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CMT > Pulm Pathophys > Flashcards

Pulm Pathophys Flashcards

1
Q

Resp System Anatomy

what is in upper respiratory tract? lower?

A
  • upper: nose, pharynx, larynx
  • lower: trachea, bronchi, lungs
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2
Q

Resp System Anatomy

conducting vs respiratory pathways

A
  • conducting: passages that serve for airway flow; nose until bronchioles
  • respiratory: alveoli and distal gas exchange regions
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3
Q

Resp System Anatomy

describe trachea

A
  • continuous superiorly w/ larynx and inferiorly becomes bronchial tree
  • cartilaginous rings support structure
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4
Q

Resp System Anatomy

differentiate R and L main bronchi

A
  • R: wider, shorter, more vertical (more frequent aspiration)
  • L: longer
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5
Q

Resp System Anatomy

anatomy of alveoli

A
  • hollow sacs that serve as site of gas exchange
  • lined by pneumocytes (type I vs type II)
  • alveolar sacs: cluster of many alveoli
  • alveolar pores: connect adjacent alveoli to help maintain equal air pressure throughout alveoli & lung
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6
Q

Resp System Anatomy

which pneumocytes secrete surfactant

A

type II

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7
Q

Resp System Anatomy

what structures pass through the hilum?

6

A
  • main bronchus
  • pulm artery
  • pulm veins
  • bronchial vessels
  • pulmonary autonomic plexus
  • lymph nodes/vessels
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8
Q

Resp System Anatomy

location/purpose of hilum?

A
  • located between T5 and T7
  • passageway for the pulm neurovasculature
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9
Q

Resp System Anatomy

differentiate R and L lungs

A
  • R: 3 lobes, 2 fissures
  • L: 2 lobes, 1 fissure, cardiac notch
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10
Q

Resp System Anatomy

differentiate parietal and visceral pleura

A
  • parietal: lines inner surface of thoracic cavity, sensitive to pressure, pain, temp
  • visceral: lines outer surface of lungs, covers fissures, not sensitive to pain
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11
Q

Resp System Anatomy

what is pleural cavity

A

space between visceral pleura and parietal pleura

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12
Q

Resp System Anatomy

purpose of pleural cavity

A

surface tension of fluid keeps lungs expanded and in contact w/ thoracic wall

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13
Q

Resp System Anatomy

which side of diaphragm is up higher?

A

R due to liver

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14
Q

Resp System Anatomy

physiology of inspiration

A
  • contraction of external intercostal muscles
  • contraction of diaphragm
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15
Q

Resp System Anatomy

physiology of exhalation

A
  • relaxation of external intercostal muscles
  • relaxaation of diaphragm
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16
Q

Resp System Anatomy

what types of pressure affect ventilation

A
  • atmospheric
  • intra-alveolar
  • interpleural
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17
Q

Resp System Anatomy

what is respiratory rate

A
  • total number of breather per minute
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18
Q

Resp System Anatomy

what is control of ventilation

A

respiratory centers located within the pons and medulla oblongata which responds to changes in CO2, O2, and pH levels within the blood

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19
Q

Resp System Anatomy

define eupnea

A

normal, relaxed, quiet breathing
12-15 breaths/min

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20
Q

Resp System Anatomy

define dyspnea

A

labored, gasping breathing
SOB

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21
Q

Resp System Anatomy

define apnea

A

temporary cessation of breathing

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22
Q

Resp System Anatomy

define respiratory arrest

A

permanent cessation of breathing

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23
Q

Resp System Anatomy

define hyperpnea

A

increased rate and depth of breathing

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24
Q

Resp System Anatomy

define hyperventilation

A

increased pulm ventilation in excess of metabolic demand (anxiety)

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25
Q

Resp System Anatomy

define hypoventilation

A

reduced pulm ventilation leading to increased CO2 concentrations

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26
Q

Resp System Anatomy

define:
* tidal volume
* residual volume
* expiratory reserve volume
* inspiratory reserve volume

A
  • TV: volume of air inhaled/exhaled with each breath under resting conditions
  • RV: volume of air left in lungs after forced exhalation
  • ERV: volume of air that can be forcefully exhaled after normal TV exhalation
  • IRV: volume of air that can be forcefully inhaled after normal TV inhalation
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27
Q

Resp System Anatomy

differentiate total lung capacity and vital capacity

A
  • TLC: sum of all lung volumes, represents total amount of air that a person can hold in lungs w/ forceful inhalation
  • VC: sum of all volumes except RV; amount of air a person can move into or out of their lungs
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28
Q

Resp System Anatomy

describe concept of V/Q coupling

A
  • perfusion: flow of blood to pulm vasculature (pulm perfusion = cardiac output)
  • ventilation and perfusion are mechanism for O2 and CO2 transport between pulmonary system and tissues
  • they must match for gas exchange to be efficient
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29
Q

Resp System Anatomy

define tissue hypoxia. What does this stimulate?

A
  • low oxygen availability to the tissues
  • sensed by the kidneys, stimulates RBC synthesis through release of EPO
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30
Q

Resp System Anatomy

define hypoxemia

A
  • low oxygen in blood
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31
Q

Resp System Anatomy

define hypercapnia

A
  • increased CO2 in blood
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32
Q

Influenza

what are the two glycoproteins?

A
  • hemaagglutinin
  • neuraminidase
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33
Q

Influenza

describe hemagglutinin (HA)

A

attaches to sialic acid containing receptors on respiratory epithelial cells

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34
Q

Influenza

describe neuraminidase

A

cleaves newly formed virions off the sialic acid containing receptor allowing the virus to exit cells

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35
Q

Influenza

differentiate M1 and M2

A
  • M1: involved in virion assembly
  • M2: involved in viral uncoating within the respiratory epithelial cells
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36
Q

Influenza

describe nucleoprotein

A

helps distinguish between 3 types of influenza viruses (A, B, C)

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37
Q

Influenza

define antigenic drift

A
  • epidemic
  • mutations accumulate in the viral genes that code for viral surface proteins resulting in new antigenic (HA or NA spikes); changes are generally minor
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38
Q

Influenza

describe antigenic shift

A
  • pandemic
  • 2+ strains of a virus combine to form a new subtype that is radically different; limited or no prior immunity
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39
Q

Influenza

MOA of neuraminidase inhibitors

A

interfere w/ release of influenza virus from infected cells and thus half spread of infection

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40
Q

Asthma

how are these asthmas mediated:
* extrinsic
* intrinsic

A
  • E: immune
  • I: non-immune
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41
Q

Asthma

what is Samter’s Triad?

A
  • ASA or NSAID use
  • Nasal Polyp
  • Asthma
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42
Q

Asthma

pathophys of extrinsic asthma

A
  • Initial Exposure to antigen: t cell differentiation into T helper cells followed by IgE antibodies binding to mast and basophil cells
  • Early phase: inhaled antigen causes IgE bound cells to degranulate which causes mediator (prostaglandin, histamine, leukotrienes) release leading to airway contraction/tightening
  • Late Phase: eosinophils increase release of inflammatory mediators which prolongs tightening/inflammation (IL-3, IL-4, IL-5, IL-13)
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43
Q

Asthma

pathophys of intrinsic asthma

A
  • non-eosinophilic, does not involve T-helper cells
  • no family hx of asthma
  • environmental factors create T helper cells which cause neutrophilic inflammation and airway hyperresponsiveness
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44
Q

COPD

describe

A

chronic lung disease characterized by progressive airflow limitation resulting from airway disease and/or parenchymal destruction

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45
Q

COPD

subtypes

A

combination of chronic bronchitis + emphysema

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46
Q

COPD

pathophys of chronic bronchitis

A

inhaled agent cause chronic inflammation in the airways which lead to progressive airway obstruction through:
* damage to endothelial cells which decreases mucociliary clearance
* mucous gland hyperplasia which leads to mucous hypersecretion and plugging
* Airway edema and smooth muscle hyper plasia leading to luminal narrowing
* peribronchial fibrosis leading to bronchial distortion

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47
Q

COPD

pathophys of emphysema

A
  • inflammatory response leads to activated neutrophils releasing proteases
  • protease activity exceeds antiprotease activity which causes tissue destruction (alveoli has less recoil, more compliance)
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48
Q

COPD

consequences of increased alveolar compliance and decreased recoil?

A
  • airway closure during expiration leading to obstruction
  • air trapping leading to lung hyperinflation
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49
Q

COPD

pathophys of healthy lungs

A
  • proteases break down elastin and connective tissue as part of normal tissue repair
  • antiproteases which act to balance protease activity
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50
Q

COPD

2 morphologic patterns associated w/ COPD

A
  • centriacinar emphysema
  • panacinar emphysema
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51
Q

COPD

describe centriacinar emphysema

A
  • associated w/ cigarette smoking/older pts
  • destruction located closer to the apices of the lungs
  • destruction of the respiratory bronchioles and a central portion of the acini
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52
Q

COPD

describe the panacinar emphysema pattern

A
  • associated with AAT deficiency, younger patients
  • more severe in the bottom of the lungs
  • destruction of all parts of the acinus (gas exchange unit of the lung)
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53
Q

COPD

what subtype is associated with weight gain? with weight loss?

A
  • gain: bronchitis
  • loss: emphysema
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54
Q

COPD

why does barrel chest develop?

A

hyperinflation in the lungs

(later stages of disease)

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55
Q

COPD

differentiate central and peripheral cyanosis

A
  • central: lips/tongue; relates to poor blood oxygenation in the lungs
  • peripheral: extremities/fingers; oxygen-depleted peripheral blood
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56
Q

COPD

define clubbing

A

bulbous enlargement of the distal fingertip and increased longitudinal and transverse nail plate curvature

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57
Q

COPD

Schamroth sign

A

loss of diamond shaped window normally visible when the dorsal surfaces of the terminal phalanges of corresponding fingers from opposite hands are placed together

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58
Q

COPD

Lovibond’s angle

A

angle located at the junction between the nail plate and proximal nail fold, which is normall less than 160 degrees

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59
Q

COPD

describe “blue bloater”

6 components

A
  • associated with chronic bronchitis
  • put on weight
  • frequent, productive cough
  • peipheral edema
  • cyanosis
  • wheezing/ronchi
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60
Q

COPD

describe “pink puffer” phenotype

8 components

A
  • classically emphysema
  • wt loss/thin
  • barrel chest
  • infrequent cough
  • pursed lip breathing
  • accessory muscle use
  • tripod positioning
  • hyperresonant chest
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61
Q

COPD

what state are COPD patients usually in?

relating to ABG

A
  • respiratory acidosis
  • but pH near normal due to renal compensation (increased serum HCO3)
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62
Q

COPD

describe blebs

A
  • small collection of air between the lung and outer surface of the lung (visceral pleura)
  • usually found in the upper lobe of the lung
  • can rupture and cause pneumothorax
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63
Q

COPD

describe bulla

A

formed from blebs that become larger/come together

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64
Q

COPD

advantage/disadvantage of SABA/SAMA

A
  • advantage: rapid onset to improve sx and lung function
  • disadvantage: relatively short duration of action
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65
Q

COPD

criteria for beginning Group E pt on ICS

A
  • eosinophil count > 300 cells/microL
  • features of asthma-COPD overlap
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66
Q

COPD

most commonly identified bacteria in acute exacerbations of COPD?

4

A
  1. Moraxella catarrhalis
  2. Streptococcus pnemoniae
  3. Haemophilus influenzae
  4. Pseudomonas aeruginosa
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67
Q

COPD

when to do noninvasive ventilation? invasive ventilation?

A
  • noninvasive: hypercapnia, hypoxemia; significant effort to breathe
  • invasive: severe respiratory failure; may be difficult to wean pts with severe COPD
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68
Q

Cystic Fibrosis

normal functioning of CFTR gene

A
  • codes for CFTR protein
  • which regulates chloride, sodium, and bicarb transport across epithelial membranes
  • water is attracted to the secretions (sodium) which thins
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69
Q

Cystic Fibrosis

pathophys of mutated CFTR gene

A
  • absent or dysfunctional chloride leading to abnormal secondary transport of sodium/water
  • THICK secretions can lead to stasis, infection, scarring
  • disease manifests only in homozygotes
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70
Q

Cystic Fibrosis

what is CFTR

A

cystic fibrosis transmembrane conductance regulator

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71
Q

Cystic Fibrosis

pathophys of cystic fibrosis

A
  • absent/dysfunctional chloride channels (dysfunctional transport of chloride –> abnormal secondary transport of Na/H2O)
  • In sweat glands: sweat with levels of sodium chloride
  • other exocrine glands: cannot secrete into lumen –> accumulation of intracellular chloride –> increased sodium/water reabsorption –> formation of hyperviscous mucus –> accumulation of secretions –> blockage of small passages –> inflammation/organ damage
72
Q

Cystic Fibrosis

pathophys of:
* male infertility
* female infertility

A
  • male: obstructive azoospemia due to bilateral aplasia/atresia of vas deferens
  • female: viscous cervical mucus, amenorrhea
73
Q

Cystic Fibrosis

mnemonic to remember common clinical features?

A

CF PANCREASS

  • C: chronic cough
  • F: failure to thrive
  • P: pancreatic insufficiency
  • A: alkalosis/hypotonic dehydration
  • N: nasal polyps, neonatal dehydration
  • C: clubbing of fingers
  • R: rectal prolapse
  • E: electrolyte elevation (sweat)
  • A: atresia, absence of vas deferens
  • S: sputum w/ S. aureus or P. aerguillas
  • S: stones in gall bladder
74
Q

Cystic Fibrosis

differentiate aplasia and atresia

A
  • aplasia: failure of an organ or tissue to develop or function normally
  • atresia: absence or abnormal narrowing of an opening or passage
75
Q

Cystic Fibrosis

describe role of IRT in cystic fibrosis

A
  • pancreatic enzyme released when there is pancreatic damage
  • if elevated: could indicate mutation analysis of CFTR
76
Q

Pneumonia- General

pathophys

A
  • exposure to pathogen and subsequent proliferation of the microbe in the lower airway and alveoli
  • local response of the alveolar epithelial cells which release cytokines into the surrounding tissue to recruit neutrophils to the site of inflammation
  • Inflammatory response (next card- depends on type)
  • systemic cytokines release as a response to invading microbe leads which disrupts hypothalamic thermoregulation (fever, chills, sweats)
77
Q

Pneumonia- General

inflammatory response to lobar pneumonia

A
  • accumulation of neutrophils and plasma exudate from capillaries into alveolar space to a lung lobe
78
Q

Pneumonia- General

inflammatory response of interstitial pneumonia

A
  • accumulation of infiltrates into alveolar walls
  • clinically: dry cough, hypoxiemia, dyspnea
79
Q

Pneumonia Severity Index (PSI)

purpose?

A
  • estimates mortality risk
  • helps to guide decisions regarding hospitalization
80
Q

Pneumonia Severity Index (PSI)

what are the classes? how do you manage them?

A
  • Class I: points < 50, manage outpatient
  • Class II: points 51-70, manage outpatient
  • Class III: points 71-90, can manage inpatient or outpatient based on risk assessment
  • Class IV: points 91-130, manage inpatient
  • Cass V: points > 130, manage inpatient
81
Q

CA- Pneumonia

CURB-65 what is evaluated for points?

A
  • each worth 1 point
  • C: confusion (disoriented to person/place/time)
  • U: uremina (BUN > 20)
  • R: Resp Rate (> 30)
  • B: BP (sys < 90, dia < 60)
  • 65: age > 65 yrs
81
Q

CA- Pneumonia

how to manage pts based on CURB-65 scoring?

A
  • 0-1 points: manage outpatient
  • 2 points: short inpatient stay/supervised outpatient stay
  • 3-5 points: manage inpatient always, assess for ICU.
82
Q

CA- Pneumonia

when to consider admission to ICU?

A

if 1+:
* hypotension that is unresponsive to volume resuscitation
* respiratory failure requiring mech vent

if 3+:
* respirations >30/min
* PaO2 < 250
* multilobar pneumonia
* confusion
* BUN > 20
* WBC < 4,000
* Platelets < 100,000
* Hypothermia
* Hypotension that is responsive to volume resuscitation

83
Q

ARDS

3 phases of ARDS?

A
  1. exudative
  2. proliferative
  3. fibrotic
84
Q

ARDS

pathophys of exudative phase

A

*6-72 hrs after eliciting factor
* initial injury: (cytokines) cause damage to pneumocytes and pulm endothelium which disrupts barriers between capillaries and air spaces (leak)
* inflammatory reaction: begins with endothelial cells secreting pro-inflammatory molecules and expressing adhesion molecules on their surface
* immune cells: neutrophils first, stick to and migrate into alveoli. Neutrophils release proteases and reactive oxygen molecules and cytokines which potentiates the cycle
* Edema: fluid, protein, cellular debris floods into the airspace.
* Disruption of Surfactant: surfactant works to increase surface tension, destroying surfactant leads to airspace collapse, V/P mismatch, L to R shunting of venous blood, pulm HTN

85
Q

ARDS

pathophys of proliferative phase

A
  • beginning stage of lung repair
  • alveolar epithelial cells begin proliferating along the alveolar basement membranes
  • macrophages clean up cellular debris and attract/activate fibroblasts
  • new pulm surfactant is produced
85
Q

ARDS

fibrotic phase pathophys

A
  • abnormal deposition of collagen in the alveolar ducts and interstitial membranes by fibroblasts
  • lung scarring: stiff lungs –> restrictive lung disease
86
Q

Pleural Effusion

describe role/pathophys of pleural fluid

A
  • hydrostatic and osmotic pressures produce pleural fluid within the capillary bed of the parietal pleural
  • pleural fluid is absorbed by lymph vessles in the diaphgragmatic and mediastinal surfaces of the parietal pleural and then into the RA
  • volume of pleural fluid turns over every hr
87
Q

Pleural Effusion

what does pleural effusion result from?

A
  • overproduction of fluid
  • inability of lymphatic system to remove fluid as it is produced
88
Q

Pleural Effusion

4 starling forces

A
  1. Capillary hydrostatic pressure (fluid pressure w/in capillaries)
  2. Interstitial Hydrostatic pressure (fluid pressure of interstitial fluid)
  3. Capillary Osmotic pressure (chemical osmotic pressure caused by proteins/molecules in the blood)
  4. Interstitial osmotic pressure (chemical osmotic pressure caused by proteins/molecules in the interstitial fluid)
89
Q

Pleural Effusion

classifications

A
  • exudative: caused by inflammation and increased capillary permeability, fluid rich in protein and LDH in the pleural space
  • transudative: caused by combination of increased hydrostatic pressure in the vasculature and decreased oncotic pressure in the plasma
90
Q

Pleural Effusion

hints for determining the etiology:
* fever, chills, productive cough
* night sweats, hemoptysis, travel out of the country
* unintentional wt loss, early satiety, loss of appetite, CP
* asbestos exposure
* wt gain, orthopnea, peripheral edema, JVD
* joint pain w/ or w/out effusion

A
  • pneumonia
  • TB
  • malignancy
  • mesothelioma
  • CHF
  • connective tissue disease
91
Q

Pleural Effusion

“if they are effusing in TWO…. think ?”

A

autoimmune

92
Q

Pleural Effusion

why can severe effusion lead to cardiac obstructive shock?

A

fluid drains into right atrium

93
Q

Pneumothorax

pathophys

A
  • as air enters pleural space, there is loss of negative pressure
  • normal opposing forces no longer pull on each other (elastic recoil in the lung tissues causes a partial or full lung collapse)
94
Q

Pneumothorax

tension pneumothorax pathophys

A
  • life threatening, can develop from any type of pneumothorax
  • one way valve for air flow into pleural space (air gets in, can’t get out)
  • air accumulates into pleural space w/ each inspiratory phase which increases pleural space pressure which shifts the mediastinum
  • contralateral lung gets compressed leading to hypoxia, hypercapnia
  • eventual compression of vena cava and atria which decreases venous return to heart and reduces cardiac function leading to rapid cardiopulmonary collapse
95
Q

Pneumothorax

mnemonic for sx of tension pneumothorax

P-THORAX

A
  • P: pleuritic pain
  • T: tracheal deviation
  • H: hyperresonance
  • O: onset sudden
  • R: reduced breath sounds and dyspnea
  • A: absent fremitus
  • X: xray shows lung collapse
96
Q

Pneumothorax

E-FAST what areas are visualized

A
  • 1: RUQ, hepatorengal recess
  • 2: LUQ, perisplenic area
  • 3: Pelvis, subrapubic window
  • 4: Cardiac, subxiphoid window
  • 5: Lungs
97
Q

Pneumothorax

describe needle decompression

A
  • 14 of 16 gauge needle inserted through chest wall
  • 2nd ICS in MCL
  • 5th ICS in MAL
  • follow decompression w/ chest tube placement
98
Q

Pneumothorax

describe chest tube thoracostomy

A
  • catheter inserted into chest wall
  • placed in the 4th to 5th ICS at MAL
99
Q

Pulmonary Embolism

3 primary contributing factors?

A

Virchow’s Triad
* circulatory stasis
* hypercoagulability
* vascular endothelial damage

100
Q

Pulmonary Embolism

what is VTE?

A
  • venous thromboembolic disease
  • spectrum of PE and DVT combined
101
Q

Pulmonary Embolism

anatomic locations of PE

A
  • move beyond bifurcation to smaller branches of pulm artery (lobar, segmental, subsegmental branches)
  • Saddle embolus: at the bifurcation of the main pulmonary trunk and may extend into the R or L main pulm artery
102
Q

Pulmonary Embolism

how does PE lead to R heart strain?

A
  • V/Q mismatch (blood pumped from RV to pulm arteries cannot pass the clot)
  • increased pulm artery pressure
  • increased pulm vascular resistance
  • R sided heart strain
103
Q

Pulmonary Embolism

pathophys of pulmonary infarction

A
  • associated w/ small emboli in the segmental and subsegmental branches causing ischemia of the lung tissue
  • causes an intense inflammatory response which leads to vasoconstriction and bronchoconstriction in the nearby areas
  • this further decreases blood flow (Q) and air flow (V)
  • decreased surfactant production + atelectasis leads to shunting (perfusion w/out ventilation) and worsens V/Q mismatch
104
Q

Pulmonary Embolism

pathophys behind d-dimer testing

A
  • > 95% sensitivity when negative (rules out VTE, pos cannot definitively dx)
  • d-dimer is a byproduct of crosslinked fibrin degradation which indicates thrombus breakdown
  • specificity of d-dimer decreases w/ age
105
Q

how to evaluate heparin? warfarin?

A
  • Heparin: PTT
  • Warfarin: PT
106
Q

Pulmonary Embolism

why should warfarin not be used?

A

warfarin causes a brief period of hypercoagulability that occurs when starting it

107
Q

Pulmonary Embolism

contraindications to anti-coag tx

4

A
  1. active bleeding
  2. acute intracranial hemorrhage
  3. major trauma
  4. severe bleeding disorders
108
Q

Pulm Nodules

what are benign causes?

A
  • Granulomatous infection: blastomycosis, histoplasmosis, TB
  • Benign tumors: lipoma, fibroma, hamartoma
  • Vascular lesion: pulm arteriovenous malformation
  • Inflammatory lesions: rheumatoid nodules, sarcoidosis
  • Infection: abscess, aspergillosis
109
Q

Pulm Nodules

what are malignant causes?

A
  • Primary lung cancer: adenocarcinoma, squamous cell carcinoma
  • Lung metastases: melanoma, sarcoma, carcinomas of breast/colon/kidney/testicles
  • Carcinoid tumors
110
Q

Coronaviruses

modes of transmission

2

A
  1. fecal oral
  2. respiratory droplets
111
Q

Coronaviruses

pathophys of respiratory transmission

A
  • inhaled
  • travels down into bronchus
  • goes into alveoli and infects them
112
Q

Coronaviruses

3 types of alveolar cells & their jobs/pathophys of coronavirus infection

A
  1. Type 1 pneumocytes: gas exchange, displays ACE 2 receptor
  2. Type 2 pneumocytes: type that secretes surfactant
  3. macrophages: release cytokines (intracellular messangers- IL-6, IL-8, TNF-alpha which recruit additional immune system cells) which makes capillaries more leaky allowing plasma (WBCs) in to the alveoli.
113
Q

Coronaviruses

what type of virus are coronaviruses

A

positive sense RNA virus- Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell.

virus doesn’t have to do anything to replicate

114
Q

Coronaviruses

MERS pathophys

A
  • stay away from camels
  • MERS binds DPP4 receptor of the lower resp tract of lungs
115
Q

Lung Cancers

pathophys

A
  • exposure to carcinogens drives acquired oncogenic mutations which allow cancerous cells to proliferate
116
Q

Lung Cancers

pathophys of adenocarcinoma

A
  • most common of lung cancers
  • peripheral tissue
  • arises from cells that line the alveoli and produce mucus
117
Q

Lung Cancers

squamous cell carcinoma pathophys

A
  • 20% of lung cancers
  • central tissue
  • arises from squamous cells which line the proximal tracheobronchial tree
118
Q

Lung Cancers

large cell carcinoma pathophys

A
  • rare
  • can affect peripheral or central tissue
119
Q

Lung Cancers

small cell lung carcinoma

A
  • 15% of lung cancers, SMOKERS
  • central tissue
  • begins in main bronchi
120
Q

Lung Cancers

describe paraneoplastic syndrome

A

set of signs/sx that can occur from underlying cancers as a result of hormone secretion from cancers

121
Q

Lung Cancers

Small cell carcinoma paraneoplastic syndrome

A
  • secrete adrenocorticotrophic hormone (ACTH): release of cortisol from adrenals, Cushing syndrome (high blood glucose, HTN, hyponatremia)
  • secrete antidiuretic hormone (ADH): water retention, pt will have edema, HTN, concentrated urine
122
Q

Lung Cancers

Large cell carcinoma paraneoplastic syndrome

A
  • can secrete beta-human chorionic gonadotropin (HCG- preg)
123
Q

Lung Cancers

Squamous cell carcinoma paraneoplastic syndrome

A
  • secrete parathyroid hormone (PTH): depletes calcium from bone causing them to be brittle, increased blood calcium”
124
Q

Lung Cancers

which nerves can be encroached on from cancers?

A
  • recurrent laryngeal nerve: hoarseness
  • phrenic nerve: diaphragmatic paralysis (nerves C3, C4, C5 form phrenic nerve)
125
Q

Lung Cancers

define components of horners syndrome

A
  • ptosis: dropping of upper eyelid due to paralysis or disease
  • miosis: excessive constriction of the pupil of the eye
  • anhidrosis: inability to sweat on one side
126
Q

Lung Cancers

CXR findings that increase suspicion for malignancy

6

A
  • new or enlarging focal lesion (coin lesion)
  • pleural effusion
  • pleural thickening
  • enlarged hilar/paratracheal lymph nodes
  • tracheobronchial narrowing
  • segmental or lobar atelectasis
127
Q

Lung Cancers

what do most cancers use for staging? what about small cell lung cancer?

A
  • most: Tumor, lymph nodes, metastases (TNM)
  • SCLC: limited, prognosis
128
Q

Lung Cancer Screenings

benefits

2

A
  • early detection leading to more effective tx and better prognosis
  • favorable associated w/ smoking cessation
129
Q

Lung Cancer Screenings

risks

4

A
  • high false pos rate
  • leads to unnecessary bx or surgery
  • increased radiation exposure
  • mental distress
130
Q

Coccidioidomycosis

60 yr old male when vacationing in New Mexico and participated in a archeological dig. What pneumonia is he presenting with?

A

coccidiodomycosis pneumia

131
Q

Coccidioidomycosis

define arthroconidia

A

type of fungal spore produced by segmentation of pre-existing fungal hyphae

132
Q

Coccidioidomycosis

what is disseminated infection defined as?

2 things

A
  • defined as disease outside thoracic cavity
  • AIDS defining illness
133
Q

Histoplasmosis Pneumonia

what does mold in the cold, yeast in the heat mean?

A

fungus exists as a mold at low temps and a yeast at high temps

134
Q

Obstructive Sleep Apnea

risk factor for children?

A

enlarged tonsils closing off airway

2-6 yrs

135
Q

Obstructive Sleep Apnea

primary causes of this in adults

A
  • obesity
  • older age
  • African american
136
Q

Obstructive Sleep Apnea

pathophys

A
  • pt experiences apneic and hyponeic episodes which
  • increases levels of arterial CO2 levels (hypercapnia) which
  • stimulates resp efforts against the narrowed upper airway until the individual wakes up
137
Q

Obstructive Sleep Apnea

pathophys of this leading to secondary tachycardia & HTN

A
  • increased resp efforts achieved by sympathetic stimulation which increases HR and BP
138
Q

Obstructive Sleep Apnea

pathophys of this leading to cor pulmonale

A
  • reduced airflow results in pulmonary hypoxia which triggers pulmonary vasoconstriction causing pulmonary HTN
  • pulm HTN can lead to R sided HF (cor pulmonale)
139
Q

Obstructive Sleep Apnea

key muscles for dilating the upper airway?

A
  • genioglossus (CN XII)
  • geniohyoid (CN I)
140
Q

Obstructive Sleep Apnea

most common site of collapse of airway

A

velum/base of tongue

141
Q

Obstructive Sleep Apnea

describe mallampati score

A

the amount of mouth opening to the size of the tongue

142
Q

Obstructive Sleep Apnea

CPAP vs BiPAP

A
  • CPAP: continuous pos airway pressure forces air in to keep the airway open (same pressure always)
  • BiPAP: provides higher pressure during inhalation and a lower one during exhalation
143
Q

Obesity Hypoventilation Syndrome

hypercapnic ventilatory response

A
  • increased pCO2 usually is part of a negative feedback loop to increase alveolar ventilation
  • central/peripheral chemoreceptors sense and respond to hypercapnia which increases the depth and frequency of breathing
144
Q

Obesity Hypoventilation Syndrome

hypercapnic ventilatory response in OHS pts

A
  • diminished resp drive
  • structural and functional resp impairment
  • sleep-related breathing alterations
  • elevated leptin levels
145
Q

Obesity Hypoventilation Syndrome

describe role/function of Leptin

A
  • peptide hormone released from adipose tissue (more leptin = more fat)
  • functions: regulates appetite, energy homeostasis, stimulatory effect on ventilatory response to CO2
  • in OHS: pts have higher leptin but are not sensitive to it, so there is reduced response to CO2
146
Q

Neonatal Respiratory Distress Syndrome

pathophys of prematurity causing this

A
  • lack of mature type II alveolar cells leads to insufficient surfactant production
  • different lipid and protein composition of surfactant in an immature lung leads to less surfactant
147
Q

Neonatal Respiratory Distress Syndrome

pathophys of surfactant inactivation causing this

A
  • meconium in the sac or blood in the alveoli
  • oxidative and mechanical stress from mech vent
148
Q

Neonatal Respiratory Distress Syndrome

pathophys for maternal DM causing this

A
  • materal hyperglycemia causes fetal hyperglycemia
  • increased insulin antagonizes the action of cortisol, delaying lung surfactant production
149
Q

Neonatal Respiratory Distress Syndrome

pathophys of scheduled C-section causing this (NO LABOR)

A
  • absence of labor = decreased cortisol production
  • altered fluid clearance from fetal lung compared w/ vaginal delivery
150
Q

Neonatal Respiratory Distress Syndrome

describe normal fetal lungs

A
  • not functional for gas exchange and are filled w/ amniotic fluid
  • placenta serves as fetus’s resp organ
151
Q

Neonatal Respiratory Distress Syndrome

fetal surfactant

A
  • lipid dense secretion
  • appears between 28-32 wks and surges after 36 wks
  • reduces surface tension in alveoli which prevents alveolar collapse at end of expiration
152
Q

Neonatal Respiratory Distress Syndrome

Fetal blood flow

A
  • enters through umbilical vein
  • liver
  • ductus venosus –> IVC
  • RA
  • foramen ovale –> LA
  • LV
  • aorta
  • brain/rest of body
  • back to mom via umbilical artery
153
Q

Neonatal Respiratory Distress Syndrome

first shunt to close?

A

foramen ovale

154
Q

Neonatal Respiratory Distress Syndrome

why don’t premature lungs work

A
  • deficient surfactant increases surface tension
  • increased pressure is required for alveolar expansion
155
Q

Croup

differentiate:
* Cheyne-Stokes
* Kussmaul breathing
* Orthopnea

A
  • CS: increase in depth of ventilation followed by periods of no breathing or apnea
  • Kussmaul: increased depth of ventilation but rate is rapid
  • Orthopnea: difficulty in respiration occuring on lying horiontal, but improves w/ sitting/standing
156
Q

Croup

aka

A

laryngotracheobronchitis

157
Q

Croup

pathophys

A
  • pathogen infects nasal and pharyngeal mucosal epithelium via aerosolized droplets
  • infection then spreads to the larynx and trachea via resp epithelium
  • infection then triggers the infiltration of WBCs leading to edema within trachea/larynx/bronchi and partially obstructs the airway
158
Q

Croup

what is Hoover’s sign?

A

inward movement of lower rib cage during inspiration

159
Q

Acute Bronchiolitis

pathophys

A
  • virus enters epithelial cells of terminal bronchioles
  • inoculation leads to inflammation causing edema, mucus secretion, and epithemlium sloughing
  • swelling leads to the narrowing of airways which causes atelectasis
  • alveoli can over-inflate and become trapped with air
160
Q

Pertussis

who gets erythromycin as PEP?

A

EVERYONE

161
Q

Interstitial Lung Diseases

what pattern on spirometry?

A
  • restrictive
  • Normal FEV1/FVC ratio
  • Reduction in TLC below 80% of predicted value
  • decreased DLCO
162
Q

Interstitial Lung Diseases

generally describe

A

collection of disorders that involves inflammation and scarring (fibrosis) of the lung interstitum

163
Q

Interstitial Lung Diseases

what is the lung interstituim

A

the space between the capillary endothelium and alveolar epithelium

164
Q

Idiopathic Pulmonary Fibrosis

pathophys

A
  • recurrent alveolar epithelial damange leads to type I pneumocyte release of transforming growth factor beta1
  • this leads to proliferation of type II pneumocytes which simulates fibroblasts
  • fibroblasts develop into myofibroblasts which secrete reticular fibers and elastic fibers
  • There is proliferation of myofibroblasts which leads to collagen accumulation (restrictive lung disease, decreased gas exchange)
165
Q

Idiopathic Pulmonary Fibrosis

what do reticular fibers do?

A

collagen which provides structural strength

166
Q

Idiopathic Pulmonary Fibrosis

what do elastic fibers do?

A

accumulation of collagen leads to thickening of interstitital layer

167
Q

Sarcoidosis

pathophys

5 steps

A
  • phagocytosis of new antigen by antigen-presenting cells (macrophages/dendritic cells)
  • activated macrophages then present the antigen to helper T cells
  • activated T cells and macrophages release inflammatory mediators (Th1 response): IL-2, interferon gamma, TNF, cytokines
  • inflammatory mediators cause macrophages to fuse into multi-nucleated giant cells which wall off the antigens forming non-caseating granuloma formation
  • fibroblasts are recruited and surround granulomas leading to fibrosis
168
Q

Pulm HTN

define

A
  • increased BP in pulmonary circulation
  • mean pulm arterial: >25 mmHg at rest or >30 mmHg during exercise
  • normal pressure: 14-20 mmHg
169
Q

which group of pulmonary HTN cannot lead to R sided HF

groups 1-5

A
  • Group 2- L sided problem
  • Group 1- some congenital problems
170
Q

Cor Pulmonale & Pulm HTN

hypoxic pulm vasoconstriction pathophys

A

limits blood flow to hypoxic alveoli, low oxygen leads to pulm vasoconstriction and diversion of blood to better oxygenated alveoli

171
Q

Cor Pulmonale & Pulm HTN

pulmonary vascular remodeling pathophys

A

vascular alterations occur: neomuscularization of arterioles, intimal thickening, medial hypertrophy

172
Q

Cor Pulmonale & Pulm HTN

what do hypoxic pulm vasoconstriction and pulm vascular remodeling lead to ? pathophys of that?

A
  • leads to pulm HTN
  • as resistance increases, pulm artery pressure and RV afterload also increase
  • RV adapts to slowly increased pulm artery pressure by dilation which leads to hypertrophy
  • eventually causes RV dysfunction and failure
173
Q

Cor Pulmonale & Pulm HTN

differentiate S3 and S4

A
  • S3: ventricular volume overload and HF, “ventricular gallop”, occurs during early diastole
  • S4: increased resistance to ventricular filling due to decreased ventricular compliance, “atrial gallop”, occurs during late diastole, ALWAYS AN ABNORMAL FINDING

CMT (72 decks)

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