilators: _______ is a bronchodilator of the methylxanthine class (caffeine). It is a PDE inhibitor (inc. cAMP = SM relax).

A

Theophylline –inhibits mucous, histamine Adverse: -cardiac stimulation (“wired” palpitations/tachy) -NO TRUE antidote for overdose NOTE: similar to milrinone (HF)

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81
Q

Obstruction drugs - Bronchodilators: _____ are muscarinic receptor antagonists (LAMAs). They are best used for patients with COPD and severe asthma.

A

Ipratropium and tiotropium (LAMAs) *synergistic w/ B2 agonists Adverse: –dry mouth (inhalation) –urine retention (BPH,)

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82
Q

Obstruction drugs - Anti-inflammatories: Coticosteroids (glucocorticoids) are anti-inflammatory drugs that act by -decrease inflammation -dec. edema -dec. histamine They come in both systemic and inhaled forms. They can be used as a prophylactic. What is important to consider with regard to using corticosteroids for Tx?

A

Still have to use rescue inhaler NOTE 2: DO NOT STOP chronic Tx abruptly (must be tapered - up to 5 days)

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83
Q

Obstruction drugs - Anti-inflammatories: Coticosteroids (glucocorticoids) are anti-inflammatory drugs that act by

  • decrease inflammation
  • dec. edema
  • dec. histamine

What are examples of orally inhaled corticosteroids (ICS)? When are they used?

A
  1. beclemthasone
  2. fluticasone
  3. budesonide (pregnancy)

*lipid soluble (control symptoms)

*adjunct to bronchodilators *slow onset - weeks

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84
Q

Obstruction drugs - Anti-inflammatories: Coticosteroids (glucocorticoids) are anti-inflammatory drugs that act by -decrease inflammation -dec. edema -dec. histamine What are examples of nasally inhaled corticosteroids (ICS)?

A
  1. Beclomethosone 2. Triamcinolone *similar to orally inhaled
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85
Q

Obstruction drugs - Anti-inflammatories: Coticosteroids (glucocorticoids) are anti-inflammatory drugs that act by -decrease inflammation -dec. edema -dec. histamine What are adverse effects of ALL inhaled steroids?

A
  1. fungal growth (candida albicans) others: hoarseness; suppress HPA-axis, growth retardation NOTE: use smallest effective dose in kids; drink water
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86
Q

Obstruction drugs - Anti-inflammatories: Mast cell stabilizers bind to and stabilize mast cells. They also prevent Ca2+ influx. They can be taken as oral or nasal inhalants, but take 2-4 weeks for effects. What is an example of a mast cell stabilizer? When is it appropriate to use?

A

Cromolyn –modest effects –safe for adults: lung irritation, mood changes –no direct anti-inflammatory effect NOTE: PROPHYLACTIC only!! (not for acute Tx) NOTE 2: Prevent exercise induced bronchospasm (1/hr pre-exercise)

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87
Q

Obstruction drugs - Anti-inflammatories: Leukotriene antagonists include _____ and ____. They act to prevent inflammation, edema, bronchoconstriction and formation of thick/viscous mucous.

A

Zafirlukast and Montelukast (singulair) *inhibit early and late phases of constriction *prevent inflammation, edema, bronchoconstrict…

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88
Q

Obstruction drugs - Anti-inflammatories: Leukotrienes are a primary mediator of asthma in humans. Leukotriene antagonists, such as Zafirlukast and Montelukast can be used as alternative Tx for 1. long term management of mild-moderate asthma 2. OR for prevention of exercise induced bronchospasm. What are contraindications of these drugs?

A

NOT for: -acute asthma -constriction -acute exercise induced bronchospasm -monotherapy (need SABA) NOTE: montelukast = less adverse effects

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89
Q

What does every person with asthma need?

A

SABA

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90
Q

Obstruction drugs - Anti-inflammatories: Zileuton is a _______. It inhibits 5-lipoxygenase (converts arachidonic acid to leukotrienes).

A

Leukotriene synthesis inhibitor *mild to moderate asthma **Expensive!! Poor compliance Adverse: headaches, respiratory infections

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91
Q

Obstruction drugs: Anti-IgE therapy may be used in asthma patients ONLY when ________. Adverse effects: -headache, injection site reactions

A

Only when known IgE-mediated allergies present ex: OmalEzumab NOTE: may cause major hypersensitivity reaction/anaphylaxis (severe)

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92
Q

Obstruction drugs: List the drugs that are contraindicated in asthma patients

A
  1. all Cholinergic Drugs
    * –M agonists (bronchoconstrict)
  2. Systemic anti-M drugs
    * –adverse effects
  3. Beta blockers (non-selective)
    * –bronchoconstrict
  4. Histamine releasing drugs
    * –constrict (tubocurarine, morphine)
  5. NSAIDS
  • –aspirin
  • ** –block PGE2, promote PGF2
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93
Q

Obstruction drugs: Strategy for Tx of Severe acute Asthma (status asthmaticus or asthma exacerbation)

A
  1. Albuterol by neb or metered dose inhalation 2. O2 (as needed) 3. IV access 4. ipratroprium (neb) 5. IV or oral corticosteroids (prednosone) 6. MgS NOTE: COPD same Tx (except last step involves Antibiotic therapy specific to cause – doxycycline is first line) *anti-viral if flue
94
Q

Drugs for Other Resp. Symptoms: Expectorants, such as _______ do NOT suppress the cough reflex. They dec. viscosity of mucous (inc. water) and inc. cough productivity.

A

Gaifenesin *brings up mucous/inc. airway secretions

95
Q

Drugs for Other Resp. Symptoms: _____ decrease viscosity of mucous and increase cough productivity.

A

Mucolytics

ex: Acetylcysteine

96
Q

Drugs for Other Resp. Symptoms: ______ (cough suppressants) suppress non-productive cough.

A

Anti-tussives *Codeine and Dextromethorphan (centrally acting; related to morphine) NOTE: minimal analgesia *high levels: recreational drug

97
Q

Drugs for Other Resp. Symptoms: Nasal decongestants (oral or nasal) are a-agonists. They act to decrease nasal congestion and open the auditory tubes. Examples include: 1. Phenylephrine 2. Pseudoephedrine What are adverse effects of these drugs?

A
  1. Adverse (nasal spray): -rebound nasal congestion (>3 days) 2. Adverse (oral) –HTN, tachy, CNS stimulation, anxiety, urine retention, **caution w/ BPH
98
Q

Drugs for Other Resp. Symptoms: Endogenous Histamine acts on the H-1 receptor. It induces: -bronchoconstriction -inc. fluid secretion -vagal mediated bronchospasm and cough Anti-histamines act to block histamine released from mast cells. What are examples of 1st generation anti-histamines (H-1 receptor antagonists)?

A
  1. Diphenhydramine (benadryl) 2. Chlorpheniramine (chlortrimeton) 3. Promethazine (Phenergan; vomiting) NOTE: 1st gen. cross BBB and have anti-muscarinic activity (sedative; anti-emetic – diphenhydramine!)
99
Q

What are the clinical uses of anti-histamines?

A
  1. allergic reactions (rhinitis; hay fever) –patient selective response 2. Motions sickness/vestibular disturbance 3. nausea and vomiting
100
Q

What are examples of 2nd generation anti-histamines (H1-receptor antagonists)?

A

–newer drugs (fewer side effects than 1st gen.) 1. Fexofenadine (allegra) 2. Loratadine (claritin) 3. Cetrizine (zyrtec) 4. desloratadine (clarinex) *GI complaints **OTC

101
Q

Drugs for Other Resp. Symptoms: Intranasal anti-histamines include ______ and _____. These drugs are used for allergic rhinitis to releive sneezing, itching and watery discharge. What are adverse effects?

A

Azelastine, Olopatadine *drowsiness, sedation **Nose bleeds**

102
Q

Drugs for Other Resp. Symptoms: Pulmonary HTN can be reveresed by Prostaglandin (prostacyclin) analogs. What are examples of PGI2 analogs?

A

Epoprostenol

MOA:

–dilate pulm. vessels –inc. pulm blood flow

Use:

–long term, continuous I.V. for PH

Adverse:

–high incidence of jaw pain – dizziness, headache, N/V, diarrhea, flushing, tachycardia

103
Q

Drugs for Other Resp. Symptoms: Bosentan and Ambrisentan are endothelin receptor antagonists. They can be used to Tx pulmonary HTN.

Endogenously, __1__ receptors vasoconstrict, while _2___ receptors vasodilate. Thus, blocking the __1___ receptors lead to vasodilation.

A
  1. ETA: constrict
  2. ETB: dilate
  3. Bosentan –non-selective antagonist (blocks both) –transiently lowers b.p (ETB) –prolonged increase in b.p. (ETA)
  4. Ambrisentan: higher affinity for ETA
104
Q

Which drugs pose a risk as teratogens and are thus Cx in pregnancy?

A

Endothelin receptor antagonists *NOT for females unless on a multi-faceted birth control *hormonal may not be as effecive *restricted access

105
Q

Drugs for Other Resp. Symptoms: Phosphodiesterase (PDE5) inhibitors include Sildenafil (Viagra) and Tadalafil (Cialis). These drugs help to induce vasodilation. How do they do so?

A

-inhibit PDE-5 – inc. cGMP – SM relax – dilate – dec. pressure *both dec. pulmonary edema and improve exercise tolerance Adverse: sustained erection w/ no refractory Cx: Nitrates; all other b.p. meds

106
Q

How does Ach trigger vasodilation via the NO pathway?

A

2 cell pathway for NO –arterial dilation via Ach release from parasympathetic axons

107
Q

What is the most likely explanation for a child that presents to the clinic with a chronic cough and negative chest X-ray?

A

Asthma –may be allergic rhinitis or post-nasal drip –MC cause of wheezing in school aged kids Causes: -environment ** –genetics ** –immunity NOTE: <1 y/o = RSV MC cause School age: rhinovirus

108
Q

Pediatric asthma: There are three typical wheezing patterns seen: 1. transient early wheezers 2. non-atopic wheezers 3. atopic wheezers True/False: Transient, early wheezers normally resolve by the age of 3 and are not family Hx associated or due to allergic sensitization.

A

True *normally dec. pulmonary function (RSV, viral) NOTE: 1/3 of children outgrow, 1/3 don’t outgrow but asthma won’t be severe, 1/3 develop persistent asthma

109
Q

What are early childhood risk factors for persistent asthma?

A

Parental asthma Allergy: atopic dermatiti (eczema), allergic rhinitis, asthma (IgE-mediated) *table

110
Q
  1. What is the most common viral cause of asthma exacerbations in older children (school aged)? 2. What is the major pathogen in children younger than 2 years of age? 3. What is the most common year round trigger? 4. What is the most common animal trigger?
A
  1. Rhinivirus – school age 2. RSV – younger than 2 3. Tobacco smoke - year round 4. Cockroach - animal
111
Q

There are two main endotypes of asthma: 1. Th-2 2. Non-Th2 (TH1) What is true about the subtypes of asthma? a. 1 phenotype may have more than one endotype b. non-allergic asthma may be either Th2 or non-Th2 c. a single endotype may contribute to more than one phenotype d. endotype ID may facilitate personalized medicine e. the most common are TH2.

A

Answer: all of the above NOTE: Th2 – contributes to allergic asthma, 1 non-allergic asthma and AERD (aspiring exacerbated resp. disease)

112
Q

Asthma endotypes are sub-classified according to the level of Th type 2 cells (high and low) 1. _____: have increased eosinophils in the sputum and airways. Tend to respond to corticosteroids. 2. _____: have normal levels of eosinophils, w/ increased (or normal) neutrophils. Tend NOT to respond to corticosteroids.

A
  1. Th2 type high –can use anti IgE or II5 (if not corticosteroid) 2. Th2 Type low
113
Q

Asthma endotypes are sub-classified according to the level of Th type 2 cells (high and low) 1. _______ secretes IL-4, IL-5 and IL-13. 2. _______ is driven by IL-17, IL-21 and IL-22 secretion.

A
  1. TH2 high –Il4, IL5, IL-13 –inc. IgE and eosinophils = AHR, mucous hypersecretion, airway obstruction (possible SM hypertrophy and fibrosis) 2. Th2 low –IL-17, 21, 22 –elevated IL-13 associated with corticosteroid resistant (contributes to AHR)
114
Q

True/False: Environmental factors and inflammatory products drive pro-inflammatory mediators and cytokines to cause acute inflammation in asthma. Persitent inflammation leads to remodeling.

A

True

115
Q

Managing Asthma involves: 1. Classification of Severity 2. Stepwise approach to therapy 3. Assessment of control This management is categorized into three groups based on age: 0-4, 4-11 , and >12. What is the gold standard for diagnosing asthma?

A

Spirometry NOTE: With the Asthma control test, a score of 19 or less indicates not controlled asthma

116
Q

Spirometry is the gold standard for determining asthma in children. It provides an objective measure for diagnosis. The following are the terminology: 1. FEV1 –forced expiration in 1 sec –under 80% is normal 2.______: forced expiratory flow between 25-75% of the vital capacity –sensitive predictor of obstruction of small airway disease –discrepancies 3. ____: decreased in obstructive disorders 4. FVC: forced vital capacity 5. FEV1/FVC = ratio that is diminished (dec.) in airway obstruction

A
  1. FEF 25-75 3. PEFR (peak expiratory flow rate) FEV1/FVC ratio <80% = airway obstruction *FEV1 can be indicator of current obstruction (predict risk) NOTE: Obstructive diseases: -inc. TLC -inc. VC -dec. FEV1 and FVC -ratio = dec. NOTE 2: Give SABA, test again (albuterol should improve breathing)
117
Q

Reversibility of asthma is determined by: 1. an increase of FEV1 of at least ____ of baseline 2. An increase of at least 10% of predicted FEV1

A

12% of baseline

118
Q

True/False: FEV1 measurements may be within the normal range for children with moderate to severe persistent asthma, and thus may be insensitive measure for diagnosing when used in isolation.

A

True *comprehensive approach: Hx, PE, risk, pulmonary function

119
Q

Describe the Stepwise approach for asthma therapy (preferred treatments) in the varying ages with regard to: 1. Step 1 (intermittent asthma) 2. Step 2 (mild asthma) 3. Step 3 (moderate to severe; 0-11) 4. Step 4 5. Step 5 *Steps 4 and 5 = 12 years and older

A

Step 1: -SABA (PRN, as needed) -all ages 2. Step 2: –low dose Inhaled corticosteroid (ICS) –all ages 3. Step 3: –Medium dose ICS (preferred; 0-4 typically) OR –low dose ICS and LABA (5 and up) 4. Step 4: –medium dose ICS + LABA 5. Step 5: –high dose ICS + LABA 6. Step 6: –High dose ICS + LABA + OCS *Steps 3-6 (also consider short course of oral steroids)

120
Q

What are the potential issues with asthma medications? (corticosteroids, short acting B-agonists, SABA’s and LABA’s)

A

Inhaled corticosteroids: –poor adherence = poor control –adverse effects: oral thrush (MC); dysphonia, height (negligible) 2. SABA –palpitations, tachycardia (non-selective) 3. Misuse of SABAs and LABAs –hypoxemia, inc. risk of death (loss of bronchoprotectice effects)

121
Q

Initial management of asthma exacerbation involves decreasing airway obstruction, correcting hypoxemia and preventing further symptom progression. Immediate goals require close patient monitoring, O2 supplementation, and administration of broncholdilators. What are the drug steps in initial management?

A

Start w/ SABA –anti-cholinergics in severe exacerbation (ibutropium bromide) 1. Inhaled SABA –nebulized/MDI –every 20min for 1 hour –initial therapy 2. Inhaled anticholinergics –improve lung function (dec. hospitalization) –give w/ first 3 albuterol Tx

122
Q

Severe asthma exacerbation has which of the following symptoms? a. diminished breath sounds (w/out wheezing) b. severe retractions (chest wall muscles) c. cyanosis d. conversational dyspnea (poor ventilation; breaths needed to complete speech patterns) e. Tripod position

A

All of the above *Diminished breath dounds without wheezing: –ominous, inability to move air NOTE:PICU patients: Heliox (open airway) and Mg2+ to relax SM

123
Q

What common oral leukotriene antagonist is sometimes used as adjuvant therapy ONLY in persistent asthma?

A

Montelukast (singulair)

124
Q

What are the biologic risk factors for asthma morbidity and mortality? a. previous severe asthma exacerbation (ICU admission, intubation) b. sudden asphyxia episodes (resp. failure) c. 2 or more hospitalizations in the past year d. 3 or more ER visits in past year e. use of <2 canisters of SABAs monthly

A

Answer: A-D **>2 canisters of SABAs per month NOTE: #ER visits, # hospitalizations, # PICU admissions, # intubations

125
Q

Transient narrowing of the airways after vigorous exercise. Common features include: 1. 10-15% decrease in FEV1 2. Decreased warming and humidification of inhaled air during exercise 3. mucous production and airway narrowing It is often provoked by cold weather, but can be improved by a slow warm up (15 min before w/ 1-2 puffs of albuterol).

A

Exercise induced asthma

126
Q

A patient presents with cough, dyspnea and wheezing 5-10 minutes after exercising. He admits that these attacks often happen after exercising, and inc. in intensity with inc. exercise. You suspect

A

Exercise induced asthma *resolves spontaneously 3o min after rest Tx: –SABA –ICS to control underlying persistent asthma –acute episodes: athlete warm up beforehand

127
Q

Recurrent wheezing in infants is more likely after what type of generalized viral airway infection?

A

bronchiolitis

128
Q

Besides inhaled medications, what medication and “dose” is most commonly given for mild asthma exacerbations?

A

loading dose of systemic corticosteroids

129
Q

What is the most common controller medication prescribed for mild persistent asthma?

A

inhaled corticosteroids

130
Q

What common medication is given as a bronchodilarot in acute asthma exacerbation?

A

albuterol (SABA) *also used for intermittent asthma

131
Q

What common medication is given as a loading dose in acute exacerbations of asthma?

A

systemic cortico-steroids (prednisone, prenisolone…)

132
Q

The volume of air remaining in the lungs that is not measurable by spirometry

A

Residual Volume *total lung capacity (because it contains residual volume)

133
Q

Normal breathing values: 1. Respiratory rate 2. PaCo2 PECo2

A

RR: 12 breaths/min PaCO2: 40 PeCo2: 100mmHg

134
Q

Volume of air in the lungs that does not participate in gas exchange. It is composed of anatomic and physiologic.

A

Dead space 1. anatomic: –volume of the conducting airways (trachea, upper resp.) 2. physiologic (functional) –alveoli that do not participate in gas exchange (ventilated, but not perfused by pulmonary capillary blood) NOTE: estimate “wasted” ventilation by comparing VT with physiologic dead space

135
Q
  1. Which type of dead space is seen in normal pulmonary functioning patients? 2. When do we see the other?
A
  1. anatomic dead space 2. Physiologic –air in lung apex, but contributes to alveolar dead space **favored location of Mycobacterium TB *
136
Q

How do you calculate physiologic dead space? (In other words, how much air is wasted in lung spaces that cannot participate in gas exchange?)

A

VD = VT x PaCo - Peco/PaCo Paco, Peco, Paco *VT = tidal volume *PaCO and PeCo = fractions that express dilution of alveolar PCO2 by dead space air

137
Q

Calculate Minute ventilation

A

Vt x breaths/min *normal VT is usually 500

138
Q

Calculate alveolar ventilation

A

VA = (VT - VD) x breaths/min ex: 500ml - 125 x 12 breaths/min = 4500ml/min

139
Q

Which values are measured on an arterial blood gas (ABG) study? a. PaO2 (oxygen in blood) b. PaCO2 (Carbon dioxide in blood) c. pH d. HCO3- e. O2 content in blood f. % sat (saO2)

A

All of the above PaO2: how well O2 moves from lungs to blood normal: 90-95 paCo2: how well CO2 moves out of blood pH: O2 delivery at tissue level %sat: Hb saturation

140
Q

True/False: Unlike anatomic dead space, which is fixed, physiologic dead space can change as lung perfusion changes (minute to minute). It can be altered w/ changes in CO and pulmonary blood flow.

A

True *chest wall = critical component of respiratory pump (diaphragm, spine, ribs, vertebrae) *diseases that alter chest wall structure - affect pump; resp. compromise NOTE: OMM can improve chest wall and normalize afferent, efferent connections.

141
Q

Optimum lung function occurs when the thorax and the lung “comply” with the inflow of air created by the negative pressure in the thorax. 1. What kinds of things can lead to increased lung compliance? 2. What decreases lung compliance?

A

Increase Compliance: 1. surfactant (type II pneumocytes) –lack of = collapse 2. Obstructive diseases –COPD (emphysema) –normal aging Decrease Compliance: 1. Restrictive disorders –pulmonary (idiopathic) fibrosis 2. Fluid/damage within functional resp. unit –pneumonia –neonatal distress syndrome (dec. surfactant; fluid/fibrin) –pulmonary edema (LVH; LHF)

142
Q

Describe respiratory function changes seen in the elderly

A
  1. Musculoskeletal restriction
  2. Increased:
  3. –compliance
  4. –A-a
  5. –ventilation-perfusion mismatch (air, not perfused)
  6. –residual volume (secondary to loss of resp. effort and chest wall restriction)
  7. Decreased
  8. –chest wall motion (musculosk. restriction)
  9. –FEV1 and FVC
  10. –muscle strength (breathing, upper airway muscles, swallowing (aspiration; bacterial issues)
  11. –CNS response to changes in O2 and CO2
143
Q

At high altitude, there is less oxygen available. This is due to differences in pressure. Other physiologic conditions within the body which may limit oxygen intake can worsen at altitude. Acute changes include: 1. less available O2 (main reason for dec. exercise tolerance and sensation of SOB/breathlessness) 2. Increased RR 3. Inc. CO2 expiration = resp. alkalosis What are chronic changes associated with high altitude?

A

–pulmonary vasoconstriction = HTN –increased EPO production = inc. Hb –Inc. 2, 3, B/DPG = right shift (O2 release to tissues) –inc. renal excretion of HCO3-

144
Q

Calculate the partial pressure of O2 in dry air at sea level (PO2 in dry air at a barometric pressure of 760mmHg)

A

Px = Pb x F Px = partial pressure of the gas Pb = barometric pressure (O2 = 760mmHg) F = fractional concentration of the gas (O2 in inspired air = 0.21) 760 x 0.21 = 159.6mmHg

145
Q

When inspired air enters the trachea, it is saturated with water vapor (humidified). What is the PO2 of humidified tracheal air?

A

Px = (Pb - PH2O) x F PO2 = (760 mmHg - 47) x 0.21 = 149.7 mmHg

146
Q

True/False: The value for PaO2 is 100mmHg. It is corrected for water vapor. This correction takes into account “continual uptake of O2 by the pulmonary capillaries” and continual diffusion of “CO2 out of the capillaries into the alveoli”

A

True *not routinely measured *calculated from blood gas measurements by alveolar gas equation

147
Q

Normally, pulmonary capillary blood equilibrates almost completely with alveolar gas. This is due to the large partial pressure driving force (higher in alveoli than in mixed venous blood of pulmonary artery). If alveolar gas PO2 = 100mmHg. What is the PO2 of pulmonary capillary blood?

A

100mmHg *O2 transfer from alveoli into blood (simple diffusion) *driving force = partial pressure different for O2 b/t alveoli and blood

148
Q

The O2 content of blood includes dissolved O2 and O2 bound to Hb (oxy-hemoglobin). Dissolved O2 in the blood is diminutive, whereas the majority of O2 is bound to Hb. What are factors that determine the amount of O2 bound to Hb?

A

-Hb conc. in blood (CBC) -O2 binding capacity (max amt. bound) -% saturation of Hb by O2 (positive cooperativity; 100% saturation = all 4 binding sites occupied)

149
Q

True/False: The PO2 at which Hb is 50% is known as the P50

A

True *amt. of O2 breathed in can alter saturation *measured by pulse ox

150
Q
  1. What is the effect of anemia on Hb? 2. What is the effect of dec. Hb on dissolved O2? 3. Will the amount of O2 bound the Hb be altered if PO2 is reduced to 50mmHg?
A
  1. anemia = dec. Hb 2. minimal; affects O2 carrying capacity 3. Yes = dec. % saturation NOTE: Amount of O2 bound to Hb depends on O2-binding capacity, Hb conc., #of binding sites open, and % saturation)
151
Q

What is the primary driver of respiration?

A

CO2 levels in the blood

152
Q

What analyte is an excellent measure of metabolic needs (during exercise or illness)

A

CO2 *produced by metabolic activity (inc. activity or sickness - inc. CO2)

153
Q

Describe respiration during exercise w/ regard to -CO2 levels -O2 -Cardiac output

A
  1. Increased CO2 2. Inc. RR to meet O2 demand –CO2 blown off 3. Inc. blood flow, Inc. CO 4. lactic acid build up = inc. RR 5. Inc. venous CO2
154
Q

Describe the process by which O2 in inspired air (ambient room air) becomes dissolved oxygen in arterial blood as it passes through the pulmonary capillary bed and becomes PaO2

A
  1. Simple diffusion –equilibration between a-A 2. O2 moves across alveolar-capillary membrane into blood 3. Most O2 binds Hb, some dissolves into the plasma 4. O2 transported from lungs into peripheral tissues –removed from the blood and used for aerobic… **3 main steps: oxygenation, oxygen delivery, oxygen consumption
155
Q

What are factors that can affect gas exchange?

A
  1. airway obstruction 2. Factors that affect diffusion –surface area (limited by COPD) –diffusion distance (limited by fibrosis) –diffusion coefficient –concentration difference across resp. surface 3. O2 exchange can be perfusion limited –requires turnover of blood in capillaries NOTE: as long as there is a concentration gradient, diffusion will continue unless blocked by mucous, fibrosis
156
Q

If a person is hypoxemic (low O2 in blood) by clinical impression or ABG measurement, what other information may need to be collected to determine diminished O2 content?

A

CBC Note: Dec. O2 delivery can be due to dec. CO or decining arterial O2 content

157
Q

Pharmacology: Empiric antibiotics are used for community acquired pneumonia (CAP) in adults. CAP is likely caused by strep. pneumo or mycoplasma pneumo. Treatment is based on patient status: 1. Outpatient 2. Inpatient, non-ICU 3. Inpatient, ICU Describe Tx for CAP in an outpatient setting where they have not taken anti-microbials in the past 3 mos

A

Macrolide (azythromycin, clarithromycin, erythromycin) *inhibit bacterial protein synthesis (50s)

158
Q

Pharmacology: Empiric antibiotics are used for community acquired pneumonia (CAP) in adults. CAP is likely caused by strep. pneumo or mycoplasma pneumo. Treatment is based on patient status: 1. Outpatient 2. Inpatient, non-ICU 3. Inpatient, ICU Describe Tx for CAP in an outpatient setting where they have a co-morbidity or HAVE taken anti-microbials in the past 3 mos

A
  1. Fluoroquinolone (levofloxacin, moxifloxacin, gemifloxacin) *inhibit DNA gyrase and type IV topoisomerase 2. B-lactam (amoxicillin/ceftriaxone_ + macrolide (if patient doesn’t tolerate Fluoroquinolones)
159
Q

Pharmacology: Empiric antibiotics are used for community acquired pneumonia (CAP) in adults. CAP is likely caused by strep. pneumo or mycoplasma pneumo. Treatment is based on patient status: 1. Outpatient 2. Inpatient, non-ICU 3. Inpatient, ICU Describe Tx for CAP in an inpatient setting not requiring ICU

A
  1. Fluoroquinolone 2. Ceftriaxone + macrolide 3. OR ampicillin-sulbactam + macrolide –instead of ceftriaxone –sulbactam = B-lactam (similar to augmentin – amoxicillin + clavulinic acid) NOTE: –ceftriaxone: 3rd gen. cephalosporin; inhibits cell wall synth. –AMP-sulbactam: extended spectrum penicillin + B-lactamase inhibitor -macrolide: protein synth. inhibitor
160
Q

Pharmacology: Empiric antibiotics are used for community acquired pneumonia (CAP) in adults. CAP is likely caused by strep. pneumo or mycoplasma pneumo. Treatment is based on patient status: 1. Outpatient 2. Inpatient, non-ICU 3. Inpatient, ICU Describe Tx for CAP in an inpatient ICU setting

A
  1. Ceftriaxone (or AMP sulbactam) + azithromycin (OR fluoroquinolone)
161
Q

A patient presents with respiratory pneumonia. A culture shows a gram + diplococcus. What is the type of pneumonia and how is it treated?

A

Strep pneumonia 1. Levofloxacin –fluoroquinolone –inhibits DNA gyrase and type IV topo –injection

162
Q

A patient presents with mycoplasma pneumonia (or chlamydia pneumonia). How can it be treated?

A
  1. Azithromycin –macrolide –inhibits protein synthesis (50s) 2. Doxycycline –tetracycline –inhibits protein synthesis (30s) 3. Levofloxacin (Moxi, Gemi) –fluoroquinolone –inhibits DNA gyrase and topo IV
163
Q

A patient presents with pneumonia from haemophilus influenza (gram - coccobacillus; facultative anaerobe). How is it treated?

A
  1. Cefotaxime or Ceftriaxone -3rd gen cephalosporins –inhibit cell wall synth. 2. Augmentin –amox + clavulinic acid
164
Q

A patient presents with atypical pneumonia. You determine she is infected with moraxella catarrhalis (gram - diplococcus) . How do you Tx her?

A
  1. Amoxicillin + Clavulanate (Augmentin) Amox: extended spectrum; inhibits cell wall synth. Clavulanate: B-lactamase inhibitor
165
Q

A patient presents with atypical pneumonia. You determine he is infected with Klebsiella (gram - rod) . How do you Tx him?

A

Imipenem *carbapanem (penicillin-like) *broad spectrum; resistant to B-lactamases *cilastatin = stabilizes (Im up in the klub)

166
Q

A patient presents with atypical pneumonia. You determine he is infected with Yersinia pestis (gram - bacilli) . How do you Tx him?

A

Gentamicin *aminoglycoside *inhibits protein synthesis (30s; misreading and insertion of wrong aa) *kidney toxicity

167
Q

A patient presents with atypical pneumonia. You determine she is infected with Bacillus anthracis (gram + rod). How do you Tx her?

A

Ciprofloxacin *fluoroquinolone *inhibits DNA gyrase and type IV topo

168
Q

A patient presents with atypical pneumonia. You determine he is infected with bordetella pertussis (gram - rod). How do you Tx him?

A
  1. Azithromycin *macrolide *inhibits bacterial protein synthesis (50s) 2. TMP-SMX (trimethoprim sulfamethoxazole) –Alternative –blocks folate synthesis
169
Q

A patient presents with atypical pneumonia. You determine she is infected with Corneybacterium diptheria (gram + bacillus). How do you Tx her?

A
  1. Erythromycin *macrolide *inhibits protein synthesis 2. Penicillin also effective
170
Q

A patient presents with atypical pneumonia. You determine he is infected with Streptococcus pyogenes . How do you Tx him?

A
  1. Pen V

–acid stable oral

–B-lactam –narrow spectrum

*inhibits cell wall synth

  1. Amoxicillin

–children like taste better

  1. Macrolide (if penicillin allergy)

–azithro, erythro

NOTE: confirm GAS before prescribing

171
Q

A patient presents with atypical pneumonia. You determine she is infected with Pseudomonas aueruginosa. How do you Tx her?

A
  1. Piperacillin + Tazobactam PIP: extended spectrum –anti-pseudomonal penicillin –inhibits cell wall TZ: B-lactamase inhibitor
172
Q

What are other possible treatments for pseudomonas aeruginosa infections?

A
  1. Imipenem
  2. Cefepime

–4th gen. cephalosporin

–inhibts cell wall

  1. Tobramycin

–aminoglycoside –protein synth

173
Q

A patient presents with atypical pneumonia. You determine he is infected with Legionella pneuophilus. How do you Tx him?

A

Levofloxacin (fluoroquinolone; inhibits DNA gyrase and type IV topo)

174
Q

List the adverse effects for the following drugs:

  1. Penicillin G/V
  2. Amoxicillin
  3. Piperacillin + Tazobactam
  4. Cefotaxime/Ceftriaxone
A
  1. Penicillin and Amoxicillin:

– Hypersensitivities

–GI distress (more in amox)

  1. Piper

–yeast infection

  1. Cefotaxime/Ceftri

–yeast infection

–cross-sensitivityw/ penicillins

175
Q

List the adverse side effects for the following drugs: 1. Levoflox/Ciproflox 2. Azithromyc/Erythromyc 3. Doxycyc. 4. Gentamicin/Tobra 5. Imipenem

A
  1. Levo/Cipro
  • –tendonitis
  • –phototoxicity
  • –prolonged QT interval
  1. Azithromycin:
    * –GI
  2. Doxy
  • –phototoxicity
  • –teeth discoloration
  • –*erythromycin: induces motilin (uncoordinated peristalsis)
  1. Gentamicin/Tobra
    * –nephro and ototoxicities
  2. Imipenem
  • –hypersensitivity
  • –cross-sensitivity with penicillins
176
Q

Respiratory drugs: Mycobacterium are obligate aerobes that thrive in O2 rich tissues (e.g. lungs). They are intracellular pathogens, that like to infect macrophages. Also, they are hydrophobic with high lipid (mycolic acid) content in their cell wall. What are the different species of mycobacterium that can contribute to respiratory distress?

A
  1. Mycobacterium tuberculosis
  2. Atypical mycobacterium

–Mycobacterium kansasii

–Mycobacterium avium-intracellular complex (MAC)

*high risk of infection in immune compromised

*prophylaxis in AIDS patients

177
Q

The following are first line drugs for the treatment of primary pulmonary TB: 1. Isoniazide (INH) 2. Ethambutol 3. Pyrazinamide 4. Rifampin Of these, which face the greatest microbial resistance? In cases of resistance, what drug can be used in their stead?

A

Isoniazid and Rifampin *replace with fluoroquinolone NOTE: Tx using all 4 meds for 2 months, then INH and rifampin for 4 more months

178
Q
  1. In a patient who is newly diagnosed with TB, what drug will be included in their treatment? 2. In exposed neonates or children, what would you use to Tx? 3. Latent TB in TST positive patients that meet one criteria would be treated with what drug?
A
  1. Newly diagnosed –Isoniazide included in Tx 2. Exposed neonates/kids –prophylactic; isoniazid alone 3 mos 3. Latent TB w/ one criteria (HIV +, Chest X-ray w/ non-progressive TB, IV drug user, Diabetes, immunocompromised) –Isoniazid alone; 9 mos
179
Q

Isoniazid is one of the 4 drugs used for the Tx of TB. What is its mechanism of action?

A
  1. INH –inhibits mycolic acid synth. (via enoyl reductase) (cell wall component) *activated by catalase peroxide (katG gene) NOTE: acetyltransferase = key metabolizing enzyme; rate of activity genetically determined (some px may need/tolerate higher dose)
180
Q

Rifampin is a second drug involved in Tx of TB. It is a broad spectrum antibiotic. It inhibits DNA transcription by binding _________.

A

DNA-dependent-RNA polymerase *selective for bacterial RNA pol

181
Q

This drug is used to treat influenza. Its is a neuraminidase inhibitor (prevents virion release from surface of infected cells). It also aids in inactivation of respiratory tract mucous.

A

Osteltamivir *dec. viral spreading and infection *dec. duration/severity *give withn 48 hours of symptom onset (prophylactic)

182
Q
  1. ________ are influenza drugs that block M2 proton selective ion channels. They prevent acidification of the virus and fusion of membranes (uncoating; transfer) 2. ______: a Cap-endonuclease inhibitor that prevents polymerase function and virus mRNA replication.
A
  1. Amantadine/Rimantidine 2. Bolaxavir marboxil (Xofluza)
183
Q

Used for Tx of RSV. It is an Ab directed at the fusion protein (prevents virus from entering cell and stops replication).

A

Palivizumab

184
Q

An anti-fungal polyene antibiotic. It selectively binds ergosterol in fungal membranes. it is used in the treatment of Blastomyces dermatitids.

A

Liposomal Amphotericin B *inc. membrane permeability and release of cytoplasmic components

185
Q

For Treatments for Cryptococcus neoformans, you use: a. FLuconazole b. Amphotericin B c. Voriconazole d. Baloxavir marboxil

A

A and B only 1. Fluconazole –inhbits enzyme that converts lanosterol to ergosterol 2. Amphotericin B –selectively binds ergosterol –polyene antibiotic

186
Q

For treatment of Aspergillus fumigatus, you would use: a. a polyene antibiotic that selectively binds ergosterol b. a drug that inhibits the enzyme responsible for converting lanosterol to ergosterol c. an antimetabolite that inhibits folate synthesis

A

Answer: B Voriconazole –inhibits lanosterol to ergosterol

187
Q

For treatment of Pneumocystis jirovecii, you would use

A

Trimethoprim + Sulfameth (TMP-SMX) –antimetabolites (inhibir folate synthesis) NOTE: This drug binds bacterial folate reductase (100,000 fold greater affinity than mammalian enzyme)

188
Q

What are the adverse effects of: 1. INH 2. Rifampin 3. Oseltamivir 4. Palivizumab

A
  1. INH –liver toxicity –peripheral neuritis (need B6) 2. Rifampin –liver tox –reddish-orange body fluids –induce Cyp 450 3. Oseltami –rare 4. Palivizumab –fever, rash
189
Q

What are the adverse effects of: 1. Fluconazole 2. Voriconazole 3. Amphotericin B 4. TMP/squaMX

A
  1. Fluconazole –drug interactions (CYP450) 2. Vori –drug interactions (P450) –liver –visual (chromatopsia, photaphobia) 3. Amphotericin –nephrotoxic 4. TMP/SMX: –Stevens Johnson syndrome (immune mediated) –megaloblastic anemia
190
Q

Treatment for Non-small cell lung cancer (NON-squamous) includes a combination of

A

Cisplatin (DNA alkylating) and Pemetrexed (anti-folate) NOTE: pemetrexed inhbits enzymes that synthesize purine/pyrimidine bases (dihydrofolate reductase; thymydilate…)

191
Q

Treatment for NSCLC squamous cells cancer involves a combination that hits 2 distinct targets: DNA and tubulin. Tx involves combining Cisplatin (DNA alkylating) with what possible drugs?

A
  1. Vinorelbine (vinca alkaloid) –inhibits tubulin polymerization (mitosis) OR 2. Gemcitabine –pyrimidne analong –inhibits S phase OR 3. Docetaxel (taxane) -inhibits tubulin Depol. (mitosis)
192
Q

Treatment of Small cell lung cancer involves combination of cisplatin and

A

Etoposide DNA topo II inhibitor *permanent strand breaks *inhibits cell division (late S-G2)

193
Q

Treatment of Mesothelioma involves a combination of Cisplatin w/

A

Pemetrexed *anti-folate *inhibits purine/pyrimidine synthesis

194
Q

Adverse effects of the small cell lung cancer drugs: 1. Cisplatin 2. All others

A
  1. Cisplatin: renal toxicity 2. Others: myelosuppression NOTE: Gemcitabine: GI ulcers too
195
Q

Restrictive Disorders: Restrictive lung disorders can be caused by 1. Extrinsic (chest wall disorders) 2. Intrinsic (acute/chronic interstitial disorders) a. fibrosis b. granulomatous c. eosinophilic d. smoking e. pulmonary alveolar proteinosis What are examples of extrinsic (chest wall) disorders that lead to restrictive disease?

A
  1. Kyphoscoliosis 2. Neuromuscular disease (myasthenia gravis) 3. polio 4. obesity (pickwickian) NOTE: These have normal A-a gradient
196
Q

Restrictive disorders cause a reduced TLC. What happens to their FEV1/FVC?

A

*Can’t get air IN *decreased lung volume (dec. FVC) *Increased FEV1/FVC = >80%

197
Q

Which of the following is an intrinsic (interstitial) restrictive disorder? a. pneumoconiosis b. sarcoidosis (granulomatous) c. idiopathic pulmonary fibrosis d. collagen vascular/autoimmune

A

All of the above **intra-alveolar (air space) component in addition to interstitial component

198
Q

Chronic interstitial diseases are characterized by inflammation and fibrosis. Clinical features include: -dyspnea (insidious) -tachypnea *end-expiratory crackles *eventual cyanosis Why cyanosis?

A

–secondary pulmonary HTN – RHF w/ cor pulmonale NOTE: NO wheezing – not airway problems like asthma, bronchitis or ectasis

199
Q

What are the imaging features seen in restrictive diseases with fibrosing pattern?

A

-bilateral -small nodules -interstitial irregular lines -ground glass shadows

200
Q

The following describes what restrictive fibrotic disorder? 1. Male >50 y/o smoker Features: 1. Repeated cycles of lung injury and healing w/ collagen deposition (TGF-B) 2. Histology: –usual interstitial pneumonia 4. fibroblastic foci, subpleural fibrosis 5. Honey-combing on CT scan *Terminal/Irreversible

A

Idiopathic Pulmonary Fibrosis Etiologies: -environment: smoking, fumes, hair dressing -genetic: mutations in TERT, TERC (telomerase); surfactant genes

201
Q

A 48 year old female presents to the clinic complaining of dyspnea and DRY cough. Histologic findings: -lymphocytes and plasma cells -fibrosing w/ diffuse or patchy infiltrates in the same stage of development PMHx: Lupus SocHx: Denies smoking What is her likely problem?

A

Non-specific interstitial pneumonia *associated w/ lupus, collagen vasc. (RA, Lupus) or HIV *insidious onset *epithelial injury/dysregulated repair *subpleural sparing *temporal and spatial homogeneity NOTE: NO honeycombing or fibroblastic foci

202
Q

A 46 year old patient presents with dyspnea and cough. Imaging reveals: -patchy, subpleural, peri-bronchial airspace consolidation. Histology reveals: -polyploid plugs of loose CT (Masson bodies) NO interstitial fibrosis or honeycomb lung was found. What is the likely diagnosis?

A

Cryptogenic organizing pneumonia (bronchiolitis obliterans organizing pneumonia - BOOP) *airspace disease *associated w/ RA, amiodarone side effect NOTE: fibroblasts IN the airspaces (alveolar ducts)

203
Q

Describe Dx and Tx of cryptogenic organizing pneumonia

A

Dx: biopsy, negative cultures (not infectious) Tx: oral corticosteroids

204
Q

Autoimmune diseases such as Lupus, RA (rheumatoid nodules; pulmonary HTN), systemic sclerosis and dermatomyositis can show what type of restrictive pneumonia?

A

Non-specific interstitial pneumonia

205
Q

A reaction to inhaled organic and inroganic particulates, fumes and vapors. Development depends on: 1. amount retained in lungs 2. size/shape, solubility of particles 3. additional effects of other irritants

A

Pneumoconiosis NOTE: -most dangerous size: 1-5 microns (small airways) -other irritants: smoking inc. asbestos (impairs mucociliary clearance)

206
Q

A generally benign condition that favors the upper lobes of the lungs. It presents with progressive dyspnea and black lung. It can be associated with Caplan syndrome (RA w/ nodules and pneumoconiosis).

A

Coal Worker’s pneumoconiosis

*no inc. risk for TB, cancer (in non-smokers)

*inc. risk of RHF

*starts as pulmonary anthracosis

– simple CWP

– complicated CWP

207
Q

A common type of pneumoconiosis seen in miners and sandblasters (foundry-work) that is characterized as a diffuse micronodular lung disease with an upper lobe predominance.

Characteristic features include:

Histologic:

  1. fibrotic nodules in upper lobes of lungs
  2. Coalescent, concentrically layered collagenous nodules
  3. Silica crystals with polarization

Imaging:

  1. multiple small, rounded opacities
  2. ground glass appearance
  3. central calcification
  4. Eggshell calcification of Hilar nodes (similar appearance to sarcoidosis)
A

SIlicosis

*crystalline form = more fibrogenic

*inc. RHF

***TB and cancer (decades after exposure)

NOTE: alveolar macrophages respond to silica in the alveoli by inc. TGF-B (fibrogenic cytokine) (impaired phagolysosome formation; dec. surveillance)

208
Q

A type of pneumoconiosis associated with construction workers, plumbers, and shipyard workers (re-modeling and demolition). It is characterized as a diffuse pulmonary fibrosis w/ asbestos bodies (dumbells). It affects the lower lobes of the lungs.

A

Asbestosis

  1. pleural plaques = MC manifestation

–ivory white appearance on CT (calcified)

–ant., posterolateral parietal pleura and over diaphragm

–plaques NOT pre-cancerous

  1. recurrent pleural effusions
  2. ferruginous bodies with iron stain
209
Q

Asbestos is associated with pulmonary fibrosis and pleural plaques. It contributes to mesothelioma (pleural and peritoneal) and bronchogenic carcinoma.

Which type of asbestos is the most carcinogenic? How does it induce tumor formation?

A
  1. Amphibole type = most carcinogenic 2

. fibrogenic, pro-inflammatory and tumor initiatior/promoter

–inc. free radical generation

**tobacco carcinogens = adsorbed onto surface (synergy)

210
Q

Lung disorders may be drug induced. Common drugs include: 1. Amiodarone

  1. Methotrexate and Methysergide
  2. Cyclophosphamide
  3. Nitrosourea and nitrfurantoin What diseases are these drugs commonly associated w/ as far as induction?
A
  1. Amiodarone

–pneumonitis

–cryptogenic oranizing pneumonia

  1. bleomycin

–fibrosis

211
Q

Radiation induced lung disorders: Describe acute vs. chronic illnesses associated w/ radiation exposure

A
  1. Acute –lymphocytic alveolitis/Hypersensitivity pneumonitis 2. Chronic: –fibrosis
212
Q

Peds - Lower Airway infections: A lower respiratory infection characterized by: -acute inflammation -edema -increased mucous -necrosis of epithelial cells lining the small airways. It is most often caused by RSV but may be due to other viral infections.

A

Bronchiolitis *rhinitis and cough -tachypnea, wheezing, crackles, use of accessory muscles (mild intercostal retractions), nasal flaring and coarse breath sounds NOTE: Leading cause of hospitaliation for infants under 1y/o

213
Q

Peds - Lower Airway Diseases: True/False: Recurrent wheezing after RSV infection may occur for months to years in affected children. Wheezing with RSV infection poses a greater risk of -prolonged airway hyperresponsiveness -later diagnosis of asthma

A

True

214
Q

To diagnose bronchilitis, assess risk factors for severity. What are these?

A
  1. <12 weeks premature 2. congenital heart defectr 3. cardiopulmonary disease 4. immunodeficiency NOTE: acoid routine CXR or lab diagnosis (won’t work) NOTE 2: NO treatment for RSV: supportive care ONLY (nasogastric or IV fluids who cannot hydrate; nasosuctioning)
215
Q

What is the diagnostic test of choice for a child with RSV?

A

Nasal secretions for RSV antigens NOTE: can do chest radiographs of hospitalized infants –can appear normal or have peribronchial thickening, interstitial pneumonia, OR segmental consolidation

216
Q

What are the indications for Hospitalization of a child diagnoed with RSV?

A
  1. Respiratory distress –are they tachypnic (breathing rapidly)? (like a freight train) 2. Signs of accessory muscle use –belly breathing –dyspnea 3. Poor feeding or inability to maintain airway 4. SIgns of respiratory failure –wheezing, cyanosis 5. Dehydration (delayed cap refill)
217
Q

Peds - Lower Airway Diseases: Chronic cough persists for > 8 weeks. When the patient’s radiograph appears normal, it can be caused by one of three things: 1. asthma 2. GERD 3. Upper airway cough syndrome (post-nasal drip) Describe these

A
  1. Asthma –MC trigger for infants/toddlers = viral upper resp. tract (URI) –cough, wheezing, SOB, chest tightness 2. Post-nasal drip –allergic rhinitis (older than 3yr) –non-allergic rhinitis –sinusitis (rhinorhea; not common < 1y/o) 3. GERD –improves by 12mos –worse at night (supine) –exercise and URI’s are uncommon precipitating factors **overfeeding
218
Q

Peds - Lower Airway disorders: Key features of this disorder are sudden, with a noxious stimulus or exertional event. Symptoms include: -normal pulse ox -failure to improve w/ B-2 agonists -clear lungs on exam -difficulty w/ INSPIRATION instead of expiration

A

Vocal cord dysfunction **paradoxic adduction of vocal cords during inspiration of rhinolarygoscopy **endoscopy = Dx NOTE: spirometry: up and then flat line

219
Q

Peds - Lower airway disorders: What should be suspected with: 1. respiratory distress or wheezing (sudden onset) in absence of clear history of choking episode 2. UNILATERAL monohonic wheeze or asymmetric breath sounds 3. poor response to expexted treatments

A

Foreign body aspiration -drooling, chest pain gagging, dysphagia, refusal to eat, cough, stridor, wheezing NOTE: foreign body hangups: thoracic inlet (MC), level of aortic arch, lower esophageal junction (pass)

220
Q

What is the gold standard for diagnosis of foreign body aspiration?

A

Rigid Bronchoscopy (Dx and management)

NOTE: Can do chest radiography (A-P exp. and insp.)

–have to have been there for at least 1 day (radioopacity and air trapping)

–esophagus: full object; trachea: side of object

221
Q

What are indirect signs of foreign body aspiration?

A
  • unilateral hyperinflation
  • atelectasis
  • mediastinal shift
  • pneumomediastinum

NOTE: expiratory chest radiographs are more sensitive than inspiratory *Many appear normal within first 24 hours

222
Q

What is a common manifestation found in children who have (or have had RSV)?

A

Apnea (absence of respiratory flow)

*infants < 6 weeks, premature or other pre-existing illnesses

223
Q

Common types of apnea are: 1. _______ in neonates can be caused by relatice immature brainstem respiratory center and is common in pre-term infancts. It can be caused by other illnesses (hypoxic injury, brain hemorrhage, etc.) 2. ______: caused by airway obstruction at any point from pharynx to distal tracha. It can occur in infants and children. 3. ______: a combintaion of central and obstructive

A
  1. Central –immature brainstem respiratory center -apnea >15-20 seconds (cyanosis, bradycardia, pallor)
  2. Obstructive (snoring!!)
    - Infants: Common causes are macroglossia, Pierre Robin sequence, and subglottic stenosis.
    - Children: enlarged tonsils, adenoids, nasal polyps, obesity, trisomy 21 *not benign condition (pulmonary HTN, death)
  3. Mixed apnea
224
Q

Describe diagnosis and Tx of Sleep Apnea in infants/children

A

Dx: neuroimaging (severe); endoscopy, sleep study (older children or suspected obstructive) Tx: theophylline, caffeine and CPAP (or nasal canula for mixed/obstructive)

225
Q

Aspiration of foreign bodies into the lower tract is common especially in children. These foreign bodies are more likely to enter the _____ primary bronchus and pass into the _____ or ______ lobe bronchi.

A

Right primary bronchus -middle or lower lobe If vertical: usually enters posterior basal segment of R. lower lobe (MC aspiration site)

226
Q

A 63 year old patient presents with cough, chest pain, fever and difficulty breathing. Chest x-ray reveals areas of opacity (white) of the lung parenchyma and enlargement of the bronchomediastinal lymph nodes (mediastinal widening)

A

Pneumonia (inflammation of the lung) *bacteria, viruses, fungi

227
Q

A patient presents with persistent productive cough and hemoptysis. Imaging reveals a tumor located near the hilus, projecting into the bronchi. Histology reveals nests of tumor cells separated by fibrous bands. You suspect

A

bronchogenic carcinoma

*early metastasis to thoracic (bronchomediastinal lymph nodes) *hematogenous spread to brain, bones, lungs, suprarenal glands

228
Q
  1. To listen to breath sounds of the superior lobes of the Right and Left lungs, where must you auscultate?
  2. T0 listen for breath sounds for the Right Inferior lobe, where must you auscultate?
  3. To listen for breath sounds from the inferior lobes, where must you auscultate?
A
  1. above 4th rib for right lung; above 6th rib for left
  2. between 4th and 6th ribs
  3. posterior chest wall
229
Q

Pneumothorax is entry of air into a pleural cavity that causes lung collapse. True/False - Open pneumothorax commonly occurs when the pleural cavity is open to outside air. Air is able to move freely through the wound during inspiration and expiration. During inspiration, the mediastinum will shift to the opposite side, and returns to original position upon expiration.

A

True *knife wound

230
Q

Anatomy: The parietal pleura is sensitive to general stimuli (pain, temperature, touch and pressure; somatosensory innervation). List the innervations of the: 1. Costal pleura 2. Mediastinal pleura 3. Diaphragmatic pleura 4. Visceral pleura

A
  1. Costal pleura –intercostal nerves 2. Mediastinal pleura –phrenic nerve 3. Diaphragmatic pleura –phrenic nerve (over domes) –lower 6 intercostals along periphery 4. Visceral pleura –sensitive to stretch –ANS from pulmonary plexus

Respiratory System (1 decks)

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