Pulm Pathophys Flashcards
1
Q
Resp System Anatomy
what is in upper respiratory tract? lower?
A
- upper: nose, pharynx, larynx
- lower: trachea, bronchi, lungs
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
3
Q
Resp System Anatomy
describe trachea
A
- continuous superiorly w/ larynx and inferiorly becomes bronchial tree
- cartilaginous rings support structure
4
Q
Resp System Anatomy
differentiate R and L main bronchi
A
- R: wider, shorter, more vertical (more frequent aspiration)
- L: longer
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
6
Q
Resp System Anatomy
which pneumocytes secrete surfactant
A
type II
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
8
Q
Resp System Anatomy
location/purpose of hilum?
A
- located between T5 and T7
- passageway for the pulm neurovasculature
9
Q
Resp System Anatomy
differentiate R and L lungs
A
- R: 3 lobes, 2 fissures
- L: 2 lobes, 1 fissure, cardiac notch
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
11
Q
Resp System Anatomy
what is pleural cavity
A
space between visceral pleura and parietal pleura
12
Q
Resp System Anatomy
purpose of pleural cavity
A
surface tension of fluid keeps lungs expanded and in contact w/ thoracic wall
13
Q
Resp System Anatomy
which side of diaphragm is up higher?
A
R due to liver
14
Q
Resp System Anatomy
physiology of inspiration
A
- contraction of external intercostal muscles
- contraction of diaphragm
15
Q
Resp System Anatomy
physiology of exhalation
A
- relaxation of external intercostal muscles
- relaxaation of diaphragm
16
Q
Resp System Anatomy
what types of pressure affect ventilation
A
- atmospheric
- intra-alveolar
- interpleural
17
Q
Resp System Anatomy
what is respiratory rate
A
- total number of breather per minute
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
19
Q
Resp System Anatomy
define eupnea
A
normal, relaxed, quiet breathing
12-15 breaths/min
20
Q
Resp System Anatomy
define dyspnea
A
labored, gasping breathing
SOB
21
Q
Resp System Anatomy
define apnea
A
temporary cessation of breathing
22
Q
Resp System Anatomy
define respiratory arrest
A
permanent cessation of breathing
23
Q
Resp System Anatomy
define hyperpnea
A
increased rate and depth of breathing
24
Q
Resp System Anatomy
define hyperventilation
A
increased pulm ventilation in excess of metabolic demand (anxiety)
25
# Resp System Anatomy
define hypoventilation
reduced pulm ventilation leading to increased CO2 concentrations
26
# Resp System Anatomy
define:
* tidal volume
* residual volume
* expiratory reserve volume
* inspiratory reserve volume
* 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
27
# Resp System Anatomy
differentiate total lung capacity and vital capacity
* 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
28
# Resp System Anatomy
describe concept of V/Q coupling
* 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
29
# Resp System Anatomy
define tissue hypoxia. What does this stimulate?
* low oxygen availability to the tissues
* sensed by the kidneys, stimulates RBC synthesis through release of EPO
30
# Resp System Anatomy
define hypoxemia
* low oxygen in blood
31
# Resp System Anatomy
define hypercapnia
* increased CO2 in blood
32
# Influenza
what are the two glycoproteins?
* hemaagglutinin
* neuraminidase
33
# Influenza
describe hemagglutinin (HA)
attaches to sialic acid containing receptors on respiratory epithelial cells
34
# Influenza
describe neuraminidase
cleaves newly formed virions off the sialic acid containing receptor allowing the virus to exit cells
35
# Influenza
differentiate M1 and M2
* M1: involved in virion assembly
* M2: involved in viral uncoating within the respiratory epithelial cells
36
# Influenza
describe nucleoprotein
helps distinguish between 3 types of influenza viruses (A, B, C)
37
# Influenza
define antigenic drift
* 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
38
# Influenza
describe antigenic shift
* pandemic
* 2+ strains of a virus combine to form a new subtype that is radically different; limited or no prior immunity
39
# Influenza
MOA of neuraminidase inhibitors
interfere w/ release of influenza virus from infected cells and thus half spread of infection
40
# Asthma
how are these asthmas mediated:
* extrinsic
* intrinsic
* E: immune
* I: non-immune
41
# Asthma
what is Samter's Triad?
* ASA or NSAID use
* Nasal Polyp
* Asthma
42
# Asthma
pathophys of extrinsic asthma
* 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)
43
# Asthma
pathophys of intrinsic asthma
* 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
44
# COPD
describe
chronic lung disease characterized by progressive airflow limitation resulting from airway disease and/or parenchymal destruction
45
# COPD
subtypes
combination of chronic bronchitis + emphysema
46
# COPD
pathophys of chronic bronchitis
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
47
# COPD
pathophys of emphysema
* inflammatory response leads to activated neutrophils releasing proteases
* protease activity exceeds antiprotease activity which causes tissue destruction (alveoli has less recoil, more compliance)
48
# COPD
consequences of increased alveolar compliance and decreased recoil?
* airway closure during expiration leading to obstruction
* air trapping leading to lung hyperinflation
49
# COPD
pathophys of healthy lungs
* proteases break down elastin and connective tissue as part of normal tissue repair
* antiproteases which act to balance protease activity
50
# COPD
2 morphologic patterns associated w/ COPD
* centriacinar emphysema
* panacinar emphysema
51
# COPD
describe centriacinar emphysema
* 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
52
# COPD
describe the panacinar emphysema pattern
* 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)
53
# COPD
what subtype is associated with weight gain? with weight loss?
* gain: bronchitis
* loss: emphysema
54
# COPD
why does barrel chest develop?
hyperinflation in the lungs
| (later stages of disease)
55
# COPD
differentiate central and peripheral cyanosis
* central: lips/tongue; relates to poor blood oxygenation in the lungs
* peripheral: extremities/fingers; oxygen-depleted peripheral blood
56
# COPD
define clubbing
bulbous enlargement of the distal fingertip and increased longitudinal and transverse nail plate curvature
57
# COPD
Schamroth sign
loss of diamond shaped window normally visible when the dorsal surfaces of the terminal phalanges of corresponding fingers from opposite hands are placed together
58
# COPD
Lovibond's angle
angle located at the junction between the nail plate and proximal nail fold, which is normall less than 160 degrees
59
# COPD
describe "blue bloater"
| 6 components
* associated with chronic bronchitis
* put on weight
* frequent, productive cough
* peipheral edema
* cyanosis
* wheezing/ronchi
60
# COPD
describe "pink puffer" phenotype
| 8 components
* classically emphysema
* wt loss/thin
* barrel chest
* infrequent cough
* pursed lip breathing
* accessory muscle use
* tripod positioning
* hyperresonant chest
61
# COPD
what state are COPD patients usually in?
| relating to ABG
* respiratory acidosis
* but pH near normal due to renal compensation (increased serum HCO3)
62
# COPD
describe blebs
* 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
63
# COPD
describe bulla
formed from blebs that become larger/come together
64
# COPD
advantage/disadvantage of SABA/SAMA
* advantage: rapid onset to improve sx and lung function
* disadvantage: relatively short duration of action
65
# COPD
criteria for beginning Group E pt on ICS
* eosinophil count > 300 cells/microL
* features of asthma-COPD overlap
66
# COPD
most commonly identified bacteria in acute exacerbations of COPD?
| 4
1. Moraxella catarrhalis
2. Streptococcus pnemoniae
3. Haemophilus influenzae
4. Pseudomonas aeruginosa
67
# COPD
when to do noninvasive ventilation? invasive ventilation?
* noninvasive: hypercapnia, hypoxemia; significant effort to breathe
* invasive: severe respiratory failure; may be difficult to wean pts with severe COPD
68
# Cystic Fibrosis
normal functioning of CFTR gene
* codes for CFTR protein
* which regulates chloride, sodium, and bicarb transport across epithelial membranes
* water is attracted to the secretions (sodium) which thins
69
# Cystic Fibrosis
pathophys of mutated CFTR gene
* 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
70
# Cystic Fibrosis
what is CFTR
cystic fibrosis transmembrane conductance regulator
71
# Cystic Fibrosis
pathophys of cystic fibrosis
* 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
# Cystic Fibrosis
pathophys of:
* male infertility
* female infertility
* male: obstructive azoospemia due to bilateral aplasia/atresia of vas deferens
* female: viscous cervical mucus, amenorrhea
73
# Cystic Fibrosis
mnemonic to remember common clinical features?
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
# Cystic Fibrosis
differentiate aplasia and atresia
* aplasia: failure of an organ or tissue to develop or function normally
* atresia: absence or abnormal narrowing of an opening or passage
75
# Cystic Fibrosis
describe role of IRT in cystic fibrosis
* pancreatic enzyme released when there is pancreatic damage
* if elevated: could indicate mutation analysis of CFTR
76
# Pneumonia- General
pathophys
* 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
# Pneumonia- General
inflammatory response to lobar pneumonia
* accumulation of neutrophils and plasma exudate from capillaries into alveolar space to a lung lobe
78
# Pneumonia- General
inflammatory response of interstitial pneumonia
* accumulation of infiltrates into alveolar walls
* clinically: dry cough, hypoxiemia, dyspnea
79
# Pneumonia Severity Index (PSI)
purpose?
* estimates mortality risk
* helps to guide decisions regarding hospitalization
80
# Pneumonia Severity Index (PSI)
what are the classes? how do you manage them?
* 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
# CA- Pneumonia
CURB-65 what is evaluated for points?
* 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
# CA- Pneumonia
how to manage pts based on CURB-65 scoring?
* 0-1 points: manage outpatient
* 2 points: short inpatient stay/supervised outpatient stay
* 3-5 points: manage inpatient always, assess for ICU.
82
# CA- Pneumonia
when to consider admission to ICU?
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
# ARDS
3 phases of ARDS?
1. exudative
2. proliferative
3. fibrotic
84
# ARDS
pathophys of exudative phase
*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
# ARDS
pathophys of proliferative phase
* 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
# ARDS
fibrotic phase pathophys
* abnormal deposition of collagen in the alveolar ducts and interstitial membranes by fibroblasts
* lung scarring: stiff lungs --> restrictive lung disease
86
# Pleural Effusion
describe role/pathophys of pleural fluid
* 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
# Pleural Effusion
what does pleural effusion result from?
* overproduction of fluid
* inability of lymphatic system to remove fluid as it is produced
88
# Pleural Effusion
4 starling forces
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
# Pleural Effusion
classifications
* 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
# 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
* pneumonia
* TB
* malignancy
* mesothelioma
* CHF
* connective tissue disease
91
# Pleural Effusion
"if they are effusing in TWO.... think ?"
autoimmune
92
# Pleural Effusion
why can severe effusion lead to cardiac obstructive shock?
fluid drains into right atrium
93
# Pneumothorax
pathophys
* 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
# Pneumothorax
tension pneumothorax pathophys
* 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
# Pneumothorax
mnemonic for sx of tension pneumothorax
| P-THORAX
* 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
# Pneumothorax
E-FAST what areas are visualized
* 1: RUQ, hepatorengal recess
* 2: LUQ, perisplenic area
* 3: Pelvis, subrapubic window
* 4: Cardiac, subxiphoid window
* 5: Lungs
97
# Pneumothorax
describe needle decompression
* 14 of 16 gauge needle inserted through chest wall
* 2nd ICS in MCL
* 5th ICS in MAL
* follow decompression w/ chest tube placement
98
# Pneumothorax
describe chest tube thoracostomy
* catheter inserted into chest wall
* placed in the 4th to 5th ICS at MAL
99
# Pulmonary Embolism
3 primary contributing factors?
Virchow's Triad
* circulatory stasis
* hypercoagulability
* vascular endothelial damage
100
# Pulmonary Embolism
what is VTE?
* venous thromboembolic disease
* spectrum of PE and DVT combined
101
# Pulmonary Embolism
anatomic locations of PE
* 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
# Pulmonary Embolism
how does PE lead to R heart strain?
* 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
# Pulmonary Embolism
pathophys of pulmonary infarction
* 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
# Pulmonary Embolism
pathophys behind d-dimer testing
* >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
how to evaluate heparin? warfarin?
* Heparin: PTT
* Warfarin: PT
106
# Pulmonary Embolism
why should warfarin not be used?
warfarin causes a brief period of hypercoagulability that occurs when starting it
107
# Pulmonary Embolism
contraindications to anti-coag tx
| 4
1. active bleeding
2. acute intracranial hemorrhage
3. major trauma
4. severe bleeding disorders
108
# Pulm Nodules
what are benign causes?
* Granulomatous infection: blastomycosis, histoplasmosis, TB
* Benign tumors: lipoma, fibroma, hamartoma
* Vascular lesion: pulm arteriovenous malformation
* Inflammatory lesions: rheumatoid nodules, sarcoidosis
* Infection: abscess, aspergillosis
109
# Pulm Nodules
what are malignant causes?
* Primary lung cancer: adenocarcinoma, squamous cell carcinoma
* Lung metastases: melanoma, sarcoma, carcinomas of breast/colon/kidney/testicles
* Carcinoid tumors
110
# Coronaviruses
modes of transmission
| 2
1. fecal oral
2. respiratory droplets
111
# Coronaviruses
pathophys of respiratory transmission
* inhaled
* travels down into bronchus
* goes into alveoli and infects them
112
# Coronaviruses
3 types of alveolar cells & their jobs/pathophys of coronavirus infection
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
# Coronaviruses
what type of virus are coronaviruses
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
# Coronaviruses
MERS pathophys
* stay away from camels
* MERS binds DPP4 receptor of the lower resp tract of lungs
115
# Lung Cancers
pathophys
* exposure to carcinogens drives acquired oncogenic mutations which allow cancerous cells to proliferate
116
# Lung Cancers
pathophys of adenocarcinoma
* most common of lung cancers
* peripheral tissue
* arises from cells that line the alveoli and produce mucus
117
# Lung Cancers
squamous cell carcinoma pathophys
* 20% of lung cancers
* central tissue
* arises from squamous cells which line the proximal tracheobronchial tree
118
# Lung Cancers
large cell carcinoma pathophys
* rare
* can affect peripheral or central tissue
119
# Lung Cancers
small cell lung carcinoma
* 15% of lung cancers, SMOKERS
* central tissue
* begins in main bronchi
120
# Lung Cancers
describe paraneoplastic syndrome
set of signs/sx that can occur from underlying cancers as a result of hormone secretion from cancers
121
# Lung Cancers
Small cell carcinoma paraneoplastic syndrome
* 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
# Lung Cancers
Large cell carcinoma paraneoplastic syndrome
* can secrete beta-human chorionic gonadotropin (HCG- preg)
123
# Lung Cancers
Squamous cell carcinoma paraneoplastic syndrome
* secrete parathyroid hormone (PTH): depletes calcium from bone causing them to be brittle, increased blood calcium"
124
# Lung Cancers
which nerves can be encroached on from cancers?
* recurrent laryngeal nerve: hoarseness
* phrenic nerve: diaphragmatic paralysis (nerves C3, C4, C5 form phrenic nerve)
125
# Lung Cancers
define components of horners syndrome
* 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
# Lung Cancers
CXR findings that increase suspicion for malignancy
| 6
* new or enlarging focal lesion (coin lesion)
* pleural effusion
* pleural thickening
* enlarged hilar/paratracheal lymph nodes
* tracheobronchial narrowing
* segmental or lobar atelectasis
127
# Lung Cancers
what do most cancers use for staging? what about small cell lung cancer?
* most: Tumor, lymph nodes, metastases (TNM)
* SCLC: limited, prognosis
128
# Lung Cancer Screenings
benefits
| 2
* early detection leading to more effective tx and better prognosis
* favorable associated w/ smoking cessation
129
# Lung Cancer Screenings
risks
| 4
* high false pos rate
* leads to unnecessary bx or surgery
* increased radiation exposure
* mental distress
130
# Coccidioidomycosis
60 yr old male when vacationing in New Mexico and participated in a archeological dig. What pneumonia is he presenting with?
coccidiodomycosis pneumia
131
# Coccidioidomycosis
define arthroconidia
type of fungal spore produced by segmentation of pre-existing fungal hyphae
132
# Coccidioidomycosis
what is disseminated infection defined as?
| 2 things
* defined as disease outside thoracic cavity
* AIDS defining illness
133
# Histoplasmosis Pneumonia
what does mold in the cold, yeast in the heat mean?
fungus exists as a mold at low temps and a yeast at high temps
134
# Obstructive Sleep Apnea
risk factor for children?
enlarged tonsils closing off airway
| 2-6 yrs
135
# Obstructive Sleep Apnea
primary causes of this in adults
* obesity
* older age
* African american
136
# Obstructive Sleep Apnea
pathophys
* 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
# Obstructive Sleep Apnea
pathophys of this leading to secondary tachycardia & HTN
* increased resp efforts achieved by sympathetic stimulation which increases HR and BP
138
# Obstructive Sleep Apnea
pathophys of this leading to cor pulmonale
* reduced airflow results in pulmonary hypoxia which triggers pulmonary vasoconstriction causing pulmonary HTN
* pulm HTN can lead to R sided HF (cor pulmonale)
139
# Obstructive Sleep Apnea
key muscles for dilating the upper airway?
* genioglossus (CN XII)
* geniohyoid (CN I)
140
# Obstructive Sleep Apnea
most common site of collapse of airway
velum/base of tongue
141
# Obstructive Sleep Apnea
describe mallampati score
the amount of mouth opening to the size of the tongue
142
# Obstructive Sleep Apnea
CPAP vs BiPAP
* 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
# Obesity Hypoventilation Syndrome
hypercapnic ventilatory response
* 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
# Obesity Hypoventilation Syndrome
hypercapnic ventilatory response in OHS pts
* diminished resp drive
* structural and functional resp impairment
* sleep-related breathing alterations
* elevated leptin levels
145
# Obesity Hypoventilation Syndrome
describe role/function of Leptin
* 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
# Neonatal Respiratory Distress Syndrome
pathophys of prematurity causing this
* 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
# Neonatal Respiratory Distress Syndrome
pathophys of surfactant inactivation causing this
* meconium in the sac or blood in the alveoli
* oxidative and mechanical stress from mech vent
148
# Neonatal Respiratory Distress Syndrome
pathophys for maternal DM causing this
* materal hyperglycemia causes fetal hyperglycemia
* increased insulin antagonizes the action of cortisol, delaying lung surfactant production
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# Neonatal Respiratory Distress Syndrome
pathophys of scheduled C-section causing this (NO LABOR)
* absence of labor = decreased cortisol production
* altered fluid clearance from fetal lung compared w/ vaginal delivery
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# Neonatal Respiratory Distress Syndrome
describe normal fetal lungs
* not functional for gas exchange and are filled w/ amniotic fluid
* placenta serves as fetus's resp organ
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# Neonatal Respiratory Distress Syndrome
fetal surfactant
* 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
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# Neonatal Respiratory Distress Syndrome
Fetal blood flow
* enters through umbilical vein
* liver
* ductus venosus --> IVC
* RA
* foramen ovale --> LA
* LV
* aorta
* brain/rest of body
* back to mom via umbilical artery
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# Neonatal Respiratory Distress Syndrome
first shunt to close?
foramen ovale
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# Neonatal Respiratory Distress Syndrome
why don't premature lungs work
* deficient surfactant increases surface tension
* increased pressure is required for alveolar expansion
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# Croup
differentiate:
* Cheyne-Stokes
* Kussmaul breathing
* Orthopnea
* 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
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# Croup
aka
laryngotracheobronchitis
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# Croup
pathophys
* 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
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# Croup
what is Hoover's sign?
inward movement of lower rib cage during inspiration
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# Acute Bronchiolitis
pathophys
* 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
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# Pertussis
who gets erythromycin as PEP?
EVERYONE
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# Interstitial Lung Diseases
what pattern on spirometry?
* restrictive
* Normal FEV1/FVC ratio
* Reduction in TLC below 80% of predicted value
* decreased DLCO
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# Interstitial Lung Diseases
generally describe
collection of disorders that involves inflammation and scarring (fibrosis) of the lung interstitum
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# Interstitial Lung Diseases
what is the lung interstituim
the space between the capillary endothelium and alveolar epithelium
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# Idiopathic Pulmonary Fibrosis
pathophys
* 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)
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# Idiopathic Pulmonary Fibrosis
what do reticular fibers do?
collagen which provides structural strength
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# Idiopathic Pulmonary Fibrosis
what do elastic fibers do?
accumulation of collagen leads to thickening of interstitital layer
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# Sarcoidosis
pathophys
| 5 steps
* 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
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# Pulm HTN
define
* increased BP in pulmonary circulation
* mean pulm arterial: >25 mmHg at rest or >30 mmHg during exercise
* normal pressure: 14-20 mmHg
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which group of pulmonary HTN cannot lead to R sided HF
| groups 1-5
* Group 2- L sided problem
* Group 1- some congenital problems
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# Cor Pulmonale & Pulm HTN
hypoxic pulm vasoconstriction pathophys
limits blood flow to hypoxic alveoli, low oxygen leads to pulm vasoconstriction and diversion of blood to better oxygenated alveoli
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# Cor Pulmonale & Pulm HTN
pulmonary vascular remodeling pathophys
vascular alterations occur: neomuscularization of arterioles, intimal thickening, medial hypertrophy
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# Cor Pulmonale & Pulm HTN
what do hypoxic pulm vasoconstriction and pulm vascular remodeling lead to ? pathophys of that?
* 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
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# Cor Pulmonale & Pulm HTN
differentiate S3 and S4
* 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
