CMT > Pulm Pathophys > Flashcards

Pulm Pathophys Flashcards

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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
# 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
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# 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
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# 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
CMT
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