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NPLEX I (2022) > Pulm > Flashcards

Pulm Flashcards

1
Q

what nerve innervates the larynx

A

CN 10

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2
Q

describe paths of sinus drainage

A

sphenoid > ethmoid > maxillary > nasal cavity

frontal > maxillary > nasal cavity

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3
Q

what are the stages of embryologic development of the respiratory tract?

A

Every Pulmonologist Can See Alveoli

Embyronic (wks 4-7)
Pseudoglandular (5-17)
Canalicular (16-25)
Saccular (26-birth)
Alveolar (36 weeks-8 years)
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4
Q

errors at the embryonic stage of development can cause what

A

tracheoesophageal fistula

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5
Q

what stage of embryologic development is respiration capable

A

Canalicular - week 25

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6
Q

what are the types of cells in the respiratory tract?

A 
Club cells:
type I pneumocytes
type II pnemocytes: produce surfactant
alveoalr macrophages (dust cells)
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7
Q

decribe anatomy of the trachea

A

9 cartilage rings

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8
Q

decribe anatomy of the bronchioles

A

smooth muscle

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9
Q

describe the boundaries of the lungs

A

MCL: lung at rib 6, pleura at rib 8
Axillary: Lung 8, pleura 10
CVA: lung 10, pleura 12
Apex of lung 4cm above rib 1

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10
Q

how many of each “type” of rib are there?

A

7 true, 8-10 false, 11 + 12 floating

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11
Q

why does pneumothorax occur?

A

blunt or penetrating chest injury, certain medical procedures, or damage from underlying lung disease. -> loss of vaccum between visceral and parietal layer of lung pleura

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12
Q

describe the circulation of blood in the lungs

A

RV > pulmonary arteries (deoxy) > lung > pulmonary veins (oxy) > LA > aorta > bronchial artery (oxy) > lung tissues > bronchial vein (deoxy) > azygos veins

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13
Q

describe the pathway of air in the lungs

A

trachea > primary bronchi > secondary/lobar bronchi > tertiary/segmental bronchi > bronchioles > terminal bronchioles > respiratory bronchioles > alveoli

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14
Q

what are the different lung volumes?

A

tidal volume: air moving into lungs with each quiet respiration

residual volume: air in lung after max expiration (cant be measured by spirometry)

inspiratory reserve volume (IRV): air that can still be inhaled after normal inspiration

expiratory reserve volume (ERV): air that can still be exhaled after normal expiration

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15
Q

what are the different lung capacities?

A

inspiratory capacity: air that can be inhaled after normal exhalation

functional residual capacity (FRC): volume of gas in lungs after normal expiration

vital capacity (VC): max vol of gas that can be expired after max inspiration

total lung capacity (TLC): vol of gas present in lungs after max inspiration

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16
Q

what are the types of ventilation?

A

minute ventilation (Ve): total vol of gas entering lungs per min

alveolar ventilation (Va): vol of gas that reaches alveoli each min

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17
Q

what is physiologic dead space (Vd)?

A

vol of inspired air that does not take part in gas exchange

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18
Q

what are the two attributes of the lung/chest wall that play a role in ventilation?

A

elastic recoil

compliance

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19
Q

what is elastic recoil? what role does it play in ventilation?

A

the lungs intrinsic nature to deflate with expiration; tendency for lungs to collapse inward and chest wall to spring outward at physiologic baseline

these opposite motinos balance each other and prevent lung collapse

at FRC, airway and alveolar pressures equal atmospheric pressure; intrapleural pressure is neg

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20
Q

what is compliance? what role does it play in ventilation?

A

changes in lung volume for a change in pressure

inversely proportional to wall stiffness (increase in compliance = decrease in stiffness)

increased by surfactant

increased compliance = lung easier to fill

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21
Q

where are the main respiratory centers that control ventilation and perfusion?

A

CNS: medulla

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22
Q

where are the various places the medullary respiratory centers get signals from?

A 
central chemoreceptors 
cerebral cortex
pontine respiratory centers
peripheral chemoreceptors
pulmonary inputs
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23
Q

the respiratory centers in the medulla control what?

A

lung movement; controlled via inspiratory and expiratory neurons (expiratory activated for deep expiration only)

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24
Q

central chemoreceptors role in ventilation control

A

on surface of medulla; detect pH changes in CSF

acidic pH > increased Co\O2

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25
Q

peripheral chemoreceptors role in ventilation control

A

on carotid and aortic bodies; detect pH, CO2, and O2 changes in blood; transmit signal via vagus and glossopharyngeal nerve

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26
Q

what is the relation between CO2/O2 and ventilation control?

A

ventilation (RR) increases with increased need for O2 (during exercise, etc)

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27
Q

what are the respiratory control centers of the medulla and describe their path to control inspiration?

A

dorsal respiratory group (inspiration)
ventral respiratory group (expiration)
pre-botzinger complex (intrinsic rhythm generator)

they interact with pons at pneumotaxic center and apneustic center to inhibit or simtulate inspiration

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28
Q

what do the mechanoreceptors in the lungs do and how?

A

assess mechanical status of lungs via vagus nerve

stretch receptors are activated when lungs are excessibly inflated > triggers inspiration reflex > stops inspiration and prolongs expiration

fibers synapse in cervical and thoracic spine and synapse with motor neurons (phrenic nerves - diaphragm, intercostol nerves - intercostal muscles)

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29
Q

what nerves affect ventilation?

A

PNS: CN10 - constrict bronchioles

Sensory: CN10

SNS (sympathetic chain ganglia): dilate bronchioles

Phrenic N

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30
Q

how are pain, emotion, and voluntary control involved in ventilation control?

A

limbic and hypothalamus send info to respiratory center; pain and emotional state change breathing

voluntary control from the primary motor cortex; communicates directly to the spinal cord, bypassing info from brainstem

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31
Q

how is carbon diozide transported through the body?

A

CO2 enters RBCs from tisues and is converted into 3 forms, where it is transported from tissues to lungs:

HCO3- (most common): via bicarb/chloride transport on RBC membrane

HBCO2: carbaminohemoglobin; CO2 bound to HB at N-terminus of globin (not heme)

dissolved CO2 (least comon)

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32
Q

what is the haldane effect?

A

oxygenation of hemoglobin promotes dissociation of H+ from hemoglobin, then equilibrium shifts toward CO2 formation, which releases CO2 from RBCs

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33
Q

explain the qualities (level of resistance/compliance) of pulmonary circulation

A

low resistance, high compliance system

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34
Q

pulmonary circulation; do oxygen and CO2 diffuse quickly or slowly across alveolar membrane?

A

oxygen diffuses slowly across alveolar membrane

CO2 diffuses rapidly across alveolar membrane

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35
Q

pulmonary diffusion increases with..

A

increased area

larger difference b/w partial pressures

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36
Q

pulmonary diffusion decreases with..

A

decreased area
less diff b/w partial pressures
thicker alveolar wall

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37
Q

pulmonary vascular resistance decreases with…

A 
increased CO
alkalosis, hypocarbia, high FiO2
increased vessel radius (vasodilation)
decreased arterial resistance
decreased blood viscosity (ex: anemia)
decreased vessel length
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38
Q

pulmonary vascular resistance increases with…

A

hypoxia, hypercarbia, acidosis

hypervolemia, polycythemia

hypothermia, atelectasis, increased airway pressure

sympathetic stimulation (ex: a agonists, N2O/ketamine)

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39
Q

during adequate gas exchange what is the ventilation to perfusion ratio?

A

V/Q = 1

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40
Q

in zone 1 (apex of lung) what is the ventilation to perfusion ratio?

A

V/Q increased

V decreases, Q decreases more

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41
Q

in zone 2 (middle of lung) what is the ventilation to perfusion ratio?

A

V/Q decreased

V increases, but Q increases more

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42
Q

what is internal vs external respiration?

A

internal respiration: capillary gas exchange in body tissues

external respiration: bulk flow of air into and out of lungs

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43
Q

what are the contributing factors to alveolar gas exchange?

A

surface area
partial pressure gradients of gasses
matching ventilation and perfusion

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44
Q

explain the relationship between rate of diffusion and partial pressures of blood gasses

A

rate of diffusion of a gas is proportional to sum of partial pressure of the gas mixture

oxygen dissociates more easily from hemoglobin at lower pH

venous blood slighlty more acidic than arterial blood because of CO2

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45
Q

pulmonary circulation; avg pulmonary arterial pressure vs systemic

A

pulmonary arterial pressure: 15mmHg

Systemic: 100mmHg

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46
Q

explain the biochemistry of surfactant

A

phospholipoprotein made by type II alveolar cells

made in saccular and alveolar phases of lung development (final 2 stages; weeks 26-birth)

20% of surfactant complex is protein

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47
Q

explain the role of nitric oxide in the pulmonary system

A

regulates vascular and bronchial tone (stimulates dilation)

formed from amino acid arginine by enzyme nitric oxide synthase

formation requires H4 biopterin as cofactor

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48
Q

what is a common feature of restrictive pulmonary diseases?

A

infiltration of inflammation and scarring of lung parenchyma

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49
Q

what is a common consequence of restrictive pulmonary diseases?

A

widespread lung fibrosis > increased lung elastic recoil > decreased lung compliance

lung smaller in vol, pt has to work harder to breathe against decreased compliance (lungs become like rubber)

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50
Q

explain the etiology/pathophys of respiratory distress syndrome

A

injury to type I pneumocytes + capillary endothelial cells in lungs

cytokines (TNF-a, IL-1) cause endothelial cells to secrete inflammatory molecules. this damage can increase risk of blood clotting, leaky endothelium (edema), and pneumocytes (I + II) die. alveoli collapse. macrophages attract and activate fibroblasts (make colalgen, leads to scar tissue > leads to restrictive lung disease)

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51
Q

common causes of respiratory distress syndrome

A

sepsis (most common), viral infections (pnemonia), burns, near-drowning, dialysis, lyme disease, pancreatitis

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52
Q

complications of respiratory distress syndrome

A 
pulmonary edema
fibrosis
infectin
poor pulmonary compliance
high mortality rate
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53
Q

clinical characteristics respiratory distress syndrome

A

SOB > respiratory failure
hypoxemia > cyanosis
edema (crackling rales sounds)

Dx:
acute (< 1 wk)
CXR/CT: opacities (white out) from pulm edema
PF ratio: RAO1/FIO2 <300mmHg
resp distress not caused by HF
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54
Q

idiopathic pulmonary fibrosis etiology

A

decreased respiratory compliance

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55
Q

pnemoconiosis etiology/types

A

dust inhalastion, upper lobes

inorganic: silicosis, asbestosis, complicated coal miners; dysnpea, incurable
organic: allergic type I IgE hypersensitivity; recover

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56
Q

sarcoidosis etiology

A

immune-mediated, widespread noncaseating granulomas

bell’s palsy, uveitis, granulomas, lupus pernio, interstitial fibrosis (restrictive), erythema nodosum, RA-like arthropathy, hypercalcemia, facial droop

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57
Q

sarcoidosis RF

A

african american females

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58
Q

sarcoidosis clinical characteristics

A

asymptomatic

large lymph nodes

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59
Q

what are obstructive pulmonary diseases and some characteristics of them?

A

airflow limitation from obstruction that is not fully reversible

lungs gradually fill with air behind obstruction + lung tissue is destroyed by chronic infection

lungs are overinflated (increased residual vol), large, missing a lot of tissue, and have increased compliance

difficult to have efficient comfortable breathing if lungs are fully expnanded when trying to overcome resistance in airways

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60
Q

what are the restrictive pulmonary diseases (names of them)

A

respiratory distress syndrome
idiopathic pulmonary fibrosis
pneumoconiosis
sarcoidosis

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61
Q

what are the obstructive pulmonary diseases (names of them)

A 
asthma
bronchiectasis
chronic bronchitis
emphysema
cycstic fibrosis
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62
Q

asthma etiology/patho

A

small bronchi abnormally responsive to stimuli causing constriction and inflammation

type I hypersensitivity from IgE, viral infections, pollution, food sensitivity, stress, aspirin

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63
Q

asthma complications

A

death - respiratory collapse and compromise

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64
Q

asthma clinical characteristics

A

cough, wheeze, dyspnea, hpoxemia, mucus plugging

elevated leukotriene D

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65
Q

bronchiectasis etiology

A

chronic dilation of bronchi from contraction of scar with secondary infection

usually lower part of lung

P aeruginosa

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66
Q

bronchiectasis complications

A

permanent dilation of airways

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67
Q

bronchiectasis clinical characteristics

A

foul smelling copious sputum usually in AM

68
Q

chronic bronchitis etiology

A

“blue boaters”
increased pCO2
lymphocytic and eosinophilic involvment (like asthma)

exacerbations typically caused by viral or bacterial infection

haemophilus influenzae, strep pneumonia, moraxella catarrhalis

69
Q

chronic bronchitis RF

A

smoking

70
Q

chronic bronchitis clinical characteristics

A

persistent cough with sputum x3 in at least 2 consecutive years

obesity, cor pulmonale, cyanotic

do not retain hypercapnic drive to breathe

71
Q

emphysema etiology

A 
"pink puffers"
normal pCO2 (chronic stimulation of EPO)
permanent dilation of part or all of the acinus with eventual destruction of alveolar walls
72
Q

emphysema RF

A

smoking (inactivated a1 antitrypsin > breakdown of lung tissue protein due to excess protease activity)

def of serum alpha 1 protease inhibitor in non-smokers

73
Q

emphysema complications

A

reactive polycythemia

74
Q

emphysema clinical characteristics

A

barrel chest, pursed lips, slow forced expiration
tympany on palpation
decreased breath sounds in lower lung fields
rely heavily on accessory muscles of inspiration (SCM, scalenes)

75
Q

acute bronchitis etiology

A

inflamed bronchial tubes, most caused by viral infection

rhinovirus, adenovirus, influenza A + B, parainfluenza

76
Q

epiglottitis etiology

A

swelling of epiflottis, blocking airflow

H influenzae, B-hemolytic strep

potentially lethal - imediate ER referral

77
Q

epiglottitis RF

A

children

78
Q

epiglottitis complications

A

airway obstruction

79
Q

epiglottitis clinical characteristics

A

sudden swelling of epiglottis and voal cords, toxin, drooling child, DO NOT OPEN THEIR MOUTH

xray: thumbprint sign

80
Q

laryngitis etiology

A

alone or as part of generalized respiratory infxn

81
Q

laryngitis RF

A

smoking

82
Q

laryngitis complications

A

carcinoma

83
Q

rhinitis etiology

A

infectious: commoncold viruses
allergic: hay fever, IgE mediated
chronic: superimposed bactterial infection on other two

84
Q

sinusitis etiology

A

(acute)

usually preceded by rhinitis, mixed normal flora

85
Q

sinusitis complications

A

can spread into orbit or penetrate bone > osteomyelitis

86
Q

pharyngitis etiology

A

group A strep

87
Q

tonsilitis etiology

A

group A strep

88
Q

pleural effusion etiology

A

fluid accumulation inside pleural cavity (b/w parietal and visceral pleura)

lymphatic, exudate (protein rich, inflammatory conditions) or transudate (protein poor, HF)

increased hydrostatic pressure/HF
increased vascular permeability, decreased oncotic pressure
increased negative intrapleural pressure
decreased lymphatic drainage

89
Q

pleural effusion RF

A

L-HF, chest infection

90
Q

pleural effusion clinical characteristics

A

tracheal deviation

Dx: decerased breath sounds, dullness to percussion, decerased tactile fremitus, CXR fluid in CVA (standing)

91
Q

compare chylothorax and hemothorax (etiology and sx)

A

chylothorax: lymph build up in pleural cavity (lympphatic system injury; truama, medical procedures)
hemothorax: blood build up in pleural cavity (blunt chest trauma, malignancy, PE)

sx (same for both): absent breath sounds on affected side, dullness to percussion (fluid in pleural space), diagnostic thoracentesis (lights criteria)

92
Q

obstructive atelectasis etiology

A

most common
collapse or incomplete expansion of acini
tumors, FB, mucus blockage
impaired gas exhange

airway obstruction prevents new air from reaching distal airways, old air resorbed

93
Q

types of atelectasis

A

obstructive (most common), compressive, contractive, adhesive

94
Q

obstructive atelectasis RF

A 
prematurity, smoking, obesity
lung disease (COPD, asthma, CF, bacterial infection)
anything leading to hypoventilation
chest wall abnormalities
surgery
95
Q

obstructive atelectasis complications

A

hypoxemia, pnemonia

96
Q

obstructive atelectasis clinical characteristics

A

SOB, cough, respiratory distress

Dx: reduced,absent breath sounds, crackles, dullness, deceased femitus, CXR, CT

97
Q

pleural fibrosis (asbestosis) etiology

A

ivory white, calcified, supradiaphragmatic and pleural plaques

98
Q

pleural fibrosis (asbestosis) RF

A

shipbuilding, roofing, plumbing

99
Q

pleural fibrosis (asbestosis) complications

A

risk of bronchogenic carcinoma, mesothelioma, caplan syndrome (RA + pneumoconiosis with intrapulmonary nodules), pleural effusions

100
Q

pleural fibrosis (asbestosis) clinical characteristics

A

affects lower lobes, asbestos bodies golden-brown, look like dumbells

101
Q

pneumothorax etiology

A

air or gas in the pleural cavity; visceral + parietal layers of pleura lose their vacuum

traumatic or spontaneous

102
Q

pneumothorax RF

A

spontaneous: tall, thin, young males and smokers

103
Q

pneumothorax complications

A

can lead to tension pneumothorax (air enters space but cannot exit)

104
Q

pneumothorax clinical characteristics

A

tympany to palpation

decreased breath sounds

105
Q

pulmonary edema etiology

A

any factor that causes pulmonary interstitial fluid pressure to rise from negative to positive

LHF, pnemonia, toxic gas inhalation, fluid overload/renal failure, decreased albumin, lymphatic obstruction

106
Q

pulmonary edema RF

A

L-HF

107
Q

pulmonary edema complications

A

can be intersitial edema or progress to alveolar edema (death)

108
Q

pulmonary emboli etiology

A

fat emboli: long bone fractures and liposuction

air emboli: nitrogen bubbles in ascending divers

amniotic fluid emboli: during labor or PP, but can be due to uterine trauma. rare.

109
Q

pulmonary emboli complications

A

large emboli - sudden death

amniotic fluid emboli - can lead to DIC, high mortality

110
Q

pulmonary emboli clinical characteristics

A

V/Q mismatch, hypoxemia, repiratory alkalaosis

sudden onset dyspnea, pleuritic chest pain, tachypnea, tachycardia

111
Q

pulmonary infarction etiology

A

lung tissue does not receive enough blood flow/oxygen

most commonly due to pulmonary thromboembolism
infection, inflammatory/infiltrative lung disease, pulmonary torsion, malignancy

112
Q

pulmonary HTN etiology

A

LHF, mitral stenosis, increased pulmonary vascular resistance, emboli, scleroderma

113
Q

adenocarcinoma etiology

A

peripheral, most common 1st degree lung cancer

114
Q

adenocarcinoma RF

A

females, non-smokers

115
Q

adenocarcinoma clinical characteristics

A

clubbing

116
Q

bronchial carcinoid etiology

A

central or peripheral

excellent prognosis, metastasis rare

117
Q

bronchial carcinoid clinical characteristics

A

sx due to mass effect or carcinoid syndrome (flushing, diarrhea, wheezing)

118
Q

laryngeal cancer RF

A

tobacco smoke

119
Q

laryngeal cancer complications

A

30-50% have metastasis at dx

120
Q

leukoplakia of larynx etiology

A

any hyperkeratonic lesion; benign or malignant, depends how much atypia is present

121
Q

leukoplakia of larynx RF

A

tobacco and alcohol

122
Q

mesothelioma etiology

A

malignancy of lungs and pleural cavity associated with asbestos

aggressive cancer that attacks mesothelium (lines organs, thoracic cavity, abdominal cavity)

involves mesothelial plaques that express calretinin (regulates calcium in the cell)

123
Q

mesothelioma RF

A

working with asbestos (paint, insulation, roofing)

smoking is NOT a RF

124
Q

mesothelioma complications

A

hemorrhagic pleural effusion (exudative), pleural thickening, poor prognosis

125
Q

mesothelioma clinical characteristics

A

chest pain, SOB, pleural effusions, bloody sputum, pneumothorax

biopsy of tumor - immunostained, rx with calretinin, “fried egg” shape
Psammoma bodies on histo
fibers most commonly found in lungs, liver, spleen, bowel

126
Q

nasopharyngeal carcinoma etiology

A

most common cancer of nasopharynx

EBV

127
Q

nasopharyngeal carcinoma RF

A

east asia, africa
males
fhx

128
Q

nasopharyngeal carcinoma complications

A

5 year survivial 60%

129
Q

polyps etiology

A

reactive nodes that rarely become cancerous

130
Q

polyps RF

A

vocal cords of heavier smokers or singers

131
Q

small cell carcinoma (squamous) etiology

A

Smoking

(oat cell), 20% of all lung cancers

132
Q

small cell carcinoma (squamous) RF

A

smoking

133
Q

small cell carcinoma (squamous) complications

A

early metastasis, secrete many hormones
pancoast tumor, rapid death
very aggressive

may produce ACTH (cushing syndrome), ADH (SIADH), or antibodies against presynaptic Ca2+ channels (Lambert-eaton myasthenic syndrome), or neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)

134
Q

non-small cell carcinoma (squamous) etiology

A

80% of lung cancers

135
Q

non-small cell carcinoma (squamous) RF

A

smoking

136
Q

congenital pulmonary disesaes

A

neonatal respiratory distress syndrome
pulmonary hypoplasia
bronchogenic cysts

137
Q

cystic fibrosis (CF) etiology

A

disease of exocrine glands which results in viscous secretions due to dysfunction of chloride channels

cystic fibrosis transmembrane conductance regulator gene (CFTR) on chromo 7 - defective chloride transport and increased sodium reabsorption

138
Q

cystic fibrosis (CF) RF

A

most lethal genetic disease in caucasion population

139
Q

cystic fibrosis (CF) complications

A

fatal before 40; pulmonary destruction, brought on by repeated infections

thick, mucus secretions block O2 exchange, increase susceptibility to infection (S aureus or H influenza)

140
Q

cystic fibrosis (CF) clinical characteristics

A

thick and viscous secretions in respiratory, GI, hepatobiliary, and reproductive tracts

wt loss, failure to thrive, nasal polyps, meconium ileus, statorrhea

dx: sweat test (elevated chloride levels) or genetic testing

141
Q

tracheoesophageal fisula etiology

A

abnormal connection, congenital

142
Q

atypical (interstitial) pneumonia etiology

A

primary (walking) pnemonia

mycoplasma
chlamydophilia pnemoniae
chlamydophilia psittaci
legionella viruses (RSV, CMV, influenza, adenovirus)
143
Q

atypical (interstitial) pneumonia clinical characteristics

A

diffuse patchy inflammation localized to interstitial areas at alveolar walls

CXR shows bilateral multifocal opacities

no exudate in alveolar spaces

144
Q

bronchopneumonia (lobular) etiology

A

patchy opportunistic infection

s pneumoniae
s aureus
h influenzae
klebsiella

145
Q

bronchopneumonia (lobular) clinical characteristics

A

Cough, fever, chills, and difficulty breathing

aspiration pneumonia usually on R upper lobe

acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving 1 or more lobe

146
Q

diphtheria etiology

A

pseudomembranous pharyngitis

corynebacterium diphtheriae

147
Q

diphtheria complications

A

LAD, myocarditis, arrhtyhmias

148
Q

diphtheria clinical characteristics

A

gray/white covering throat

preventable by vax

149
Q

fungal pnemonia etiology

A

histoplasma capsulatum

150
Q

lobar pnemonia etiology

A

strep pnemonia (+) diplococcus (rusty brown sputum)

klebsiella p (-) rods (alcoholics)

legionella

151
Q

lobar pnemonia clinical characteristics

A

intra-alveolar exudate > consolidation

152
Q

lung abscess etiology

A

cavity filled with pus

infected teeth, gums, tonsils, obstructed bronchus, cancer, septic pulmonary emboli

bacertiodes, fusobacterium, peptostreptococcus, s aureus

153
Q

lung abscess RF

A

pts predisposed to LOC (alcoholics, epileptics) or bronchial obstuction (cancer)

154
Q

lung abscess clinical characteristics

A

lung abscess 2 to aspirations most often in R lung

155
Q

pertussis etiology

A

whooping cough

bordetella pertussis

156
Q

pertussis complications

A

dangerous for infants

157
Q

pertussis clinical characteristics

A

violent uncontrollable cough

158
Q

respiratory synctial virus (RSV) etiology

A

viral infection

159
Q

respiratory synctial virus (RSV) complications

A

dangerous for infants and older adults

160
Q

respiratory synctial virus (RSV) sx

A

mild cold sx

161
Q

tuberculosis (TB) etiology

A

delayed hypertensitivity type IV

mycobacterium TB

caseating granulomas
primary + secondary reactivation > apices of lung/high O2
acid-fast bacilli

162
Q

tuberculosis (TB) complications

A

every organ system can have TB, usually starts in lungs. if not tx, can spread everywhere

163
Q

tuberculosis (TB) sx

A

night sweats, fever, wt loss

164
Q

goodpastures syndrome etiology

A

antibodies against basement membrance of kidneys and lungs

type II immune injury

165
Q

goodpastures syndrome sx

A

coughing up blood

166
Q

laryngotracheobronchitis etiology

A

parainfluenza virus

NPLEX I (2022) (20 decks)

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