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Preclerkship > Resp Review > Flashcards

Resp Review Flashcards

1
Q

4 stages of pulmonary consolidation in pneumonia

A

1) Congestion (exudate enters alveoli) 2) Red hepatization (RBCs, fibrin) 3) Grey hepatization (RBC breakdown) 4) Resolution (sputum)

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2
Q

Basic pathophys of pneumonia

A

Bacterial toxins/PAMPs –> histamine release, vascular permeability –> alveolar edema

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3
Q

Community acquired pneumonia most common pathogen

A

Streptococcus pneumoniae

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4
Q

Pneumonia caused by a pre-existing condition

A

Secondary pneumonia

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5
Q

Hospital-aquired pneumonia happens when?

A

>48 hours after admission

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6
Q

3 main types of pneumonia based on locations in lungs

A

1) Lobar (consolidation of 1 lobe) 2) Bronchopneumonia (bronchioles + adjacent alveoli, patchy) 3) Interstitial (inflamm/fibrosis of interstitium - bilateral opacities, may be indolent)

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7
Q

Percussion in pneumonia

A

Dull

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8
Q

Why does alcohol increase pneumonia risk? (3)

A

1) Impairs activity of macrophages/mucociliary/NK cells/other WBCs 2) Aspiration 3) Alters normal URT flora

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9
Q

What might you see on palpation in lobar pneumonia?

A

Unilateral expansion

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10
Q

In pneumonia you might hear what breath sounds in the parenchyma (auscultation)

A

Bronchial

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11
Q

CO2 and O2 in pneumonia?

A

Hypoxemic Not necessarily hypercapnic, may be hypocapnic due to hyperventilation

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12
Q

CXR signs for the 3 pneumonia types

A

1) Lobar –> lobar opacity, air bronchograms 2) Bronchopneumonia –> patchy reticular/reticulonodular infiltrates, bilateral, base of lungs 3) Interstitial - reticular opacities (diffuse lines) mostly around hila

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13
Q

What are the 2 scoring systems for pneumonia (one in detail)

A

1) CURB-65: confusion, high serum urea, RR >=30, BP syst <=90 or diast <=60; >=65 years old; 2+ = hospitalize, 3+ = consider ICU Also pneumonia severity index ^mortality risk

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14
Q

In Fick’s law, rate of diffusion depends on… (4)

A

Surface area Membrane thickness Diffusivity of the gas Partial Pressure gradient

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15
Q

2 ways that endotracheal tube increase infection risk

A

Prevent closure of glottis May act as a fomite

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16
Q

Viral RTIs make susceptible to bacterial 2o infection via…

A

1) Impairing mucociliarty escalator 2) Upregulating adhesion proteings 3) Paralyzing macrophages

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17
Q

Biggest risk factor for COPD?

A

Smoking

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18
Q

Drugs that reduce fever (acetaminophen, ibuprofen) inhibit what?

A

Cyclooxygenase

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19
Q

Bleeding from upper GI tract

A

Hematemesis

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20
Q

Blood from lower GI tract

A

Hematochezia

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21
Q

Blood from airway (lungs, nose)

A

Hemoptysis

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22
Q

Nosebleed proper term

A

Epistaxis

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23
Q

Pneumothoax vs atelectasis

A

Atelectasis = collapse of lung tissue w/ loss of volume Pneumothorax = air in IP space –> loss of neg pressure b/w pleural membranes –> partial or complete lung collapse

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24
Q

Resp distress vs failure vs arrest?

A

Distress = struggling to breath Failure = inability to regulate blood parameters through breathing (ABG-diagnosed!) Arrest = cessation of breathing

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25
Q

What test is used for clubbing?

A

Schamroth’s test

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26
Q

Clubbing occurs in what diseases?

A

ILD, CF, cancer, congenital heart disease, cardiac shunting NOT COPD

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27
Q

Most dependent part of pleural cavity when upright = ? What is this called on radiograph?

A

Costadiaphragmatic recess (parietal pleura at base of lung b/w diaphragm and ribs) Costaphrenic angle

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28
Q

Bronchioles are composed almost entirely of

A

Smooth muscle

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29
Q

Without cartilage, how are the bronchioles and alveoli kept open?

A

Transpulmonary pressure

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30
Q

In normal conditions, most airway resistance is in the…

A

Larger bronchioles/bronchi near trachea (few vs terminal bronchioles)

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31
Q

Distribution of receptors for nervous control of airway diameter

A

BR ARs in periphery, MAch in central airways

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32
Q

Control of airway diameter mainly regulated by… (SNS or PSNS)

A

PSNS (SNS weak)

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33
Q

B2 ARs bind which catecholamine more strongly?

A

Epinephrine

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34
Q

B2 agonist

A

Salbutamol (ventolin)

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35
Q

PSNS fibres that release acetylcholine to lung parenchyma are derived from ___ nerve

A

Vagus

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36
Q

Microembolism occluding small pulmonary arteries triggers…

A

Bronchiolar constriction reflex

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37
Q

Acetylcholine leads to broncho…

A

constriction

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38
Q

Give an example of a local secretory factor that leads to bronchoconstriction

A

Histamine

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39
Q

Define asthma (3 things)

A

1) Bronchial hyperresponsiveness (inflamm + narrowing)
2) Episodic exacerbations
3) Reversible airway obstruction

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40
Q

Genetic predisposition to immune hyperresponsiveness may manifest in what combination of disorders?

A

Atopic triad: atopic dermatitis (eczema), asthma, allergic rhinitis

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41
Q

Genetic predisposition to hypersensitivity/allergy

A

Atopy

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42
Q

What is AERD?

A

Aspirin-Exacerbated Respiratory Disease (Samter’s Triad)

  1. Asthma
  2. Nasal polyps
  3. ASA sensitivity
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43
Q

What causes ASA sensitivity?

A

COX-1 inhibition

Arachadonic acid metabolized by lipooxygenase instead –> leukotrienes (instead of prostaglandins)

–> bronchospasm, vascular permeability, mucus production

Submucosal edema + airway obstruction!

“Pseudoallergic reaction” - like type 1 hypersensitivity but not IgE-mediated

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44
Q

Why do beta blockers trigger asthma?

A

Inhibit E/NE binding of B2ARs

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45
Q

2 main categories of asthma

A
  1. Allergic (extrinsic) - atopy; environmental allergens
  2. Nonallergic (intrinsic) - neutrophil-mediated; cold, stress, GERD, chemicals, meds, RTIs
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46
Q

Endobronchial obstruction in asthma mainly due to:

A

Bronchospasm

Submucosal edema

Mucus production

Hypertrophy of SM

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47
Q

Allergic (extrinsic asthma) primarily mediated by

A

IgE –> FcERI binding, mast cell degranulation, histamine release

(Type I hypersensitivity)

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48
Q

Nonallergic (intrinsic) asthma primarily mediated by

A

Neutrophils (–>submucosal edema + obstruction)

e.g. aspirin-induced asthma

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49
Q

Chronic asthma can lead to…

A

Fibrosis (scarring, BM thickening, irreversible obstruction –> COPD)

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50
Q

Summary of pathophys of asthma

A

Allergen phagocytosed by APC

Presented on MHCII to CD4+ T cells (differentiate into TFH and TH2)

IL4/IL5 release

IL4 –> IgE –> mast cell degranulation –> histamines + leukotrienes

IL5 –> eosinophils –> leukotrienes/cytokines, proteases

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51
Q

How to histamines impact the bronchioles?

A

Histamines –> SM constriciton in bronchioles!

Vascular permeability, inflammation, mucus production

(submucosal edema)

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52
Q

What are the 2 phases of the asthmatic immune response?

A
  1. Mast cells recognize cross-linked IgE –> rapid degranulation/bronchoconstriction, mucus production
  2. Eospinophil/neutrophil recruitment takes time, they are part of later phase
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53
Q

Percussion in asthma

A

HYPERresonance (air traipping!)

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54
Q

Auscultation in asthma

A

Prolonged exp + exp wheeze, decreased breath sounds

(quiet chest = badbadbad!)

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55
Q

Mucus/epithelial cells clogging bronchioles in asthma that can be coughed up

A

Curschmann spirals

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56
Q

Charcot-Leyden crystals

A

Pigments of broken-down eosinophils, seen in sputum analysis in asthma

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57
Q

FEV1 increase after bronchodilator required for asthma diagnosis

A

12%

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58
Q

If asthma patient asymptomatic what test could you do (instead of bronchodilator test)

A

Bronchoprovocation test = Methacholine challenge (muscarinic agonist)

Positive = 20% drop in FEV1

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59
Q

FEV loop in asthma appears

A

Concave on top

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60
Q

PFT result in asthma

A

Decreased FEV1/FVC (FVC may decrease due to gas trapping)

Reversible 12% post bronchodilator test

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61
Q

Initial ABG for asthma

Severe late-stage ABG for asthma

A

Initial: hypoxemic, hypocapnic, alkalotic (Type 1 RF)

Final: hypoxemic, hypercapnic, acidosis (Type 2 RF)

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62
Q

CXR in asthma

A

If severe: Hyperinflation - flat diaphragm, increased intercostal space, barrel chest

(but in most asthma mainly used to exclude differentials)

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63
Q

3 main categories of asthma treatment

A

1) Causal
2) Relievers (treat symptoms) - SABA/LABA, SAMA/LAMA
3) Controllers (treat underlying inflammation) - e.g. ICS

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64
Q

Emergency asthma med (IV)

A

IV magnesium sulfate (blocks Ca channels to relax SM)

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65
Q

SAMA and LAMA examples

A

SAMA = ipratropium bromide

LAMA = tiotropium bromide

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66
Q

What is a test that can be done during acute exacerbation of asthma, and as a way for patients to monitor if their meds are working before symptoms increase?

A

Peak Expiratory Flow Rate (hsould be >70% of expected)

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67
Q

Describe some treatment modalities for asthma

A
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68
Q

The mucous membrane in the bronchial tree changes from _______ in the main bronchi, lobar bronchi, and segmental bronchi to _______ with some _____ in larger bronchioles, to mostly ________ with no _____ in smaller bronchioles, to mostly_____ in terminal/respiratory bronchioles. ______ lines the alveoli (_____)

A

The mucous membrane in the bronchial tree changes from ciliated pseudostratified columnar epithelium in the main bronchi, lobar bronchi, and segmental bronchi to ciliated simple columnar epithelium with some goblet cells in larger bronchioles, to mostly ciliated simple cuboidal epithelium with no goblet cells in smaller bronchioles, to mostly nonciliated simple cuboidal epithelium in terminal/respiratory bronchioles. Simple squamous epithelium lines the alveoli (pneumocytes)

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69
Q

4 layers of tracheal tissue (lumen to outer)

A
  1. Innermost mucosa: resp epithlium (PSCC w/ goblet/basal cells) + BM
  2. Submucosa: mixed seromucous glands
  3. Hyaline cartilage anteriorly, trachealis muscle fibres posteriorly
  4. Adventicia: areolar CT w/ small BVs/nerves
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70
Q

SM in bronchi vs trachea?

A

Complete encircles the lumen in bronchi

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71
Q

Basement membrane connects ____ to ____. What are the 2 parts?

A

Epithelial cells to CT

  1. Basal lamina (secreted by epi cells, attach them to BM)
  2. Reticular lamina (close to CT, contains collagen)
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72
Q

What’s measured in an ABG? (8)

A
  1. PaO2
  2. PaCO2
  3. SaO2
  4. HCO3-
  5. pH
  6. Base excess
  7. Anion gap
  8. Other: Hb, electrolytes, glucose, etc…
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73
Q

ABG normal range for…

PaO2

A

80-100 mmHg

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74
Q

ABG normal range for…

PaCO2

A

35-45 mmHg

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75
Q

ABG normal range for…

pH

A

7.35-7.45

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76
Q

ABG normal range for…

HCO3-

A

21-27 mEg/L

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77
Q

ABG normal anion gap

A

12 mEq/L

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78
Q

Test to perform before ABG

A

Modified Allen’s test (compress both wrist arteries, release from ulnar artery –> colour should rapidly return if collateral circulation present)

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79
Q

ABG usually performed from which artery?

A

Radial

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80
Q

Anion gap and non-anion gap apply to which AB disorder subtype?

A

Metabolic acidosis

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81
Q

Steps of ABG interpretation

A
  1. Look at O2 for hypoxemia
  2. Alkalosis vs acidosis
  3. Resp or metabolic
  4. Metability acidosis –> check anion gap
  5. Check for other primary metabolic disorders by checking AG/bicarb ratio
  6. Check for other primary resp disorders using CO2 Winters Formula (bicarb x 1.5+8 +/-2)
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82
Q

Describe interpretation of AG/bicarb ratio

A

< 1 –> concurrent primary metabolic non-AG acidosis

>2 –> concurrent primary metabolic alkalosis

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83
Q

2 types of restrictive lung diseases + examples

A
  1. Intrinsict (ILD)
  2. Extrinsic (pleura/pleural cavity, chest wall, resp muscles/NM disease)
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84
Q

Examples of obstructive lung diseases (4)

A

COPD, CF, asthma, bronchiectasis

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85
Q

Obstructive lung diseases are issues with ____

Restrictive lung diseases are issues with _____

A

Obstructive = resistance

Restrictive = compliance

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86
Q

An extra big expiratory scoop on a flow-volume curve indicates what disease and why?

A

Emphysema –> airways collapse during expiration

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87
Q

What does a restrictive lung disease look like on a flow-volume loop?

A

Compressed bc air comes out faster all at once (think of tight elastic band snapping back)

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88
Q

3 main steps of interpreting PFT

A
  1. Spirometry
  2. Lung volumes
  3. DLCO
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89
Q

Summary of spirometry interpretation

A
  1. Flow-volume loop (obstructive fixed/variable, intra/extra; restrictive)
  2. FEV1/FVC ratio –> obstruction (<0.7 actual value, or <lln></lln>

<p>3. <strong>FEV1</strong> --&gt; severity of obstruction (&lt;70 = moderate, &lt;50 = severe)</p>

<p>4. If ratio normal, low <strong>FVC</strong> --&gt; restriction</p>

<p>5. Post-bronchodilator measurements (reversibility)</p>

</lln>

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90
Q

What are things to look for in lung volumes of PFT?

A

TLC –> restriction (low), hyperinflation (high)

RV –> obsety/restriction (low), gas-trapping (high)

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91
Q

DLCO interpretation

A

Intraparenchymal vs extraparenchymal restriction

If only abnormal thing –> blood issue (anemia, PE…)

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92
Q

2 main components of interstitial lung disease

A

1) Alveolitis (inflammation, usually first step)
2) Fibrosis (primary process in IPF)

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93
Q

Steps leading to fibrosis in ILD

A

Tissues damage or Ag

Inflammation, cytokines

Proteases/oxidants (more damage! Degrading CT)

Fibroblasts recruited (building CT)

–> abberant CT formation

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94
Q

Explain what happens with fibroblasts in ILD

A

Type II pneumocytes stimulate fibroblasts to differentiate into myofibroblasts –> secrete collagen

Overproliferation, too many myofibrocytes that aren’t properly apoptosing

–> thick IL layer

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95
Q

Most common type of ILD

A

Idiopathic pulmonary fibrosis

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96
Q

ILD is triggered by ____ exposures/stimuli

A

Chronic! Long-term

97
Q

Pneumoconioses

A

ILDs caused by inhalation of inorganic dusts

98
Q

Auscultation for ILD

A

Inspiratory dry/fine crackles/rales

Elevated diaphragm (restriction)

Egophony will stay as EEE (differentiate from alveolar filling which would cause wet crackles)

99
Q

PFT changes in ILD

A

FEV1/FVC - high/normal (elastic recoil)

FVC - low

TLC - low

FRC - low (reduced compliance, increased recoil)

DLCO - low

100
Q

Radiological sign of ILD

A

Reticular opacities (fibrosis)

Honeycombing (air-filled fibrotic cysts)

101
Q

ABG in ILD

A

Increased A-a gradient

Hypoxemia

Hypocapnia/resp alkalsos at first

Most of type: hypocapnia + neutral pH (metabolic compensation!)

Late stage - hypercapnic

102
Q

Treatment for ILD

A

Treat underlying cause (AB, steroids)

Lung transplants

Generally irreversible :(

103
Q

Acute Respiratory Distress Syndrome

A

Severe inflammatory reaction of lungs

Hypoxemia + bilateral pulmonary infiltrates not accounted for by heart failure/fluid overload

104
Q

Main differential for ARDS

A

Cardiogenic pulmonary edema

(both call alveolar edema - different causes, similar outcomes)

105
Q

Is ARDS always initiated with lung injury?

A

NO. Systemic inflammatory response, which is why opacities are always bilateral

106
Q

Most common cause of ARDS?

A

Sepsis

107
Q

Berlin criteria for ARDS

A

MUST MEET ALL 4 CONDITIONS

  1. Acute onset (resp failure <1 week after potential trigger)
  2. Bilateral opacities not explained by pleural effusions
  3. Hypoxemia: PaO2/FiO2 <300 mmHg (mod <200, severe<100, normal = 500)
  4. Resp failure not fully accounted for by heart failure or fluid overload
108
Q

Pathophys of ARDS

A

Damage –> inflammatory cascade

  1. Exudative phase: excess fluid in interstitium and on alveolar surface
  2. Hyaline membrane formation: neutrophils/protein rich exudate in alveolar space –> hyaline membranes form (fibrin + debris + RBCs), impair gas exchange, hypoxemia

Damage to pneumocytes –> less surfactant –> alveolar collapse, reduced compliance, shunting

Vascular occlusions –> dead space

  1. Organizing phase: type II pneumocyte prolif, fibroblasts infiltrate –> IL fibrosis can occur
109
Q

Edema in ARDS is caused by destruction/failure of what?

A

Alveolar-capillary membrane

  • Endothelium* - activated, swelling/leaking
  • Epithelium* - flooding, decreased surfactant/resorption (both type II pneums)
110
Q

Is the disease in ARDS gravity-dependent?

A

The opacities are NOT but atelectasis is!

111
Q

Primary imaging test for ARDS

How to distinguish from cardiac issue?

A

CXR: peripheral bilateral opacities

Distinguish from CHF: no (or small) pleural effusions, no cardiomegally, no pulmonary edema (septal lines)

112
Q

ABG in ARDS

A

PaO2: low

pH: high; pCO2: low (initially resp alkalosis)

Increased A-a gradient

PaO2/FiO2 <300 mmHg

…Eventual resp exhaustion (hypercapnia/acidosis)

113
Q

Major physiological changes in ARDS:

A

^ A-a gradient

Lower: compliance, FRC

^WOB

R-L shunting + Dead space

Hypoxemia

^pulmonary vascular resistance (fibrin, vasoconstriction, edema)

114
Q

Ventilation strategy for ARDS?

A

Lung-protective ventilation (low TV & plateau pressure, lowest FiO2 possible)

115
Q

Severe bilateral opacities in ARDS can lead to what appearance on x-ray?

A

“White out”

116
Q

Prognosis in ARDS?

A

Usually full resolution if patient recovers, improvement starts after 1-3 weeks

If complicated by interstitial pulmonary fibrosis –> prolonged ventilator dependence

40% mortality if simultaneous organ failure

117
Q

Infant respiratory distress syndrome is what?

A

Surfactant deficiency disorder

118
Q

Diseases that can be classified as COPD

A

Mainly: chronic bronchitis + emphysema

Also: CF, bronchiectasis, asthma (irreversible)

119
Q

Common etiologies of COPD

A

SMOKING

Environmental exposures

Genetics: alpha-1 antitrypsin deficiency

120
Q

Why does alpha-1 antitrypsin deficiency beget COPD?

A

It is an protease inhbitor that inhibits elastase (secreted by neutrophils)

Without it –> unopposed elasteolysis in alveoli

121
Q

In COPD, lung inflammation and proteases lead to proteolytic destruction of the lung parenchyma. What are the effects of this?

A
  1. Reduced elastic recoil –> air trapping
  2. Reduced airway patency –> narrowing/collapse
  3. Enlargement of alveoli –> hyperinflation, bullae

Result = emphysema

122
Q

Why is hypoxemia not observed as early in emphysema as in chronic bronchitis?

A

Matched V/Q defect (both terminal bronchioles/alveoli and capillary bed are destroyed!)

123
Q

2 main types of emphysema

A
  1. Centriacinar Emphysema - destruction of respiratory bronchiole (central acinus, alveoli ok), usually upper lobe - associated with smoking
  2. Panacinar Emphysema - destruction of entire acini (incld alveoli); usually lower lobe/lung bases but can be entire lung - associated with a1-antitrypsin deficiency
124
Q

R heart failure due to respiratory system failure

A

Cor pulmonale

125
Q

How would A-a gradient be impacted by COPD or during asthma exacerbation?

A

Incraesed due to shunting, V/Q mismatching

126
Q

In COPD, inflammation leads to chronic bronchitis through what pathological changes?

A
  1. Airway fibrosis/narrowing
  2. Hypertrophy/hyperplasia of mucus glands + goblet cells –> mucus production
  3. Death of airway epithelium cilia cells (mucus plugs –> air trapping!)
  4. SM hypertrophy
  5. Pulmonary hypertention (V/Q mismatch, hypoxemic vasoconstriction)
127
Q

Diagnostic criteria for chronic bronchitis

A

Productive cough on most days in 3 consecutive months for 2 consecutive years

128
Q

Does COPD cause more issues with inspiration or expiration?

A

Expiration (for both CB and E)

129
Q

How does pursed-lip breathing help patients with emphysema?

A

Prolongs expiration

Maintains PEEP to keep airways open

130
Q

Auscultation in COPD

A

Expiratory wheeze

Inspiratory crackles/rales (airways “popping” open)

Emphysema: decreased breath sounds (alveolar hyperinflation/destruction)

Chronic Bronchitis: Rhonchi (gurgling due to mucus)l

131
Q

Percussion in COPD

A

Hyperresonant (gas trapping)

132
Q

Change in chest appearance in COPD

A

Barrel-chested

(^ant-post diameter due to hyperinflation caused by collapsed airways)

133
Q

PFT changes in COPD

A

Decreased: FEV1, FVC (or normal), FEV1/FVC (<70%), DLCO (emphysema)

Irreversible (<12% recovery)

Increased: TLC, RV (gas trapping)

134
Q

ABG in COPD

A

Increased: PCO2

Decreased: PO2, pH

135
Q

COPD Radiography

A

Evidence of air trapping: hyperinflation, barrel chest, flat diaphragm, ^AP diameter; air pockets visible in emphysema

136
Q

Best treatment for COPD

A

Smoking cessation!

Doesn’t improve lung structural damage but reduces mucus/hyperrresponsiveness, normalizes FEV1

137
Q

Giving too much O2 in COPD patient can lead to…

A

CO2 narcosis

138
Q

List some COPD treatment modalities (other than smoking cessation and vaccines) (6-8)

A

Long-term oxygen therapy (LTOT) - aim for sats 88-92%

Bronchodilators (SAMA + SABA or LAMA + LABA)

Steroids: ICS (maintenance), IV/PO (acute exacerbations)

PDE inhibitors (SM relaxation) - theophylline

ABs

Pulmonary rehab

(Lung resection)

(Mucolytics)

139
Q

Complications of COPD (8)

A
  1. AECOPD (mucus trapping)
  2. Pneumonia (mucus trapping)
  3. Macro-nutrient deficiency (inflammation –> hypermetabolism)
  4. Wasting/muscle atrophy (inactivity/deconditioning, nutrient deficiency)
  5. Secondary polycythemia (hypoxemia –> kidney EPO –> erythropoiesis)
  6. Pulmonary hypertension + cor pulmonale (hypoxic pulmonary vasoconstriction)
  7. Depression
  8. Pneumothorax (bullae rupture, creating leak into pleural space)
140
Q

Define Acinus

A

Distal to terminal bronchiole, comprised of resp bronchiole + alveolar ducts + alveoli

141
Q

DIfference between acinus, primary lobule, secondary lobule?

A

Primary lobule = distale to resp bronchiole (alvelar ducts + sacs + alveoli)

Acinus = distal to terminal bronchiole (inclds resp bronchiole); 4-5 primary lobules

Secondary lobule = 3-25 acini

142
Q

Branching of bronchial tree in the conducting zone

A

Trachea –> mainstem (1o) bronchi –> lobar (2o) bronchi –> segmental (3o) bronchi –> bronchioles (no cartilage!) –> terminal bronchioles

143
Q

Internal ridge at bronchial junciton = ?

Chalk-full of what?

A

Carina

Irritant receptors (cough reflex)

144
Q

Which lung are we more likely to aspirate into and why?

A

R (bronchus is wider/more vertical)

145
Q

How is a bronchopulmonary segment defined?

A

Supplied by a tertiary bronchi; structurally/functionall indepdendent

146
Q

Adam’s apple = ?

Describe

A

Laryngeal prominance (2 sides of thyroid cartilage come together)

147
Q

What fully closes the airway during swallowing?

A

Vocal ligaments (vocal chords) close the glottis

Vestibular ligaments (false vocal chords) keep the remainder of the glottis closed

148
Q

Costale cartilage and cartilage in the airways is what type?

A

Hyaline (weak cartilage, flexible/resilient gel)

149
Q

What are the false ribs

A

5 ribs total

Ribs 8-10 connect to sternum indirectly via costal cartilate of 7th rib

Ribs 11-12 are “floating ribs”

150
Q

Main anatomy of sternum

A

Manubrium –> manubriosternal joint (sternal angle, angle of Louis) –> body –> xiphisternal joint –> xiphoid progess

151
Q

Which costal cartilage articulates with the sternal angle?

A

2nd

152
Q

Describe locations of superior and inferior mediastinum

A

Superior = T1-4, just behind manubrium

Inferior = T4-12 (ends at diaphragm)

153
Q

Inferior mediastinum is divided into anterior, middle, and posterior. The heart/pericardium are in which compartment?

A

Middle inferior mediastinum

154
Q

Superior thoracic aperature

A

T1 + 1st rib + upper manubrium

Passage of vasculature/nerves into thoracic cavity

155
Q

Inferior thoracic aperature

A

T12, 11th/12th ribs, 7th-10th costal cartilages

Where structures exit thorax into abdominal cavity; closed by diaphragm

156
Q

What nerve supplies the diaphragm, and what cervical segments does it come from?

A

Phrenic nerve

“C3, 4, and 5 keep the diaphragm alive!”

157
Q

Describe paradoxical movement of diaphragm

A

If one side paralyzed, moves up with inspiration due to decrease in intrathoracic pressure

158
Q

How are external intercostals oriented?

A

Hands-in-pockets

159
Q

External intercostals supplied by what nerves?

A

Intercostal nerves, come off spine @ same level

160
Q

Accessory muscles of inspiration

A

Scalenes (elevate first 2 ribs)

Sternocleidomastoids (elevate sternum)

Pectoral girdle (pectoralis minor, serratus anterior, trapezius)

161
Q

Accessory muscles of expiration

A

Internal intercostals

Abs: rectus abdominus, internal/external obliques, transversus abdominis

162
Q

What are the main muscles in forced inspiration?

A

STILL DIAPHRAGM AND EXTERNAL INTERCOSTALS!

163
Q

Origin and insertion of external intercostals

A

Origin = upper rib

Insertion = lower rib

(Pull insertion toward origin!)

164
Q

Diaphragm insertion

A

Central tendon

165
Q

Describe locations of the VAN and the collateral branch

A

VAN is in costal groove on inferior upper rib

Collateral branch on upper part of lower rib

166
Q

What is the point of tripoding when in resp distress?

A

Fixes the upper shoulder girdle –> allows better activation of accessory muscles for deeper inspiration

167
Q

Intercostal veins drain posteriorly into what? What is this system for?

A

Azygous/hemiazygous veins

Alternative route for inferior vena cava (which can be compressed during pregnancy e.g.)

168
Q

Blood supply to VAN comes from ___ posteriorly, ___ anteriorly

A

Aorta posteriorly

Internal thoracic arteries anterioly

169
Q

What is pulmonary arterial pressure?

What is pulmonary venous pressure?

A

PAP = Pressure generated by R ventricle

PVP ~ L atrial pressure

(very small gradient compaire to systemic!)

170
Q

Describe the path of the pulmonary circulation

A

R atrium

Pulmonary trunk

R/L pulmonary arteries –> arterioles –> capillaries

Pulmonary venules/veins

4 pulmonary veins (2R/2L return blood to L atrium)

171
Q

In the bronchial circulation, what is unique about circulation to the bronchioles?

A

Bronchioles don’t have veins but they do have arteries

Blood enters pulmonary veins = anatomical shunt

172
Q

What’s the difference between thoracic aorta and abdominal aorta?

A

Same struction but name changes when passes through diaphragm

173
Q

Intrapleural pressure is always…

A

Negative compared to alveolar/atmospheric

(elastic recoils of lungs inward, chest wall outward)

174
Q

Transpulmonary pressure =

If higher, lungs are…

A

alveolar - intrapleural pressure

Higher –> lungs larger!

175
Q

Is inspiration or expiration longer?

A

Expiration

176
Q

How does IP pressure change during inspiration/expiration

A

Declines throughout insp (-5 –> -8)

Lower peak at end of insp

Increases throughut exp

177
Q

How does alveolar pressure change throughout insp/exp?

A

Insp: Decrease then increase back to atm

Exp: increase then decrease back to atm

178
Q

Poiseuille Relationship and flow

A
179
Q

Define lung compliance (ratio)

A

dV/dP

180
Q

Define eupnea

A

Quiet breathing

181
Q

In the cough reflex, afferent impulses sent to medulla via ____

A

Vagus nerve

182
Q

What do the peripheral chemoreceptors sense?

Where are they?

What is their afferent innervation?

A

O2/CO2/pH

Aortic bodies (aortic arch) –> vagus nerve (X)

Carotid bodies (carotid arteries) –> glossopharyngeal nerve (IX)

183
Q

Central chemoreceptors respond to what?

A

pH, CO2

(more robust response to H+ changes than peripheral bc less buffering proteins)

184
Q

Describe medullary resp centre

A

Dorsal respiratory group (inspiration, diaphragm/intercostals via phrenic/intercostal nerves)

Ventral respiratory group (forced breathing, accessory muscles)

185
Q

What/where is the respiratory “pacemaker”

A

Pre-Botzinger complex in VRG

186
Q

Describe the pontine respiratory group

A

Apneustic centre - simulates DRG neurons to increase depth of breathing

Pneumotaxic centre - inhibits DRG neurons via apneustic centre

187
Q

What would happen if there was damage to your pneumotaxic resp centre?

A

Prolonged inspiration + short gasping expiration (bc not inhibiting the medullary centre/DRG!)

188
Q

Where is the pressure cutoff for PO2 where things start getting real bad?

A

60 mmHg (90% Hb sats)

189
Q

Changes in O2 that trigger chemoreceptors to induce respiration are what particular O2 in the blood?

A

Free O2!

So that’s why you need large drop - some will release from Hb to buffer it

190
Q

Hering-Breuer reflex:

A

Baroreceptors in bronchi/bronchioles stretch during lung overinflation –> vagus nerves –> DRG inhibition

191
Q

Define the 4 types of hypoxia

A
  1. Hypoxic (hypoxemia) hypoxia - low pO2 in arterial blood
  2. Anemic hypoxia - lack of functional Hb
  3. Ischemic hypoxia - lack of blood flow to tissue
  4. Histotoxic hypoxia - tissues can’t use O2 (e.g. cyanide)
192
Q

Define hyperpnea and hypopnea

A

High/low TV

(does not refer to speed!)

193
Q

Define hyperventilation

A

overall alveolar minute ventilation exceeds metabolic needs à hypocapnia/respiratory alkalosis

194
Q

Define hypoventilation

A

Minute volume does not meet metabolic needs (low TV or RR) –> resp acidosis

195
Q

Define tachypnea and bradypnea

A

RR high or low

196
Q

Unifying factor for hypercapnia

A

Alveolar hypoventilation!

197
Q

Define alveolar ventilation

A

AV = volume of gas reaching alveoli per min

(tidal volume - physiologic dead space) x RR

198
Q

Define minute ventialtion

A

Volume of air a person breaths per mind

= TV x RR

199
Q

Define the types of dead space

A

Physiologic dead space =

Anatomical dead space (conducting airways) +

Alveolar dead space (V in alveoli that don’t partake in gas exchange)

200
Q

Reference blood levels for PO2 and PCO2

A

O2: 100 –> 40 mmHg

CO2: 40 –> 45 mmHg

201
Q

Majority of muscles in pharynx, soft palate, larynx have motor innervation from….

name a few actions

A

Vagus nerve

(swallowing, phonation, coughing)

202
Q

Name the 4 tonsils

What are they called all together?

A

Pharyngeal (adenoids) - roof/posterior wall of nasopharynx

Palantine - sides of oropharynx

Lingual - base of tongue

Tubal - lateral wall of basopharynx

Together = Waldeyer’s ring

203
Q

Main causes of platypnea-orthodeoxia syndrome

A

V/Q mismatch

Pulmonary arteriovenous shunts

Intracardiac shunts

204
Q

In platypnea orthodeoxia syndrome why are symptoms alleviated by lying down?

A

Diseased basal lung (V/Q mistmach)–> more perfusion of apical lung!

Hepatopulmonary syndrome –> intrapulmonary vascular dilation more at base of lung

205
Q

O2 binding to Hb involves ____ binding resulting in sigmoidal curve

A

Cooperative

206
Q

What is the effect of 2,3-BPG on Hb binding?

A

Allosteric effector

Lowers O2 affinity to ^unloading @ tissues (stablizes reduced Hb)

207
Q

Bohr effect

A

Shift of O2-Hb curve right/down

  • Hypoxic/acidotic area (lactic acid formation due to anaerobic metabolism)
  • pH drop raising the P50 of Hb (pressure at which 50% of receptor saturated)
208
Q

What are 4 things that shift the Hb-O2 binding curve right?

A
  1. H+ (low pH)
  2. High CO2
  3. High temp
  4. 2,3-BPG
209
Q

At what point is the steep drop-off in the Hb-O2 dissociation curve?

A

60 mmHg

90% saturation

210
Q

Describe the major and minor phenomena in the Haldane effect

A

Minor: Hb bound to O2 has lower affinity for CO2 (but most CO2 transported as bicarb)

Major:

O2 binds Hb making it more acidic –> H+ release –> shifts bicarb equilibrium L generating CO2 + H2O (in the lung)

Then CO2 can diffuse into alveoli for expulsion

211
Q

What is the reciprocal of compliance?

A

Elastance

212
Q

If IP pressure is still negative during expiration, why do the lungs shrink?

A

Because it’s less than the elastic recoil pressure, leading to net positive pressure in the alveoli

213
Q

If a patient’s O2 sats are 100% do you know they have enough O2?

A

No! Other types of hypoxia, e.g. anemia

214
Q

Pressure of pulmonary circulation (R heart) vs systemic circulation (L heart)

A

10-20 mmHg (pulmonary)

80-100 mmHg (systemic MAP)

215
Q

If drive doesn’t lead to muscle tension =

If tension doesn’t lead to movement =

A

Weakness

Impedance

216
Q

Pneumothorax:

Negative IP pressure comes from recoil forces of _____ and _____ and the fact that the body gets rid of air pockets. If air enters IP space due to puncture, these forces disappear leading to…

A

Lung inward

Chest outward

^lung deflation and chest wall moves outward due to no more opposing recoil forces

217
Q

Describe the V/Q ratios in diff parts of the lung

A

0.3-2.5 from base –> apex

~0.8 average

218
Q

Ventilation is ~50% greater in what part of the lung when standing and why?

A

Base because weight of pleural fluid increases intrapleural pressure at the base to a less negative value –> alveoli less expanded and more compliant to increase V on inspiration

219
Q

All V no Q =

All Q no V =

With increasing V/Q, O2/CO2 values approach what?

A

Absolute dead space

Absolute shunting

Approach inspired air

220
Q

What does the A-a gradient say about cause of hypoxemia?

A

Normal –> issue extrinsic to lungs; e.g. neuromuscular disorder, high altitude

Elevated –> lung issue: V/Q mismatch, shunting, diffusion impariment, alveolar hypoventilation

221
Q

If PaCO2 and PaO2 are both low then what must you see with the A-a gradient?

A

Elevation!

222
Q

What are the 2 types of pulmonary shunts and how do they respond to supplemental O2?

A

Anatomic - alveoli bypassed, unresponsive

Physiological - non-ventilated alveoli are perfused; responsive

223
Q

Describe anatomical R-L shunts that move blood directly from pulmonary arteries –> veins

A

Arteriovenous malformations

Dilated, high capacitance, don’t regulate diameter via V/Q matching

224
Q

Define shunt fraction

A

% blood distributed by L ventricle that is not completely oxygenated

225
Q

Define apneusis

A

Protracted/deep/gasping inhalation + short exhalation (think of apneusic centre!)

226
Q

Is O2 supplementation effective for hypoventilation?

A

Yes for hypoxemia but not for hypercapnia

227
Q

Is O2 supplementation effective for impaired membrane diffusion

A

Yes (^gradient)

228
Q

Cyanosis is caused by what? What patients would you be VERY likely to observe cyanosis in?

A

Deoxy-Hb

Anemic patients

229
Q

Hypercapnia seen in what 2 causes?

A

Hypoventilation (CO2 transfer impacted as much as O2)

Circulatory deficiency (CO2 affected much less than O2 due to ^^^ blood transport capacity)

230
Q

Does super high CO2 increase respiration?

A

Actually depresses it

231
Q

Dyspnea =

A

Shortness of breath, “air hunger”

232
Q

Why doesn’t asthma necessarily cause hypercapnia?

A
  • Not everyone with COPD or asthma is a CO2-retainer
  • There are still parts of the lungs working well in these diseases so can compensate if the V-Q mismatch is accounted for appropriately
233
Q

Is providing O2 helpful if just parts of the lung are underventilated? (COPD, asthma, emphysema, ILD, pneumonia)

A

YUPPERS

234
Q

Important history considerations for ongoing dyspnea/cough

A

Smoking

Occupation

235
Q

Tests if you suspect COPD?

A

Spirometry (to confirm)

CXR (to rule out, e.g. cancer)

236
Q

1 predictor if someone will quit smoking

A

Whether or not they are personally motivated to do so (e.g. after health diagnosis, pregnancy)

237
Q

12% increase for reversibility in asthma is in what parameter?

A

FEV1

238
Q

What med used in bronchodilator test?

A

SABA (e.g. salbutamol = ventolin = albuterol)

239
Q
A

Preclerkship (25 decks)

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