Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Resp System Anatomy

describe trachea

A
  • continuous superiorly w/ larynx and inferiorly becomes bronchial tree
  • cartilaginous rings support structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Resp System Anatomy

differentiate R and L main bronchi

A
  • R: wider, shorter, more vertical (more frequent aspiration)
  • L: longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Resp System Anatomy

which pneumocytes secrete surfactant

A

type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Resp System Anatomy

location/purpose of hilum?

A
  • located between T5 and T7
  • passageway for the pulm neurovasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Resp System Anatomy

differentiate R and L lungs

A
  • R: 3 lobes, 2 fissures
  • L: 2 lobes, 1 fissure, cardiac notch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Resp System Anatomy

what is pleural cavity

A

space between visceral pleura and parietal pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Resp System Anatomy

purpose of pleural cavity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Resp System Anatomy

which side of diaphragm is up higher?

A

R due to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Resp System Anatomy

physiology of inspiration

A
  • contraction of external intercostal muscles
  • contraction of diaphragm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Resp System Anatomy

physiology of exhalation

A
  • relaxation of external intercostal muscles
  • relaxaation of diaphragm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Resp System Anatomy

what types of pressure affect ventilation

A
  • atmospheric
  • intra-alveolar
  • interpleural
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Resp System Anatomy

what is respiratory rate

A
  • total number of breather per minute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Resp System Anatomy

define eupnea

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Resp System Anatomy

define dyspnea

A

labored, gasping breathing
SOB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Resp System Anatomy

define apnea

A

temporary cessation of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Resp System Anatomy

define respiratory arrest

A

permanent cessation of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Resp System Anatomy

define hyperpnea

A

increased rate and depth of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Resp System Anatomy

define hyperventilation

A

increased pulm ventilation in excess of metabolic demand (anxiety)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Resp System Anatomy

define hypoventilation

A

reduced pulm ventilation leading to increased CO2 concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Resp System Anatomy

define hypoxemia

A
  • low oxygen in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Resp System Anatomy

define hypercapnia

A
  • increased CO2 in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Influenza

what are the two glycoproteins?

A
  • hemaagglutinin
  • neuraminidase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Influenza

describe hemagglutinin (HA)

A

attaches to sialic acid containing receptors on respiratory epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Influenza

describe neuraminidase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Influenza

differentiate M1 and M2

A
  • M1: involved in virion assembly
  • M2: involved in viral uncoating within the respiratory epithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Influenza

describe nucleoprotein

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Influenza

MOA of neuraminidase inhibitors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Asthma

how are these asthmas mediated:
* extrinsic
* intrinsic

A
  • E: immune
  • I: non-immune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Asthma

what is Samter’s Triad?

A
  • ASA or NSAID use
  • Nasal Polyp
  • Asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

COPD

describe

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

COPD

subtypes

A

combination of chronic bronchitis + emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

COPD

2 morphologic patterns associated w/ COPD

A
  • centriacinar emphysema
  • panacinar emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

COPD

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

A
  • gain: bronchitis
  • loss: emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

COPD

why does barrel chest develop?

A

hyperinflation in the lungs

(later stages of disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

COPD

define clubbing

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

COPD

describe “blue bloater”

6 components

A
  • associated with chronic bronchitis
  • put on weight
  • frequent, productive cough
  • peipheral edema
  • cyanosis
  • wheezing/ronchi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

COPD

describe bulla

A

formed from blebs that become larger/come together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

COPD

advantage/disadvantage of SABA/SAMA

A
  • advantage: rapid onset to improve sx and lung function
  • disadvantage: relatively short duration of action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

COPD

criteria for beginning Group E pt on ICS

A
  • eosinophil count > 300 cells/microL
  • features of asthma-COPD overlap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Cystic Fibrosis

what is CFTR

A

cystic fibrosis transmembrane conductance regulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 (78 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions